Gut hormones in Addiction Flashcards

1
Q

What are the key factors involved in regulating eating behaviour?

A

External cues (sight, smell, taste)

Internal cues (hormones, autonomic nervous system, gut and fat tissue)

Psychological cues (eating behaviour, reward sensitivity, food preference).

This system is under homeostatic control.

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2
Q

What are some brain regions activated in response to food cues?

A

Amygdala- emotional respones.

Nucleus accumbens- reward expectancy, motivation ,drive

Dorsal striatum- habitual behaviours, learned association

Insula- taste cortex, decision making, multimodal integration.

Orbitofrontal cortex- salience. Repeated food tastes less pleasant as its activation decreases.

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3
Q

How do you measure food responses?

A

fMRi, measure CBF.

Show photos of healthy and unhealthy food. (low energy and high energy).

Rate how appealing the pictures are.

You can see network of activation and identify regions of interest (ROIs).

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4
Q

What were the ROIs identified?

A
Orbitofrontal cortex
Amygdala
Nucleus accumbens
Putamen
Anterior insula
Caudate
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5
Q

What is the food reward in obesity?

A

In response to food cues, people with obesity have heightened response.

Giving the food gives less activity with a higher BMI in the dorsal striatum and caudate.

The ability to suppress desire is impaired.

Different studies show different activation in obese vs thin patients.

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6
Q

What were the problems with the review that said obesity is not a measure of food reward?

A

BMI is not a measure of adiposity.

Not a measure of hormonal mediators.

There is heterogeneity of obese phenotype.

BMI not a behavioural measure

Source of obese patients

Nutritional state (fasted/fed)

Inter- individual differences in food preference

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7
Q

What are some criteria for food addiction?

A

Substance taken in larger amount and for longer period than intended.

Persistent desire to quit/

Important social activities reduced.

Tolerance

Withdrawal symptoms (taken substances to relieve withdrawal)

Clinical significant impairment or distress.

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8
Q

How would you assess food addiction?

A

Yale food addiction scale. 25 questions.

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9
Q

What was found on a study in imaging the brain in people with high scores on the scale?

A

In anticipation of receiving a chocolate milkshake, there was increased activation in the vmPFC and amygdala.

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10
Q

Are we unnecessarily medicalising food addiction?

A

Finlayson considered addiction as just hedonic overeating- that is just a summation of various eating disorders- emotional eating, uncontrolled eating, binge eating, hedonic heating. We NEED food to survive, but we don’t need drugs to survive.

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11
Q

What is the difference in food bias when you are fasted?

A

You are biased towards high energy foods- it gives an increased activation signal.

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12
Q

How does the brain know you have eaten?

A

Hormones.

Peripheral signals when you eat from intestine- PYY, GLP-1.

Increased weight- leptin increases.

Losing weight- leptin and hormones go down.

Fasting- ghrelin increases.

These signals are proportional to the amount we have eaten. Act on brainstem/hypothalamus/indirectly through vagus nerve?

THESE CIRCUITS ALTER THE RESPONSES TO FOOD CUES.

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13
Q

What is the action of injected ghrelin and GLP-1?

A

Ghrelin mimics fasting, and increases brain hedonic response to food- increases appeal.

Giving GLP-1 reduced response to food cues.

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14
Q

What was the effect of gastric bypass and banding surgery?

A

Bypass had a large effect on weight loss. Bypass stomach- undigested food straight to small bowel, so huge increases in PYY and GLP1. Less response to food cues and activation in response to taste compared to banding patients.

Banding had a lower effect- increases vagal signals by stretching stomach.

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15
Q

How did somatostatin work?

A

Supposed to supress PYY and GLP-1, to reverse the bypass the procedure.

Went down more in the bypass than the banding because they were higher in the bypass. Increased reactivity and appeal of food cues.

Therefore you can reverse the reduced food reward.

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16
Q

What other contributions might these gut hormones have?

A

Reduces stress and monetary stress. HAs a role in other behaviours.

17
Q

What effect does ghrelin have?

A

It mediates the stress induced response to food.

Knocking out the receptor reduces the reward

18
Q

What was found when using the hormones in food reward in drugs?

A

Exerts effects on the mesolimbic system- reduces reward response to other drugs.

Analogue GLP-1 Reduces alcohol intake, food intake

Ghrelin increases alcohol intake ad reward in mice.

19
Q

What can the inactive ghrelin do to the active version?

A

It can block it. Desacyl ghrelin analogue reduced body wight in overweight/obese humans.

Reduced the intake of sugars in a buffet meal.

20
Q

What are the aims of the GHADD study?

A

Investigate if acute desacyl ghrelin or GLP-1 analogue (Exendin-4) administration reduces brain reward response with high energy food, cigarettes or alcohol, and monetary reward anticipation.

Addictive behavioural components e.g negative emotional reactivity, compulsivity, attentional bias.

Appetite and food taste hedonics.

fMRI (cue reactivity), questionnaires on appetite and craving, computer tasks, food picture task.

Preliminary findings: Reducing response to food and alcohol and cigarettes mediated by Exendin-4.