PYB304 Motivation: Hunger, Eating, & Health Notes

Eating & Digestion

• Digestion provides energy in the form of:
  • Lipids (fats)
  • Amino acids
  • Glucose
• Energy intake is infrequent, so energy is stored as:
  • Fats (long term, adipose tissue: 85%)
  • Protein (muscles: 14.5%)
  • Glycogen (liver: 0.5%)

Storage and Release of Energy

• Glucose:
  • Primary energy source for the brain.
  • Stored as glycogen in the liver and easily converted back to glucose.
• Pancreatic hormones:
  • Glucagon: converts glycogen to glucose.
  • Insulin: converts glucose to glycogen.
• Fat:
  • Preferred energy storage; provides twice the energy of glycogen.
  • Glycogen attracts water and is heavy.
  • Fat comes from food or is produced from glucose.

Steps in Digestion

• Chewing: breaks up food & mixes with saliva.
• Saliva: lubricates food & begins digestion.
• Swallowing: moves food to the stomach.
• Stomach: storage reservoir; hydrochloric acid breaks food into small particles, pepsin breaks down protein to amino acids.
• Duodenum: digestive enzymes break down protein to amino acids, starch, and complex sugars to simple sugars, which pass into the bloodstream.
• Fats: emulsified by bile from the gall bladder, transported through lymphatic system.
• Large Intestine: absorbs remaining water and electrolytes.

3 Phases of Energy Metabolism

• Cephalic Phase
  • Preparatory phase triggered by sight, smell, or expectation of food.
  • High insulin, low glucagon.
  • Promotes the use of blood glucose, conversion of excess glucose to glycogen and fat, and amino acids to proteins.
  • Inhibits conversion of glycogen, fat, and protein into glucose, free fatty acids, and ketones
• Absorptive Phase
  • Nutrients from a meal meet immediate energy requirements; excess is stored.
  • Insulin levels high, glucagon levels low.
  • Promotes utilization of blood glucose, conversion of excess glucose to glycogen and fat, and conversion of amino acids to proteins, storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle.
  • Inhibits conversion of glycogen, fat, and protein into directly utilizable fuels (glucose, free fatty acids, and ketones)
• Fasting Phase
  • Energy is withdrawn from stores to meet immediate needs.
  • Glucagon levels high, insulin levels low.
  • Promotes conversion of fats to free fatty acids, glycogen to glucose, free fatty acids to ketones, and protein to glucose.
  • Inhibits utilization of glucose by the body (but not the brain), conversion of glucose to glycogen and fat, and amino acids to protein, storage of fat in adipose tissue.

Energy Metabolism - Preparatory Phase (Cephalic Phase)

• Starts with the thought/sight of food, ends with start of absorption into bloodstream.
• Conditioned, high release of insulin, but little glucagon, in anticipation of glucose increase.
• Insulin lowers bloodborne fuels by promoting:
  • Use of glucose as primary energy source.
  • Conversion of bloodborne energy sources to storage of fuel (glucose to glycogen & fat, amino acids to proteins).
  • Storage of glycogen in liver & muscle, fat in adipose tissue, proteins in muscle.

Energy Metabolism – Immediate Energy Needs (Absorptive phase)

• Digestion promotes release of gut hormones, some of which stimulate insulin release.
• More insulin is released by the pancreas (stimulated by glucodetectors in liver).
• Increased insulin release means glucose can be used immediately.
• Glucose imported into cells via glucose transporters (require insulin for functioning).
• Glucodetectors also exist in the brain (circumventricular organs).

Energy Metabolism – Fasting Phase

• Period between meals.
• Low insulin, high glucagon levels in the blood.
• Low insulin levels:
  • Glucose is no longer the main energy source (reserved for the brain).
  • Conversion of glycogen & protein to glucose is promoted (gluconeogenesis = protein to glucose; glycogenolysis = glycogen to glucose).
• Pancreas secretes glucagon: high levels of glucagon result in:
  • Release of free fatty acids from adipose tissue (converted to ketones – used by muscles).
  • Conversion of glycogen back to glucose.

