Effects of Negative Affect in Individuals With Binge Eating Episodes
| Status: | Recruiting |
|---|---|
| Conditions: | Obesity Weight Loss, Psychiatric, Psychiatric, Eating Disorder |
| Therapuetic Areas: | Endocrinology, Psychiatry / Psychology |
| Healthy: | No |
| Age Range: | 18 - 55 |
| Updated: | 4/17/2018 |
| Start Date: | February 1, 2018 |
| End Date: | October 31, 2022 |
| Contact: | Megan E Shott, BS |
| Email: | megan.shott@ucdenver.edu |
| Phone: | 720-777-4026 |
Neural Effects of Negative Affect on Food Choices and Reward In Individuals With Binge Eating Episodes
Binge-eating is characterized by recurrent episodes of eating large amounts of - typically
high calorie - foods, eating much more rapidly than normal and until feeling uncomfortably
full, as well as feeling disgusted with oneself, depressed, or guilty after those episodes.
Two eating disorders are characterized by binge-eating as central diagnostic criteria,
binge-eating disorder (BED) and bulimia nervosa (BN). Binge-eating episodes in BN, but not
BED, are typically followed by compensatory mechanisms such as self-induced vomiting, and BED
is typically associated with obesity, while BN is not. Behavior studies such as ecological
momentary assessment (EMA) research of affect in an individual's naturalistic environment
have shown that negative affect and negative urgency (the tendency to act rashly when
distressed) often precede binge-eating.
The Investigators want to answer the following questions: Can negative affect in BN and BED
be linked to 1) altered dopamine related brain reinforcement learning, 2) to food value
computation and cognitive control circuit function, and 3) can dopamine related brain
activation predict eating and negative affect, indicating a brain based neurobiological
vulnerability. Answering those questions will help to define binge-eating based on regulation
of brain reward, cognition, and emotion circuit function and point toward potential
psychopharmacological interventions to normalize brain function and behavior.
high calorie - foods, eating much more rapidly than normal and until feeling uncomfortably
full, as well as feeling disgusted with oneself, depressed, or guilty after those episodes.
Two eating disorders are characterized by binge-eating as central diagnostic criteria,
binge-eating disorder (BED) and bulimia nervosa (BN). Binge-eating episodes in BN, but not
BED, are typically followed by compensatory mechanisms such as self-induced vomiting, and BED
is typically associated with obesity, while BN is not. Behavior studies such as ecological
momentary assessment (EMA) research of affect in an individual's naturalistic environment
have shown that negative affect and negative urgency (the tendency to act rashly when
distressed) often precede binge-eating.
The Investigators want to answer the following questions: Can negative affect in BN and BED
be linked to 1) altered dopamine related brain reinforcement learning, 2) to food value
computation and cognitive control circuit function, and 3) can dopamine related brain
activation predict eating and negative affect, indicating a brain based neurobiological
vulnerability. Answering those questions will help to define binge-eating based on regulation
of brain reward, cognition, and emotion circuit function and point toward potential
psychopharmacological interventions to normalize brain function and behavior.
Specific Aim 1: To test on two study days, one neutral affect and one negative affect day
(affect induction) whether negative affect alters brain reinforcement learning in a dopamine
system anchored taste reward learning paradigm (a task for prediction error and reward value
computation) during functional magnetic resonance brain imaging (fMRI). Hypothesis 1: In
response to negative and compared to neutral affect induction, binge eating disorder (BED)
and bulimia nervosa (BN) will show increased positive prediction error and taste valuation
regression with striatum and insula activation compared to obese (OB) and healthy control
(HC) groups. This will be an indication that negative affect excessively activates dopamine
related reward circuit response in BED and BN. Specific Aim 2: To study during a food choice
paradigm the effects of negative affect on brain circuitry for cognitive control and food
valuation. Specific Aim 2a: To study brain circuitry for food valuation in response to
neutral or negative affect. Hypothesis 2a: In response to negative and compared to neutral
affect induction, BED and BN groups will show greater striatal activation when rating food
for taste, compared to OB and HC. This will indicate that BED and BN are associated with
increased affect-regulated motivation to approach high calorie foods after negative affect
induction and compared to OB and HC. Specific Aim 2b: To study brain control circuitry during
food choice in response to neutral or negative affect. Hypothesis 2b: In response to negative
and compared to neutral affect induction, BED and BN groups will show increased insula and
striatal, but lower dorsolateral prefrontal cortex (DLPFC) activation compared to OB and HC
groups. This will indicate that negative affect activates automatic food reward circuit
response, but reduces cognitive control circuitry during food choice in BED and BN. Specific
Aim 3: To test whether brain activation predicts food intake or negative affect. Specific Aim
3a: To test whether brain activation can predict food intake during a post-fMRI scan test
meal. Hypothesis 3a: On negative- versus neutral-affect days, BN and BED will select more
food in a post-fMRI scan test meal; lower DLPFC and higher striatal activation during food
choice, and higher (prediction error) taste reward activation in insula and ventral striatum
will predict greater food intake. Specific Aim 3b: To test whether brain activation during
reward learning or food choice predicts negative affect measured by EMA on the study day, as
well as measured between study days in the individual's naturalistic environment. Hypothesis
3b: Insula, ventral striatum and DLPFC activation (taste prediction error task, food choice
task) during the negative affect condition will predict the intensity of negative affect
immediately after fMRI, as well as intensity of negative affect episodes during the days
between brain scans in the individual's naturalistic environment, suggesting a
neurobiological affective vulnerability.
