Motivation and Hunger

Question 1

What is eating and digestion and how does it work?

Answer 1

Digestion is the process of converting food into energy and nutrients.

Energy is supplied to the body in the form of lipids (fats), amino acids, and glucose. Energy usage is constant but intake is relatively infrequent, so energy is stored as fats (in adipose tissue, 85%), protein (in muscles, 14.5%), and glycogen (in the liver, 0.5%)

Question 2

What is the stomach and pancreases roll in the digestion process?

Answer 2

The stomach uses hydrochloric acid to break down food and transfer it to the upper level of the intestine. The pancreas provides enzymes and peptides, and the liver stores glycogen

Question 3

How does the brain and body store and release energy, what are the roles of glucose, glucagon and insulin - what are the pancreatic hormones that help regulate this process?

Answer 3

Glucose is the brains energy source and needs to be readily available. It is stored as glycogen in the liver and easily converted back to glucose.

Two hormones regulate this conversion process: glucagon (stimulates conversion from glycogen to glucose) and insulin (stimulates conversion from glucose to glycogen). Fat is the preferred energy store as it provides 2x as much energy as glycogen.

Question 4

What are the 3 phases of energy metabolism?

Answer 4

Cephalic phase:
the body prepares for a meal and releases insulin

Absorptive phase:
Nutrients from a meal meet the body’s immediate energy requirements, with the excess being stored.

Fasting Phase:
Energy is withdrawn from stores to meet the body’s immediate needs

Question 5

What does the cephalic and absorptive phase promote and inhibit ?

Answer 5

Promotes:
1. High insulin, low glucose
2. blood glucose as energy source
3. conversion of excess glucose to glycogen and fat
4. conversion of amino acids to proteins
5. storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscles

Inhibits:
Conversion of glycogen, fat, and protein into utilisable fuels

Question 6

What does the fasting phase promote and inhibit?

Answer 6

Promote:
1. Conversion of fats to free fatty acids
2. Converts glycogen to glucose, free fats acids to ketones, and proteins to glucose

Inhibit:
1. Utilisation of glucose by the body not the brain
2. Conversion of glucose to glycogen and fat, amino acids to protein
3. Storage of fat in adipose tissue

Question 7

In the preparatory phase of energy metabolism, seen in the cephalic phase of eating. How does it begin?

Answer 7

Starts with thought/sight of food, ends with start of absorption into bloodstream.

Conditioned, high release of insulin from the pancreas (but comparatively little release of glucagon) in anticipation of glucose increase in the bloodstream.

Question 8

In energy metabolism, what are the immediate energy needs in the absorptive phase?

Answer 8

GET GLUCOSE INTO THE CELLS

gut hormones -> insulin release -> pancreas glucodectors release more insulin -> glucose imported into cells

Question 9

In energy metabolism what happens in the fasting stage?

Answer 9

Low levels of insulin but high levels of glucagon in the blood

Due to low insulin levels:
Glucose no longer main energy source (reserved for the brain)
Conversion of glycogen and protein to glucose is promoted

Pancreas starts secreting glucagon

Question 10

What is gluconeogenesis and Glycogenolysis?

Answer 10

Protein converted to glucose

Glycogen converted into glucose

Question 11

What does high levels of glucose result in?

Answer 11

1. Release of free fatty acids from adipose tissue (converted to ketones)
2. Conversion of glycogen back to glucose

Question 12

How does insulin normally function in the body?

Answer 12

Insulin binds to insulin receptors and triggers the opening of glucose transporters in fat and muscle cells, allowing glucose removal from the bloodstream.

Question 13

What causes Type 1 diabetes?

Answer 13

Insulin is not produced by beta cells in the pancreas and hence glucose is not removed from the blood stream, causing diabetes.

Question 14

What causes type 2 diabetes?

Answer 14

Prolonged overproduction of insulin dulls insulin receptors, therefore glucose is not removed from the bloodstream, causing diabetes.

Question 15

What is the energy set-point assumption?

Answer 15

homeostatic, negative feedback system where monitoring and feedback trigger changes in temperature to bring us back to an ideal set point.

Question 16

What is glucostatic set-point theory?

