Ch. 4 Physiological Mechanisms of Regulation Flashcards
Homeostatic Regulation
- Regulatory mechanisms exist within the body that sample the internal environment
- When the body is above or below some optimal value, these mechanisms alert the brain
- The brain activates the necessary actions to return the organism to a balanced state
- Your body may also be designed to regulate homeostasis both in the short and long-term
Why do we eat?
- Cues in our environment
- Memory of last time we ate
- Our perception of how much we have eaten in the moment
- Variety of food available
- Sensory specific satiety
- But of course, to maintain homeostatic balance and provide energy to our bodies
- Low blood glucose signs glucoreceptors which trigger the motive to eat
- Short-term and long-term homeostatic mechanisms
Short-Term Regulation of Hunger
- Controls when we eat a meal and how much we eat
- Gut sends signals to brain to stimulate or stop eating
Various structures detect nutrients (or lack thereof) and communicate to the brain via the vagus/vagal nerve, responsible for parasympathetic control of the heart and digestive tract
Stretch receptors
- Receptors in the wall of the stomach that stretch when stomach is full
Nutrient detectors
- Cells/molecules in stomach that detect the presence of specific nutrients (e.g., carbohydrates, proteins, fats)
Ghrelin
- hormone produced by the stomach lining to stimulate appetite
Obestatin
- hormone that suppresses appetite
Duodenum
- Secretes various hormones, including CCK (cholecystokinin) to signal the presence of glucose to the brain
- Genetically obese mice have 25% of the amount of CCK present in their brains as normal mice
Liver
- Liver receives nutrients from gastrointestinal tract via the hepatic portal vein
- Injections of glucose into portal vein suppresses feeding, indicating this as another cite at which glucose is detected and signaled to the brain
Pancreas
- Beta cells in the pancreas detect changes in glucose and release hormones insulin and amylin to signal glucose accessibility to the brain
- Insulin helps transport glucose into cells
- In addition, sight, smell, and taste can promote/inhibit eating
Crum et al., 2011 - Method
- Within-subjects design
On both occasions, participants drank a 380-calorie milkshake - Ghrelin was measured via blood samples three times at each visit:
- at baseline (before reading about milkshake) – 20 mins into experiment
- after learning about the milkshake, but before drinking it – 60 minutes in
post-consumption – 90 minutes in (had 30 minutes to drink milkshake) - After baseline, participants asked to view one of two labels
- One portrayed milkshake as an “indulgent” 620 calories
- One portrayed milkshake as a “sensible” 140 calories
Long-Term Regulation of Hunger
- Maintains adequate energy stores so that if short-term energy intake is inadequate, body can maintain normal functions
- Body weight appears to be relatively well-regulated
We maintain a particular weight quite consistently
Set-Point Theory (Lipostatic Theory)
- Lateral hypothalamus (LH) and Ventralmedial hypothalamus (VMH)
- May be the structures in the brain that regulate weight set-points
- Lesions to LH, lower set-point; Lesions to VMH, higher set-point
Leptin
- Hormone produced by fat cells and released into the bloodstream
Insulin
- Insulin levels in the blood are also related to glucose and fat storage
- When weight is reduced, insulin and leptin levels drop
Arcuate nucleus (in hypothalamus)
- Detects leptin and insulin levels In blood
- When levels drop, arcuate nucleus secretes neuropeptide Y (NPY), a neurotransmitter that is an appetite stimulant
Dissenting Theories
- Glucose-driven hunger may be triggered in only rare or emergency situations
- People typically eat well before conditions produce low glucose
- Eating occurs based on various environmental cues
People eat because food is available or based on times of day - Conditions that promote eating are both behavioral and metabolic
Complicated process!
Conceptual Diagram of Hunger Regulation (Berthoud & Morrison, 2008)
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Burnette & Finkel, 2012
- 169 participants (80% female) who were currently trying to lose weight
Longitudinal experiment
Randomly assigned participants to a growth mindset, knowledge, or control condition for a 12-week intervention (five biweekly emails) - Growth mindset manipulation: Participants received messages about the malleability of body weight, but no information about exercise or nutrition
- Goal: buffer dieters against inevitable dieting setbacks
Information manipulation: Participants received scientifically validated information for promoting weight loss
Control group: No information about body weight
- Participants weighed again 12 weeks after Time 1
Their “setback severity” was also assessed
Setback severity did not differ across conditions
Results:
- At Time 2 (post-intervention), people in the growth mindset condition reported higher growth mindset toward weight than participants in the other two conditions
- Although, overall, participants failed to lose weight, those in the growth mindset and knowledge conditions gained less weight than those in the control condition; Weight loss in growth and knowledge condition did not differ significantly
- In the growth mindset condition, increases in growth mindset predicted decreases in weight
Setback severity predicted weight gain in the control and knowledge conditions, but not in the growth mindset condition
Thus, growth mindset condition buffered participants against setback-related weight gain
Anorexia
- Restriction of food intake due to intense fear of gaining weight or becoming fat
- 15% below expected body weight
Negative effects: Loss of period, low blood pressure, brain shrinks, learning deficits, elevated cortisol, perverted hunger drive
- Serotonin hypothesis
Bulimia
- Binge eat large quantities of food in a short amount of time
- At least once a week for 3 months
- Sense of lack of control during bingeing; attempt to regain control through purging behaviors
- Causes of a binge eating episode: difficulty handling emotions, restrictive dieting, interpersonal conflict, loss or separation
Approaches to understanding bulimia:
- Sociocultural approach
- Clinical/psychiatric approach
- Epidemiological approach
- Social contagion approach
- Serotonin and norepinephrine
Obesity
- Long-term imbalance between energy intake and energy usage
Causes of Obesity:
- Adaptiveness gone wrong
- Genetic predisposition
- Obesity maintains obesity
- Socioeconomic status/location
- Culture
- Habituation
- Addiction
- Stress
- Not enough sleep?
Wagner et al., 2014
- Tested whether comfort food really improved mood
- Across 4 studies, asked people about their food preferences
Including what their comfort foods were - First three studies were within-subjects design
Participants were tested on separate occasions and those scores were compared to one another - Put everyone in a negative mood at beginning of study
Study 1 – Participants got their comfort good at one visit and an equally liked non-comfort food in a second visit (counterbalanced)
Study 2 – Participants got their comfort food at one visit and a neutral food in a second visit (counterbalanced)
Study 3 – Participants got their comfort food at one visit and no food at a second visit (counterbalanced)
Study 4 - between-subjects design – four groups: No food, comfort food post-film, gift of chocolate before film not-eaten, and comfort food pre-film