Diabetes

• Type I Diabetes:
  • Insulin is not produced by beta cells in the pancreas.
  • Glucose is not removed from the bloodstream, causing diabetes.
• Type II Diabetes:
  • Prolonged overproduction of insulin leads to desensitization of insulin receptors.
  • Glucose is not removed from the bloodstream, causing diabetes.

Set-Point Assumption

• Energy Set-point: Homeostatic, negative feedback system.
• Homeostasis: Glucostatic and Lipostatic set-point.

Theories of Hunger and Eating

• Body heat and food & water intake regulated via elaborate physiological regulatory systems.
• Homeostatic: fairly constant levels are kept.
• Negative feedback systems: set-point assumption.

Glucostatic and Lipostatic Set-Point Theories

• Glucostatic theory:
  • Blood-glucose (short term regulation).
  • Responsible for initiating and terminating meals.
• Lipostatic theory:
  • Body fat (long-term regulation).

Weaknesses of Set-Point Theories

• Eating disorders, obesity epidemic.
• Inconsistent with evolutionary pressures (banking food when available).
• Major predictions of theories not confirmed.
  • Changes in glucose needed to increase eating, not natural.
  • People with excess fat don’t adjust meal size.
• Fail to recognize taste, learning, social influences.

Positive-Incentive Perspective

• Developed to overcome shortcomings of set-point.
• Positive incentive value (vs deficit).
• Emphasize anticipated pleasure of eating & craving.
• Animals eat in response to:
  • Preferred flavours.
  • Past experiences.
  • Time since last meal.
  • Others eating.

Factors That Influence What We Eat

• Animals:
  • Prefer sweet and salty.
  • Aversion to bitter.
  • Conditioned taste aversions.
  • Conditioned taste preferences.
• Culture specific for humans.
• Cravings for deficiencies:
  • Sodium, other vitamins.
  • Dietary deficiencies?
• Manufacturing of food to maximise profit.
• Difficulty to learn.

Factors That Influence When We Eat

• When food is readily available:
  • Animals eat many small meals.
  • Humans focus on a few large meals.
• Eating as a stressor.
  • Eating stresses the body (Woods et al).
  • Malaise/unpleasant feelings -> effects of cephalic stage.
• Weingarten research:
  • Rat experiments (ate each time the conditioned stimulus was presented).
  • Hunger caused by expectations not energy deficit.
  • We eat when we are used to eating.

Factors That Influence How Much We Eat

• Satiety: motivational state that causes us to stop eating when there is food remaining.
• Satiety Signals:
  • Volume.
  • Nutritive density (calories per unit volume).
  • Sham models: eat how much they are used to eating.
  • Eating a small amount before meal increases size of meal (Appetizer effect).
  • Serving size.
  • Social influence.
  • Increased variety of food.
  • Cafeteria-style diet/Sensory-specific satiety.

Sensory-Specific Satiety

• Encourages consumption of a varied diet.
• Encourages taking full advantage of abundance.

The Role of the Hypothalamus

• Myth of hunger & satiety centres.
• Dual-centre model:
  • Early work (1950s):
    • VMH: was implicated in satiety
    • Lesions à hyperphagia (over-eating)
      • dynamic phase
      • static phase
    • LH: was implicated in feeding
    • Lesions à aphagia
    • Accompanied by adipsia
    • Partial recovery through tube feeding
• Hypothalamic nuclei now focus for research (e.g., arcuate nuclei).

Ventromedial Hypothalamic Lesions

• Rats overeat (dynamic phase) until a higher body weight is attained, then maintain that weight (static phase), even with forced feeding or food deprivation.

