Summarize evidence of the physiological factors implicated in the regulation of hunger.
Explain how food availability, situational factors, culture, and learning influence hunger.
Describe evidence of the prevalence, health consequences, and roots of obesity.
Hunger is a complex motivational system, not a simple one.
Early theories linked stomach contractions to hunger, based on observations.
Walter Cannon and A. L. Washburn (1912) verified the association between stomach contractions and hunger.
Cannon theorized that stomach contractions cause hunger.
This theory was discredited because people still experience hunger after stomach removal (Wangensteen & Carlson, 1931).
Current theories focus on:
The role of the brain
Digestive factors
Hormones
Research with lab animals suggested that hunger is controlled in the brain, specifically the hypothalamus.
The hypothalamus regulates biological needs related to survival.
Lateral Hypothalamus (LH):
Destroying the LH in rats led to a decrease or loss of interest in eating
Ventromedial Nucleus of the Hypothalamus (VMH):
Destroying the VMH in rats led to excessive eating and rapid weight gain - ability to recognise satiety (fullness) had been neutralised
Early conclusion: LH and VMH were the brain's on-off switches for hunger (1940s and 1950s)
The dual-centres model of hunger was later undermined .
Current thinking: LH and VMH are elements in the neural circuitry that regulates hunger, but are not key on-off centers.
Arcuate Nucleus and Paraventricular Nucleus:
These areas are believed to play a larger role in modulating hunger.
The arcuate nucleus is considered especially important.
Contemporary theories focus on neural circuits that pass through areas of the hypothalamus, not anatomical centres.
These circuits depend on neurotransmitters and are more complicated than previously thought.
The neural circuits regulating hunger are interconnected with extensive parallel processing.
This complex circuitry is sensitive to a diverse range of physiological processes.
The digestive system has mechanisms that influence hunger.
Walter Cannon's hypothesis that the stomach regulates hunger was partially correct.
The stomach sends signals to the brain to inhibit further eating after food consumption (Woods & Stricker, 2013).
Vagus Nerve: Carries information about the stretching of stomach walls, indicating fullness.
Other nerves carry satiety messages based on the nutrient content of the stomach.
Hormones contribute to the regulation of hunger.
Ghrelin: Secreted by the stomach when the body goes without food, causing stomach contractions and promoting hunger.
CCK: Released by the upper intestine after food consumption, delivering satiety signals to the brain and reducing hunger.
Leptin: Contributes to long-term regulation of hunger and other bodily functions.
Produced by fat cells and released into the bloodstream.
Provides the hypothalamus with information about the body's fat stores.
High leptin levels diminish hunger; low leptin levels promote increased hunger.
Insulin: Secreted by the pancreas and sensitive to fluctuations in body fat stores.
Hormonal signals (insulin, ghrelin, CCK, and leptin) converge in the hypothalamus, especially the arcuate and paraventricular nuclei..
Eating is influenced by social and environmental factors.
Physiological regulation of hunger assumes homeostatic mechanisms are at work.
Incentive Value: Humans are motivated to eat by the anticipated pleasure of eating, not just energy deficits.
Environmental variables influence food consumption:
Palatability: The better food tastes, the more people consume.
Quantity Available: People consume what is put in front of them
Larger plates and dinnerware increase consumption.
Variety: Increased variety leads to increased consumption
Sensory-Specific Satiety: Incentive value of a specific food declines as you eat it.
Buffets lead to overeating due to the availability of many foods.
According to incentive models, availability and palatability are key factors regulating hunger.
Presence of Others: Individuals eat 44\% more when eating with others.
People use each other as guides and eat similar amounts.
Women may reduce intake in the presence of an unfamiliar opposite-sex person.
Obesity is assessed by Body Mass Index (BMI): weight (in kilograms) divided by height (in metres) squared (kg/m^2).
BMI of 25.0-29.9 is overweight, and over 30 is obese.
About 31\% of adults are obese and 58\% are overweight in South Africa (Chooi et al., 2019).
The obesity epidemic is a global problem (Lobstein, 2017).
Humans evolved to consume more food than necessary due to competition for limited resources.
Excess calories were stored as fat for future shortages.
Modern societies have abundant, reliable supplies of palatable food, leading to chronic overconsumption.
Obesity increases mortality risk.
Associated with coronary disease, stroke, hypertension, diabetes, respiratory problems, gallbladder disease, arthritis, muscle and skeletal pain, sleep apnea, and some cancers.
May promote inflammatory and metabolic changes contributing to Alzheimer's disease.
Obesity is partly hereditary.
Identical twins reared apart are more similar in BMI than fraternal twins reared together (Stunkard et al., 1990).
Genetic factors account for 61\% of weight variation in men and 73\% in women (Allison et al., 1994).
Overweight people eat too much in relation to their exercise level.
Modern society provides tasty, high-calorie foods everywhere.
Marketing efforts increase consumption of unhealthy foods.
Highly processed, high-fat, high-sugar foods may be addictive.
Modern societies create an 'obesogenic' environment.
Decline in physical activity due to modern conveniences.
Overeating contributes more to obesity than lack of exercise.
Food industry downplays overconsumption and frames the issue as balancing consumption with exercise.
About one-half of the public believes exercise is more influential than diet in determining weight.
People who think exercise is more influential are more likely to be overweight.
People tend to regain weight after losing it, suggesting homeostatic mechanisms defend against weight loss.
Metabolic and neuroendocrine processes resist weight loss.
Energy expenditure declines after weight loss.
Reduced fat stores result in reduced leptin levels, fueling increased hunger.
The body is also wired to resist weight gain.
Adaptive mechanisms maintain a stable body weight, suggesting a set point for weight.
The set point is an individual's natural point of stability for weight.
South Africans experience two extremes: poverty leading to underfeeding and rising obesity rates.
Many individuals lack access to healthier food options.
Affordable and easily available food is often unhealthy.
Many South Africans cannot afford a healthy diet.
People may choose unhealthy food due to palatability, variety, and convenience.
The 'sugar tax' is an attempt to reduce intake of unhealthy foods.
Food preferences are acquired through learning.
People prefer familiar foods.
Geographical, cultural, religious, and ethnic factors limit exposure to certain foods.
Repeated exposure to a new food increases liking.
Forcing a child to eat a specific food can backfire.
Taste preferences are learned associations formed through classical conditioning.
Youngsters can be conditioned to prefer flavors paired with pleasant events.
Taste aversions can be acquired through conditioning.
Eating habits are shaped by observational learning.
The set point concept suggests the body has a natural weight range.
A key question is why obesity has increased if the body defends a weight range.
The body defends against weight loss more strongly than weight gain.
This is likely because in ancestral times, defending against weight loss was more crucial for survival due to food scarcity.