(affect induction) whether negative affect alters brain reinforcement learning in a dopamine
system anchored taste reward learning paradigm (a task for prediction error and reward value
computation) during functional magnetic resonance brain imaging (fMRI). Hypothesis 1: In
response to negative and compared to neutral affect induction, binge eating disorder (BED)
and bulimia nervosa (BN) will show increased positive prediction error and taste valuation
regression with striatum and insula activation compared to obese (OB) and healthy control
(HC) groups. This will be an indication that negative affect excessively activates dopamine
related reward circuit response in BED and BN. Specific Aim 2: To study during a food choice
paradigm the effects of negative affect on brain circuitry for cognitive control and food
valuation. Specific Aim 2a: To study brain circuitry for food valuation in response to
neutral or negative affect. Hypothesis 2a: In response to negative and compared to neutral
affect induction, BED and BN groups will show greater striatal activation when rating food
for taste, compared to OB and HC. This will indicate that BED and BN are associated with
increased affect-regulated motivation to approach high calorie foods after negative affect
induction and compared to OB and HC. Specific Aim 2b: To study brain control circuitry during
food choice in response to neutral or negative affect. Hypothesis 2b: In response to negative
and compared to neutral affect induction, BED and BN groups will show increased insula and
striatal, but lower dorsolateral prefrontal cortex (DLPFC) activation compared to OB and HC
groups. This will indicate that negative affect activates automatic food reward circuit
response, but reduces cognitive control circuitry during food choice in BED and BN. Specific
Aim 3: To test whether brain activation predicts food intake or negative affect. Specific Aim
3a: To test whether brain activation can predict food intake during a post-fMRI scan test
meal. Hypothesis 3a: On negative- versus neutral-affect days, BN and BED will select more
food in a post-fMRI scan test meal; lower DLPFC and higher striatal activation during food
choice, and higher (prediction error) taste reward activation in insula and ventral striatum
will predict greater food intake. Specific Aim 3b: To test whether brain activation during
reward learning or food choice predicts negative affect measured by EMA on the study day, as
well as measured between study days in the individual's naturalistic environment. Hypothesis
3b: Insula, ventral striatum and DLPFC activation (taste prediction error task, food choice
task) during the negative affect condition will predict the intensity of negative affect
immediately after fMRI, as well as intensity of negative affect episodes during the days
between brain scans in the individual's naturalistic environment, suggesting a
neurobiological affective vulnerability.
Inclusion Criteria:
Healthy Controls
- Age 18-55 years old
- Healthy body weight between 90 and 110 % average body weight since puberty.
- Regular monthly menstrual cycle (if applicable)
- Edinburgh Handedness Inventory Revised (EHI-R) LQ* score > +200
Obese
- Age 18-55 years old
- Current body mass index (BMI) > 30 kg/m2.
- Stable food intake regimen in previous 4 weeks.
- Edinburgh Handedness Inventory Revised (EHI-R) LQ* score > +200
- Obese for at least one year
Binge Eating Disorder
- Age 18-55 years old
- Edinburgh Handedness Inventory Revised (EHI-R) LQ* score > +200
- DSM 5 diagnosis of Binge Eating Disorder A. Recurrent episodes of binge eating B.
Binge eating episodes are associated with three (or more) of the following
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically hungry.
4. Eating alone because of embarrassment.
5. Feeling disgusted with oneself, depressed, or very guilty after overeating. C.
Marked distress regarding binge eating is present. D. At least once a week for 3
months. E. The binge eating is not associated with the recurrent use of
inappropriate compensatory behavior.
Bulimia Nervosa
- Age 18-55 years old
- Edinburgh Handedness Inventory Revised (EHI-R) LQ* score > +200
- DSM 5 diagnosis of Bulimia Nervosa A. Recurrent episodes of binge eating Eating, in a
discrete period of time, an amount of food that is definitely larger than most people
would eat during a similar period of time and under similar circumstances.
A sense of lack of control over eating during the episode. B. Recurrent inappropriate
compensatory behavior in order to prevent weight gain, such as self-induced vomiting;
misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.
C. At least once a week for 3 months. D. Self-evaluation is unduly influenced by body shape
and weight.
Exclusion Criteria:
Healthy Controls
- Current pregnancy or breast feeding within last 3 months
- First degree relative with current or past eating disorder
- Current Medications other than BCP or IUD
- Past or present Axis I psychiatric disorder including substance or alcohol use
disorder as determined through SCID-5 clinical interview
- First degree relative with an eating disorder
- Major Medical illness
- Recent history of suspected substance abuse or a lifetime history of psychostimulant
abuse and/or dependence
- Metal implants or braces
Obese
- Current pregnancy or breast feeding within last 3 months
- First degree relative with current or past eating disorder
- Current or previous eating disorder diagnosis
- Current Medications other than BCP or IUD
- Past or present Axis I psychiatric disorder including substance or alcohol use
disorder as determined through SCID-5 clinical interview
- Major Medical illness
- Recent history of suspected substance abuse or a lifetime history of psychostimulant
abuse and/or dependence
- Metal implants or braces
Binge Eating Disorder
- Pregnancy or breast feeding within last 3 months
- Lifetime history of bipolar disorder or psychosis
- Use of a psychostimulant within the prior 6 months
- Recent history of substance abuse or dependence (except for alcohol and cannabis use)
- Major Medical illness
- Metal implants or braces
Bulimia Nervosa
- Pregnancy or breast feeding within last 3 months
- Lifetime history of bipolar disorder or psychosis
- Use of a psychostimulant within the prior 6 months
- Recent history of substance abuse or dependence (except for alcohol and cannabis use)
- Major Medical illness
- Metal implants or braces
We found this trial at
1
site
Aurora, Colorado 80045
Principal Investigator: Guido KW Frank, MD
Phone: 720-777-4026
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