Lateral Hypothalamic Lesions

• LH lesioned rats do recover but regulate their weight at a lower level
• Recovery suggests feeding & satiety are regulated elsewhere, & not in the LH
• LH lesions à wide range motor disturbances & general lack of responsiveness to sensory input

Problems with the VMH as a Satiety Centre

• Primary role of hypothalamus is regulation of energy metabolism, not eating.
• Obese because rats overeat; overeat because they become obese.
• Bilateral VMH lesions increase insulin -> lipogenesis, ↓lipolysis.
• Fat converted at high rate; eating continues to ensure calories in blood to meet energy demands.
• Many effects of VMH lesions are not attributable to VMH damage.
  • Bilateral lesions of noradrenergic bundle or the paraventricular nuclei produce hyperphagia just as VMH lesions do.

Early Studies: The Gastrointestinal Tract & Satiety

• Cannon & Washburn (1912):
  • Hunger pang thought to implicate role of stomach contractions.
  • But, animals with stomachs removed eat what is needed to maintain body weight.
• Koopmans (1981) second-stomach preparation:
  • Transplanted stomach connected to circulatory system.
  • Eating decreased both in terms of amount & calories.
  • Conclusion: satiety information reaches the brain through signals released by stomach.

Hunger & Satiety Peptides

• Stomach & gastrointestinal tract release peptides:
  • Satiety (↓ appetite):
    • CCK (Cholecystokinin).
    • Bombesin.
    • Glucagons.
    • Alpha-melanocyte-stimulating hormone.
    • Somatostatin.
  • Hunger (­ appetite):
    • Neuropeptide Y (NPY; released from paraventricular nuclei and arcuate nucleus).
    • Galanin (this & NPY both ­ eating when injected into the paraventricular nuclei).
    • Orexin-A.
    • Ghrelin.
• Renewed focus in hypothalamus (receptors).

Why Losing (or Gaining) Weight Is Difficult

• 33% of energy supplied by food is spent in digestion.
• 55% used for basal metabolic processes (e.g., heat production, maintaining membrane potentials).
• 12% used to fuel behavioral processes (comparatively more if great exertion is required).
• Diet-induced thermogenesis: amount of energy expended is adjusted in response to over- or under-nutrition.
• With ↓ (less than a sixth) in caloric intake, basal metabolism rate also declines (by 16%); body weight declines only by 6% .

Why Settling Point and Not Set Point?

• The equilibrium is neither predetermined nor actively defended.
• Enduring changes in the parameters that affect body weight (e.g., major increase in positive-incentive value).
• Metabolic changes limit further weight changes rather than eliminate weight changes.
• Return to previous weight in individuals can be explained just as well by settling point model.

Obesity: Why Is There an Epidemic?

• “Fast food” society, “obesogenic environment”.
• Evolution (not adaptive when food is readily available & high calorie):
  • Prefer high-calorie foods.
  • Eat maximum capacity.
  • Store energy as fat.
  • Use calories efficiently.
• Social/cultural factors:
  • Eat at specific times.
  • Eat maximum amounts.

Why Do Only Some People Become Obese?

• Food preferences.
• Social factors.
• Basal metabolism.
• Differences in consumption & energy expenditures.
• Differences in nonexercise activity thermogenesis.
• Differences in gut microbiome composition?
• Genetics.

Leptin & the Regulation of Body Fat

• 1950s genetically obese mouse (can’t produce leptin) ob/ob mouse.
• Leptin:
  • Hormone produced by fat cells.
  • In animals ↓ eating
  • ↓ body fat.
  • Correlated with subcutaneous fat.
  • Receptors in arcuate nucleus (of hypothalamus).
  • In (the minority of) humans who have low levels, administration can maintain reasonable weight.
• Insulin:
  • Positively correlated with body fat.
  • Receptors found in brain, mostly hypothalamus (arcuate nucleus).
  • Low doses reduce eating & body weight.

Leptin & the Regulation of Body Fat - Links to Hypothalamus (Arcuate Nucleus)

• Located in 2 classes of neurons that release:
  • Hunger peptides (Neuropeptide Y).
  • Satiety peptides (melanocortins).

