ELM-4: Hedonism

What is the Homeostatic Regulation of Feeding

• The interplay between normal hunger and satiety

• Hedonic eating occurs with food that provides pleasure

• Negative reinforcement promotes eating to remove the negative valence of hunger

• Positive reinforcement of feeding produces a positive valence or incentive salience → linked to the motivation of wanted and is linked to reard

• Homeostatis and reward are not mutally exclusive → can interact

What is the effect of 2-deoxyglucose and THC on feeding behavior in rats, and how does it relate to homeostatic and hedonic drives to ea

• 2-deoxyglucose is a glucose analogue that cannot be phosphorylated by hexokinase, preventing ATP production.

• Injection of 2-deoxyglucose into rats increases food intake, as glucose is not taken up and produces negative valence, driving homeostatic feeding.

• A similar feeding response is observed with THC (the active cannabis ingredient), but it is effective only in pre-fed rats, when no more energy is needed.

• If rats are not pre-fed, THC does not increase food intake.

What is Hedonism in Feeding?

• It is the motivation to eat based on the reward value of food and is dependent on cognitive brain regions, where tasty food induces positive valence and leads to eating.

• Pudding after-meal effect is a hedonic drive to eat, driven by the reward value of food

What did fMRI studies show about the brain activity of rats following hemopressin injection and how does cannabis influence feeding motivation?

• Hemopressin, a novel peptide, increases food intake by activating homeostatic systems.

• fMRI with BOLD mapping was used to track brain activity in rats following systemic hemopressin injection, showing activation in the Ventromedial Hypothalamus (VMH).

• Statistical maps from group studies show specific brain regions activated before and after hemopressin injection, highlighting areas involved in homeostatic feeding.

What did fMRI studies about the brain activity of rats following AM251 injection?

• AM251 is a drug that activates cannabinoid receptors, and activates brain areas including the hypothalamus, ventral tegmental areas, nucleus accumbens, orbitofrontal cortex, and prefrontal cortex.

• These areas are part of the brain's reward circuitry, indicating that cannabis affects motivation to eat by influencing higher reward pathways.

What are the two aspects of motivation to eat and how do they differ?

• Liking: Experienced when tasting something pleasant; an innate, survival-based response evoked by food.

  • Associated with hedonic hotspots in the reward structures of the brain, but does not involve dopaminergic signalling.

• Wanting: Motivated by the desire to eat, related to the anticipation of pleasure and reward.

  • Linked to dopaminergic signalling (reward-driven motivation) and the incentive salience to eat.

• Liking involves pleasure from tasting food, while wanting is related to incentive salience (desire for the food).

How Can Liking Responses to Taste be Measured in Animals?

• Using Innate orofacial responses: e.g., tongue protrusion in response to sweet tastes (e.g., sucrose), indicating positive reactions.

  • seen in non-human primates and rodents

  • IOR requires the brainstem; to modify these responses postively or negatively, higher brain regions are required

• Negative reactions: E.g., gapes and head shakes in response to bitter tastants (e.g., quinine), indicating aversive responses.

• These responses are innate and help with survival.

How Can Taste Responses Be Modified?

• Modification through experience

  • Conditioned taste aversion: Pairing a neutral/positive taste (e.g., sweet taste) with something aversive (e.g., lithium chloride or GDF15) can induce negative responses.

  • Learned associations: Tastes can become aversive or pleasant depending on conditioning.

• Brain Stimulation

  • Stimulation of specific brain regions, involved in pleasure-related responses to food (hedonic hotspots) with opioids and cannabinoids to enhance taste reactivity and pleasure

What is the function of the mesolimbic dopamine (DA) reward pathway?

• It links DA neurons in the midbrain with the forebrain's limbic system.

• Main function is to signal the value or incentive salience of rewards – it indicates how much we want to repeat a rewarding stimulus.