Answer 16

Hunger is driven by the need to have a certain set point of glucose in our bloodstream.

Question 17

What is the lipostatic set-point theory?

Answer 17

hunger, eating, and appetite are driven by an ideal weight based on fat levels

Question 18

How are body heat, and food and water intake regulated according to theories of hunger and eating?

Answer 18

elaborate physiological regulatory systems that are homeostatic and involve negative feedback systems with a set-point assumption. As energy levels deplete, we look for energy sources in food.

Question 19

What are the two set-point theories and how do they function?

Answer 19

The glucostatic theory focuses on short-term regulation of blood-glucose and is responsible for initiating and terminating meals. The lipostatic theory focuses on body fat for long-term regulation

Question 20

What are the weaknesses of the set-point theories?

Answer 20

Inconsistencies with evolutionary pressures

Fail to make accurate predictions

Fail to recognise the impact of taste, learning, and social influences on eating behaviour

Question 21

What is the positive-incentive perspective of eating?

Answer 21

Emphasises the anticipated pleasure of eating and craving. It suggests that animals eat in response to preferred flavours, past experiences, time since the last meal, and the eating behaviour of others.

Question 22

What factors influence what we eat?

Answer 22

Preferences for sweet and salty foods, aversions to bitter foods, conditioned taste aversions and preferences, cravings for deficient nutrients, and cultural factors can all influence what we eat

Question 23

What factors influence when we eat?

Answer 23

Food availability, stress, expectations, and habitual eating times can all influence when we eat.

Question 24

What factors influence how much we eat?

Answer 24

Satiety signals, the volume and nutritive density of food, serving size, social influence, and the variety of food available can.

Question 25

What are the effects of Ventromedial Hypothalamic (VMF) lesions in rats?

Answer 25

VHM lesions lead rats to overeat during the dynamic phase of weight gain until a higher body weight is attained. They continue to maintain this new weight during the static phase, even with forced feeding or food deprivation.

Question 26

What are the effects of Lateral Hypothalamic (LH) lesions in rats?

Answer 26

satiety are regulated elsewhere

result in a wide range of motor disturbances and a general lack of responsiveness to sensory input.

Question 27

Why isn’t Ventralmedial Hypothalamus (VHM) considered a satiety centre?

Answer 27

The primary role of hypothalamus is the regulation of energy metabolism when not eating. Overeating following VMH lesions is more due to an increase in lipogenesis and decrease lipolysis.

Question 28

What are the hunger (increase appetite) and satiety (decrease appetite) peptides released by the stomach and gastrointestinal tract?

Answer 28

Hunger peptides that increase appetite include: Neuropeptide Y, Galanin, Orexin-A, and Gherlin.

Satiety peptides that decrease appetite include: CCK, Bombesin, Glucagons, Alpha-melanocyte-stimulating hormone, and Somatostatin.

Question 29

Why is losing or gaining weight difficult?

Answer 29

about 33% of energy from food is spent on digestion, 55% on basal metabolic processes, and 12% on behavioural processes. Diet-induced thermogenesis adjusts energy expenditure in response to over- or under-nutrition, meaning our bodies become more efficient at using stored energy when we consume fewer calories.

Question 30

What is the difference between a set-point and a settling point in weight regulation?

Answer 30

A settling point is a balance that is neither predetermined nor actively defended, unlike a set-point. Changes in parameters affecting body weight or metabolic changes can shift this equilibrium.

Question 31

What are some reasons for the obesity epidemic?

Answer 31

The obesity epidemic is due to a combination of factors such as fast food consumption, evolutionary traits favouring high-calorie foods, social factors, and genetics.

Question 32

What is the role of Leptin and Insulin in the regulation of body fat?

Answer 32

Leptin, a hormone produced by fat cells, decreases eating and body fat in animals. Insulin, positively correlated with body fat, has receptors found mainly in the hypothalamus and low doses reduce eating and body weight.

Question 33

What are some eating disorders and their characteristics?

Answer 33

Anorexia Nervosa involves self-starvation and psychological disturbances.

Bulimia involves binge-eating and purging without extreme weight loss.