Leptin in Humans

• Obese humans found to have high, rather than low levels of leptin.
• Injections of leptin did not reduce either eating or the body fat of obese humans.

How to Treat Obesity

• Increase satiety signals (e.g., serotonin agonists; but side effects).
• Reducing digestion/absorption of fat (e.g., gastric banding, gastric bypass surgery).
• “New generation anti-obesity drugs” (aka diabetes drugs)? – semaglutide (“Ozempic” etc) & GLP-1 receptor agonist drugs.
• Intermittent fasting and ketogenic diets?
• Relapse with cessation of treatments.
• Permanent change in lifestyle.

Eating Disorders

• Anorexia Nervosa:
  • Self-starvation plus psychological disturbances.
  • 1-2% of population.
• Bulimia: related disorder (underconsumption).
  • Binge-eat & purge in absence of extreme weight loss.
  • Erratic cycles, suggesting hypothalamic involvement.
  • Dangers of repeated vomiting (e.g., poisoning & result in heart failure; can affect heart rhythms & damage kidneys, stomach, oesophagus, teeth).
• Variations of same disorder?
  • Distorted body image; movement between diagnoses; population distribution; OCD & depression correlations; poor treatment response.

Avoidant/Restrictive Food Intake Disorder (ARFID)

• Persistent & disturbed pattern of feeding/eating limited in variety &/or volume -> failure to meet nutritional/energy needs.
• NOT ‘picky’ or ‘fussy’ eating.
• Differs from AN: do not restrict food to control weight or change body size/shape; not assoc. with weight/shape concerns.

Types of ARFID

• Sensory-based ARFID: Being sensitive to the taste, texture, temperature, smell, or appearance of a specific food.
• Trauma-related ARFID: Had a distressing experience with food.
• Restrictive ARFID:
  • Not being able to recognize hunger and fullness.
  • Lack of interest in food and eating.
  • Poor appetite.

Psychological Signs of ARFID

• Worsening picky eating.
• Avoiding or refusing an entire food group.
• Sensitive to smell, texture, and temperature.
• Only eating food of a similar color or brand.
• Lack of interest in food.
• Anxiety around new foods.
• Fears around food like fear of vomiting, choking, allergy.
• Avoid social events.

Neuroscience of ARFID

• Limited, but rapidly growing research area (see Scharner, 2024).
• Genetics: highly heritable (0.79), even after excluding autism (0.77) Dinkler et al., 2021); genes associated with taste perception & neurodivergence may confer increased risk for ARFID.
• Endocrinology: higher satiety-promoting (Peptide YY, cholecystokinin, oxytocin) hormone levels & lower hunger-promoting (ghrelin) hormone levels – may contribute to etiology &/or maintenance?

Neuroscience of ARFID

• Neuroimaging: ­ activation in reward circuitry (esp. OFC, also anterior insula) when viewing high-calorie food images in fasting state in youth with ARFID who were also overweight/obese vs those of normal weight; kids with ­OFC activity pre-meal were less satiated after the meal, hunger group (OV/OB vs HW) difference mediated by OFC activation (Kerem et al., 2021).
• More common in Ms, but no sex differences found in activation in OFC & hypothalamus after viewing high-calorie food image; no sex differences in ghrelin (hunger) & peptide YY (satiety) (Getachew et al., 2021).
• Comorbidities complicate interpretation; more studies needed.

Eating Disorders & Comorbidity

• Some groups are disproportionately at higher risk of an eating disorder – e.g., neurodivergence, anxiety and mood disorders, T1DM
• Est. 37% comorbidity with autism (Westwood et al., 2017); shared traits/factors; poorer treatment outcomes with existing approaches (Tchanturia et al., 2020)
• ADHD: youth 3-6 x more likely to develop an ED than youth without
• ADHD; also higher rates of eating pathology, body dissatisfaction, desire to lose weight/ drive for thinness (Curtin et al., 2013)