• The system evolved to reinforce behaviours that support survival, such as sex and eating energy-dense foods (positive valence)

• Pleasurable stimuli (e.g., sweet or fatty food) trigger the release of DA from the midbrain (VTA), reinforcing the behaviour.

• Drugs of abuse and substances like cannabis, cocaine, and amphetamines flood the forebrain with DA, amplifying feelings of reward.

How Is Postiive Reinforcement Demonstrated Through Operant Conditioning?

• Operant conditioning is used in experimental rodents, where the rats work for the reward of cocaine by pressing a lever

• They will press the level more for the reward of sucrose

What does PET scanning reveal about brain activity in obese individuals, particularly regarding dopamine (DA) receptors?

• PET Scan with radioactive glucose shows similar overall brain activity in both normal-weight and obese humans.

• PET Scan with Radiolabelled DA Agonists to measure binding at DA receptors.

  • Obese Patients have a decreased number of DA receptors in the forebrain, particularly in the nucleus accumbens.

• There is a negative correlation exists between DA agonist binding and BMI, suggesting a downregulation of DA receptors.

• Obese individuals may no longer experience the same reward from food, and so require more food to satisfy their drive

Why are Homeostatic and Hedonistic Eating Said To Be ‘inextricably linked’?

• Homeostatic and hedonistic eating are inextricably linked, with the salience or reward value of food dependent on nutritional status

  • Food looks and tastes better when we are hungry

• Food pictures produce a much stronger activation of reward areas in the brain compared to non-food pictures, when hungry

• When subjects are fed the differnce is less pronounced→ both pictures induce little activity in reward centres

What did the functional MRI study on leptin-deficient children reveal about food motivation and brain activation?

• Leptin-deficient individuals have a constant drive for food, even after eating.

• Their brain activity in reward areas, like the nucleus accumbens and striatum, is stronger when shown food pictures, regardless of recent food intake.

  • subjective score for food pictures>non-food pictures even after eating; still prefer food items on a visual analogue scale

• The difference in brain activation between food and non-food pictures shows significant differences in reward areas, but not in areas just involved in vision.

What did the functional MRI study on leptin-deficient children reveal after leptin treatment?

• After 7 days of leptin treatment, there was no significant change in body weight, but the children's responses to food pictures changed.

  • The reward areas in the forebrain (dopamine-driven) no longer showed stronger activation for food pictures → after feeding, children no longer gave food pictures high liking scores

  • no difference in the activation of reward areas of the forebrain that recieved DA input between food and non-food pictures → lost some of their motivation for food

  • No obvious change in the visual cortex

• The study suggests leptin signals body adiposity and can affect higher cognitive function, and confirms that food is more rewarding when in a negative energy balance or are hungry

Why is It Believed That We Don’t Bcome Addicive to Certain Types of Food

• While we may crave certain types of food, e.g. sugar, there is no reliable evidence for this phenomenon

• When craving and then eating foods like chocolate will activate reward centres, causing you to want to eat more, you don’t become dependent on it, and don’t exhibit withdrawal if not consumed

Why is it an evolutionary benefit to respond to decreased energy stores with increased hunger?

• When our energy stores decrease, hunger and homeostatic feeding are triggered (increase). This response has evolutionary benefits → protection against low body weight .

• It allows animals to stock up on energy-dense food when available (e.g., ripe fruit), ensuring survival during lean times and helping prepare for winter or migration by storing energy.

• Wild animals and early humans couldn't afford to become too fat, as excess weight would make foraging and escaping predators difficult.

  • There was an evolutionary pressure to avoid putting on too much weight for survival.

How Has the Modern Environment Contributed to the Obesity Epidemic?

• Unlike wild animals and early humans, evolutionary pressures to keep weight down have been removed in modern times.

  • We now live in warm, safe homes and have easy access to food (e.g., drive to supermarkets).

• The modern environment is obesogenic, with continuous exposure to highly palatable foods which are easy to obtain without effort, contributing to the obesity epidemic.

  • This combination of easy access to food and a lack of necessity to work for it is driving the rise in obesity.