11. Brain and Food

• phase after eating

• anabolic phase (storage molecules are synthesized)

• phase between meals

• storage molecules are broken down

not enough energy is taken up to meet the needs of the body

intake & storage of energy consistently exceeds the energy usage

• underneath thalamus in walls of 3 brain ventricle

• connected with pituitary (hormoe releasing)

Homeostasis (regualtion of body temperature, compostition of blood and fluids..)

1. periventricular - receives input from other zones

2. medial - secretes hormones into blood stream

3. lateral - secretes hormones into blood stream

Posterior Pituitary (Neurohypophysis):

• Releases hormones directly into the blood

• Hormones are produced in the hypothalamus

• Neurons from the hypothalamus project into the posterior pituitary

• oxytocine

Anterior Pituitary (Adenohypophysis):

• Produces its own hormones

• Regulated by releasing hormones from the hypothalamus (e.g. CRH, TRH)

• Hypothalamic hormones arrive via the hypophyseal portal system

• thyreotropin

sympathic:

• activity

• nordadrenaline

parasympathetic:

• rest

• acetylcholine

• enteric nervous system

• embedded in the inner walls of esophagus, stomach, gut, pancreas & gall bladder

• # neurons = # neurons spinal cords

• 
  

• because of the more or less autonomous functions that include sensory neurons connecting to motor neurons that control gut movements but alsp the production of enzymes

• integrated with CNS via sympathetic and parasympathetic fibers

• Leptin is a hormone produced by fat cells when they are filled with lipids.

• Sensor location: Hypothalamic nucleus arcuatus (ARC)

• It signals the brain that the body has enough energy stored (fat).

• In ob/ob mice, the leptin gene is defective, so the brain does not get the signal – leading to overeating and obesity.

• Giving external leptin to ob/ob mice makes them slim again.

• In humans, true leptin deficiency is rare.

• Most obese people have enough or even high leptin, but their brain may be resistant to it.

• Therefore, leptin treatment usually does not help with common obesity in humans.

to varying levels of leptin in blood stream

disruption of food intake - anorexia

overeating and accumulation of food

• When the stomach is empty, it releases ghrelin, a hormone that stimulates hunger.

  → Ghrelin activates NPY/AgRP neurons in the nucleus arcuatus, which promote feeding.

• During and after eating, satiety signals (e.g. stomach stretching, nutrients, hormones like CCK, insulin) are released.

  → These inhibit appetite and end the meal.

1. gastric distension

2. cholecystokinin (cck) releas

3. insulin

leptin and insulin

• Two neuron populations in the arcuate nucleus (ARC) detect hormonal signals (e.g. leptin, insulin).

• These neurons control the hypothalamic melanocortin system via the MC4 receptor in the lateral hypothalamus.

• This system influences hunger and energy expenditure.

1. Arcuate nucleus (ARC): – Acts as the sensor for hormones like leptin, ghrelin, insulin – Contains two key neuron types:

   • NPY/AgRP neurons → activated by hunger, stimulate feeding

   • POMC/CART neurons → activated by satiety, reduce feeding

2. Paraventricular nucleus (PVN): – Activated by POMC/CART signals – Promotes satiety and metabolism via hormones like ACTH, TSH

3. Lateral hypothalamus: – Activated by NPY/AgRP signals – Drives hunger and food-seeking behavior

The ARC receives hormonal input, then directs signals either to PVN (to suppress hunger) or to the lateral hypothalamus (to increase feeding).

1. Hindbrain:

   – Controls meal size

   – Receives signals via vagal afferents and circulating hormones – Coordinates ingestion, digestion, and absorption

2. Hypothalamus:

   – Central for the drive to eat

   – Modulates autonomic and endocrine systems (e.g. hormone release, organ function)

3. Cortico-limbic system (cortex, basal ganglia, hippocampus, amygdala):

   – Controls the emotional, cognitive, and decision-making aspects of eating

   – Involved in reward, memory, habits, and impulse control

orbitofrontal cortex & amygdala

insule processes

Nucleus accumbens & dorsal striatum

lateral hyppthalamus

They show that dopamine is critical for the motivation to seek food ("wanting"), but not necessary for enjoying food("liking").Rats that could self-stimulate dopamine release preferred stimulation over eating, while rats with damaged dopamine pathways still liked food when offered, but stopped seeking it.