Avoidant/Restrictive Food Intake Disorder (ARFID) involves a persistent and disturbed pattern of feeding or eating.

Question 34

What are some comorbidities associated with eating disorder?

Answer 34

Eating disorders are often comorbid with conditions like autism, ADHD, mood disorders, and Type 1 Diabetes Mellitus (T1DM).

ADHD youth are more likely to develop an eating disorder with higher rates of eating pathology, body dissatisfaction, desire to lose weight/drive for thinness.

Question 35

How is glucose depletion related to ‘Ego’ or ‘Regulation Depletion’ Theory?

Answer 35

Low glucose levels lead to energy deficiency and difficulty in regulating emotions and behaviour, often causing irritability, or “hanger”. This aligns with the ‘ego-depletion’ theory, which posits that self-control depletes limited mental resources.

Question 36

What does the psychological constructionist theory explain about being “hanger”?

Answer 36

Our brain interprets physical sensations and if unsure of their cause, may attribute them to emotions, leading to feelings of hanger.

Question 37

What is the evolutionary perspective on “hanger”?

Answer 37

adaptive response, motivating aggressive food-seeing behaviour when energy levels are low.

Question 38

What is the physiological perspective on “hanger” (beyond glucose)?

Answer 38

hormones gherlin and leptin, and stress hormones like cortisol and adrenaline, can contribute to hanger.

Question 39

What is the main perspective adopted in the MacCormack and Lindquist (2018) article?

Answer 39

This is a psychological constructionist view. Emotions and physiological experiences like hunger are not distinct biological systems, but a shared core affect. Emotions and experiences like hunger are constructed by the brain using contextual information and body states.

Question 40

What were the main findings of the MacCormack and Lindquist (2018) study?

Answer 40

1. Hunger doesn’t automatically lead to negative emotions
2. Individuals usually conceptualise hunger as emotion when not explicitly focused on the emotional nature of their feelings.
3. The presence of an emotion label can lead to implicit regulation of the emotion, reducing the likelihood that hunger results in the experience of negative, high arousal emotions.

Question 41

What are the implications of the MacCormack and Lindquist (2018) findings?

Answer 41

They challenge the traditional understanding that separates bodily changes like hunger and emotions as distinct biological systems, suggesting they instead interact and reciprocally influence each other.

Question 42

What is the bio psychological perspective of the MacCormack and Lindquist (2018) findings and future directions?

Answer 42

From a bio psychological perspective, the findings underscore the complex interplay between physiological states, emotional processing, and motivational states. They suggest potential biological pathways (like hunger signals - gherkin or satiety signals - leptin) through which hunger might influence emotional states. Future research could delve further into these biological pathways, investigate the impact of other physiological states on emotional processing, and explore the implications of these interactions on social and cognitive processes.

Question 43

What is a major strength of the Swami et al. 2022 study in terms of research design? why?

Answer 43

It is its longitudinal experience sampling methodology, providing a more ecologically valid assessment of the associations between hunger and emotional outcomes.

Question 44

What are the main findings of the Swami et al. 2022 study?

Answer 44

That hunger was significantly associated with greater feelings of anger and irritability, as well as lower ratings of pleasure. These associations were consistent when considering each emotional construct individually and when combined into a compound measure.

Question 45

What are the implications of the Swami et al. 2022 study?

Answer 45

They are relevant for understanding the everyday experiences of emotions and the impact of hunger on emotional states.

Question 46

In what ways do Swami et al.s findings extend from those of MacCormack and Lindquist?

Answer 46

It provides further evidence for the association between hunger and negative emotions in everyday life. The longitudinal nature of Swami et al. study and the inclusion of a wider range of emotional states provide a more comprehensive understanding of the hunger-emotion relationship.

Question 47

How do the Swami findings provide additional points to consider alongside physiological and bio psychological explanations?

Answer 47

It suggests that the subjective experiences of hunger and the awareness of hunger cues play a meaningful role in emotional outcomes, highlighting the importance of psychological and contextual factors in understanding the link between hunger and emotions. The study emphasises the complex interplay between physiological, psychological, and situational factors in shaping emotional experiences.