Cognitive neuroscience of food intake control
26 important questions on Cognitive neuroscience of food intake control
Where in the body are these genes expressed?
The genes involved in obesity are mostly expressed in the central nervous system, not only in hypothalamus and pituitary gland that regulate appetite, but also in brain areas that are implicated in learning, reward, cognition, emotion and memory
What characterises overeating?
What role does reward play in our behaviour?
- ‘Wanting’ / Behavioral activation / invigoration – motivational transformation of previously learned stimuli, incentive salience into action (Berridge; Robbins & Everitt; Niv)
- ‘Liking’ – hedonic impact, pleasure (during consumption) (Wise)
- Learning – reward prediction and formation of associative reward links (Schultz; Dayan; Montague)
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Compulsive overeating (binge eating) =
eat a lot of food, only for comfort without hunger.
Measuring dopamine with PET
- Dopmaine-producing neuron
- Neuron in striatum
- measuring trait differences: dopamine receptor availability
PET and individual differences.
Striatal dopamine receptor availability is lower in
- amphetamine users versus non-users (volkow et al. 2001)
- obese vs. Normal-weight individuals
(Wang et al 2001 (replicated in 5 other studies, but also 3 contradictory studies)) smokers versus non-smokers
Both addiction and obesity are accompanied by abnormalities in the dopamine system
- Reduced dopamine receptor binding in the striatum
- Reduced dopamine synthesis capacity in the striatum
Overeating is also accompanied by strong craving / wanting elicited by food-related cues
- Obese, relative to normal-weight, individuals show increased food cue-related BOLD responses in the striatum
- Food cue-induced dopamine release in the striatum predicts the severity of the disorder in binge eaters
Can we use a behavioral training program to reduce this neural food cue reactivity?
- mindless eating
- inattentive, habitual, externally-triggered
- mindful eating
- awareness of taste, hunger, satiety and eating triggers
Mindful eating research
Interventions: Educational cooking training (ECT) program
8 weekly group sessions (2.5h); 0.5h homework a day
Model-based vs model-free learning
- Goal-directed -> U-shape
- Methamphetamine dependents show decreased
- BED -> main effect of reward
- Obese -> U-shape
- HV -> bigger w-term.
- For the OCD and Meth -> significant effect
- similar to meth-dependents, binge eaters show decreased model-based learning. Obese individuals do not differ from controls.
Experiment: habitual versus goal-directed behaviour:
- standard
- congruent
- incongruent
If you are goal-directed -> incongruent you get totally confused.
Alcohol dependents show increased responses in posterior putamen during habitual responding
Fixed response-outcome association
Second phase: selective satiation: Eat as much as you can
Third phase: extinction test. "no outcomes, but computer counts and you get outcomes afterward.
change your behaviour dependent on which food you're salivated on.
Obesity is accompanied by reduced adaptation of food choices after selective satiation, i.e. reduced goal-directed control
Habitual behaviour is mediated by the posterior putamen showing:
- Increased BOLD responses during habitual behaviour in addiction
- Increased gray matter volume in obesity
Attentional bias - stroop task
It depends on your mindset how you respond to it -> if you're hungry you are slower.
Drug users have greater attentional bias to drug words than controls
-> PFC activity
Obese children in stroop task
- Obese children were slower in naming the color of food words than those of control words, i.e. They showed an attentional bias to food cues
- this effect was absent in lean children
Result: stroop task in fMRI
Obesity is accompanied by reduced dorsolateral prefrontal cortex responses during overcoming attentional bias
Both addiction and obesity are characterized by
Do you think drug addicts show more or less differences in dopamine release before versus after drug use?
The ‘consumption’ of a drug leads to less changes in the striatum in addicts than in controls
FMRI and reward consumption: Consuming milkshake versus tasteless solution
- The consumption of a milkshake leads to less changes in the striatum in people with a high than a low BMI especially when carrying a risk allele of a dopamine gene
- Decreased striatal activity predicted future weight gain in the risk allele carriers
Neurocognitive parallels between addiction and obesity:
- decreased availability of dopamine receptors and decreased dopamine
synthesis (PET) - – increased sensitivity to reward cues (fMRI)
– Increased ‘habits’ at the expense of goal-directed/model-based behaviour
• accompanied by increased posterior putamen responses/volume – Decreased cognitive control (e.g. increased attentional bias)
• accompanied by prefrontal cortex differences
– decreased sensitivity to consumption of reward (PET and fMRI)
Addiction models of obesity:
- Increased striatal responses to reward anticipation reflect heightened reward sensitivity
- decreased striatal responses to reward receipt reflect reduced reward-related learning rather than reward deficiency
If we regard overeating as an addiction, what would be the consequences for treatment or prevention?
- Treatment: If overeating resembles addiction, similar treatment strategies could be used
- pharmacological/behavioral therapies that target the striatal dopamine system to reduce cue-induced habitual food/drug seeking
- pharmacological/behavioral therapies that target the frontal cortex to enhance goal-directed control
- Prevention: If certain foods – high in fat, salt and sugar – are similar to addictive substances, policy makers could
- tax those foods, similar to tobacco and alcohol
- prohibit those foods, similar to cocaine and heroin
How convincing is the addiction model of obesity?
Evidence for compulsive overeating (and lack of goal-directed control?) Mostly comes from binge eating disorder
- binge eating disorder is not the major cause of obesity/excessive eating -> its prevalence is much lower than obesity
Withdrawal symptoms during dieting?
- Dysphoria and distress?
- no shakes and sweats
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