1. The brain becomes less sensitive to the reward from "yummy" food over time.

2. This is shown by a higher reward threshold — more stimulation (or more food) is needed to feel the same pleasure.

3. As a result, overconsumption can lead to reward deficits, driving the animal to eat even more to compensate.

4. This creates a vicious cycle of eating and weight gain that worsens energy imbalance.

• D2 receptors are part of the brain's reward system and help regulate dopamine signaling.

• They act like a brake, preventing overstimulation from rewards like food.

• In obesity, D2R levels are often reduced, making food less rewarding.

• As a result, individuals may eat more to reach the same level of pleasure, contributing to overeating.

• This mechanism is similar to addiction.

• Carbohydrates increase the uptake of tryptophan, the precursor to serotonin, into the brain.

• Serotonin levels rise during and after a meal, especially if it's rich in carbs, which can improve mood.

• This explains the soothing effect of foods like pasta or sweets, especially under stress, when serotonin is low.

• Serotonin is key for mood regulation, and some drugs that boost serotonin also suppress appetite.

• However, such drugs (e.g. dexfenfluramine) had serious side effects and were withdrawn.

• The central nucleus (CN) of the amygdala is involved in evaluating food and guiding threat avoidance.

• Two key cell types in the CN have opposing roles:

  • PKC-delta cells detect bad or harmful food and suppress eating

  • Htr2a cells promote appetitive behavior and increase food intake

• Optogenetic experiments show that activating Htr2a cells makes food more rewarding, while inactivating them reduces consumption

• These cells receive input from areas processing taste, body signals, and energy balance and send output to appetite-related brain regions

Activation of neurons in the deep cerebellar nuclei increases the baseline dopamine level, which reduces the typical phasic dopamine spike that occurs when food is presented.As a result, food feels less rewarding, which leads to reduced food intake.This suggests the cerebellum acts as a “brake” on reward-driven eating behavior.

It refers to the interaction and conflict between two systems:

• Bottom-up (metabolic drive): Signals from the body (e.g. hunger, leptin) regulate food intake to maintain energy balance and body weight.

• Top-down (hedonic/cognitive drive): Emotions, thoughts, and decisions (e.g. dieting, emotional eating) can override metabolic signals.

Eating behavior depends on which system dominates — the body’s needs or the brain’s desires and choices.

• biological factors

• psychological factors

• social factors

• While there is no single clear neurobiological model of AN, several findings suggest imbalances in brain chemistry and function.

• AN patients often show increased serotonin (5-HT) and decreased dopamine (DA) activity:

  • Serotonin is linked to inhibition, anxiety, and self-control

  • Dopamine is linked to reward and motivation

• This imbalance may contribute to symptoms like anhedonia, perfectionism, and self-denial.

• Brain imaging shows altered activation in areas like the insula (taste processing), ventral striatum, and prefrontal cortex.

• AN patients may even show stronger reward responses to food than others, but this doesn’t translate into eating behavior — possibly due to overriding inhibitory control.

• In BE, impulsive and fast decisions about food are linked to increased activation in brain regions involved in reward and valuation:

  • Medial prefrontal cortex (mPFC)

  • Medial orbitofrontal cortex (OFC)

  • Ventral striatum

  • Left posterior hippocampus

  These areas process immediate rewards, with less involvement of executive control.

  This supports the idea that BE shares features with impulse control disorders and addictions – driven by reward sensitivity rather than long-term planning.

Yes. A healthy microbiome supports normal brain function.Dysbiosis (microbial imbalance), often caused by poor diet, is linked to anxiety, depression, stress sensitivity, and cognitive issues.Probiotics may help improve these symptoms.

Studies show that men activate the orbitofrontal cortex (OFC) more strongly when viewing food while hungry.This activation is linked to a reduction in hunger, suggesting greater cognitive control over food desire.Women showed less OFC activation, possibly indicating a lower ability to suppress hunger, which may contribute to gender differences in obesity risk.