What is the primary functional difference between the Lateral Hypothalamus (LH) and the Ventromedial Hypothalamus (VMH)?

The LH acts as an 'on-switch' for hunger, initiating feeding behaviour when energy is low. In contrast, the VMH acts as an 'off-switch' or satiety center, signaling the body to stop eating once nutritional needs are met.

How do the roles of Ghrelin and Leptin differ in terms of energy regulation timing?

Ghrelin is a short-term regulator that fluctuates before and after meals to trigger immediate hunger. Leptin is a long-term regulator that reflects the total amount of body fat, helping to maintain stable body weight over weeks and months.

Compare the effects of a lesion in the LH versus a lesion in the VMH.

A lesion in the LH leads to a total lack of hunger (aphagia) and weight loss because the 'start eating' signal is destroyed. A lesion in the VMH leads to uncontrollable overeating (hyperphagia) and obesity because the 'stop eating' signal is removed.

What is a common misconception regarding the relationship between Leptin levels and obesity?

While it seems logical that more fat (and thus more leptin) should stop overeating, many individuals with obesity develop 'leptin resistance.' This means their brain no longer responds effectively to the hormone, so they never feel full despite having high energy stores.

Why is it incorrect to say that the stomach being 'empty' is the only cause of hunger?

Hunger is a multi-faceted neural process; while an empty stomach releases Ghrelin, hunger can also be triggered by low blood glucose levels, external cues (smell/sight of food), and the Arcuate Nucleus integrating various neural inputs.

What error is made when assuming the hypothalamus works in total isolation to control eating?

The hypothalamus is the control center, but it relies on constant feedback from the peripheral nervous system (like the vagus nerve) and the endocrine system (hormones). Ignoring these external inputs overlooks how the brain 'knows' the body's status.

Define 'Orexigenic' and provide an example of a hormone with this effect.

Orexigenic refers to any substance or neural pathway that stimulates appetite. Ghrelin is the primary orexigenic hormone, as its rise in the bloodstream directly correlates with increased hunger and food seeking.

What is the 'Set-Point Theory' in the context of eating behaviour?

The Set-Point Theory suggests that the hypothalamus maintains a specific 'target' body weight for an individual. It adjusts hunger and metabolic rate to return the body to this weight if it deviates significantly.

Define 'Hyperphagia' and identify its typical neural cause.

Hyperphagia is the medical term for excessive, uncontrollable overeating. It is typically caused by dysfunction or damage to the Ventromedial Hypothalamus (VMH), which prevents the sensation of satiety.

How does the Arcuate Nucleus (ARC) act as an integration center?

The ARC contains two sets of neurons: one that stimulates appetite and one that suppresses it. It receives hormonal signals like Leptin and Ghrelin from the blood and then sends instructions to other hypothalamic areas to coordinate the body's response.

The Role of Neural & Hormonal Mechanisms in Eating Behaviour | AQA A-Level Psychology

Eating behaviour: Option Topic (Section C)

The Role of Neural & Hormonal Mechanisms in Eating Behaviour

Summary

Eating behaviour is governed by a complex homeostatic system that integrates neural signals from the hypothalamus with hormonal feedback from the digestive system and adipose tissue. This system ensures energy balance by triggering hunger when reserves are low and inducing satiety when nutritional needs are met.

1. Definition & Core Concepts

Homeostasis: The physiological process by which the body maintains a stable internal environment, specifically regulating energy balance through the control of food intake and expenditure.
The Hypothalamus: A critical brain region that acts as the control center for eating behaviour, processing various signals to initiate or terminate feeding.
Orexigenic vs. Anorexigenic: Orexigenic mechanisms are those that stimulate appetite and food seeking, while anorexigenic mechanisms suppress appetite and promote a feeling of fullness (satiety).

Flowchart showing the feedback loop between the hypothalamus, stomach (Ghrelin), and adipose tissue (Leptin).

2. Neural Mechanisms: The Dual-Center Model

Lateral Hypothalamus (LH): Historically identified as the 'hunger center,' the LH is responsible for initiating eating behaviour; damage to this area typically leads to aphagia (refusal to eat).
Ventromedial Hypothalamus (VMH): Known as the 'satiety center,' the VMH signals the body to stop eating; lesions in this area often result in hyperphagia (overeating) and significant weight gain.
The Arcuate Nucleus (ARC): A specialized cluster of neurons in the hypothalamus that integrates various hormonal signals from the body to coordinate the activity of the LH and VMH.

3. Hormonal Regulation: Ghrelin and Leptin

Ghrelin: A fast-acting hormone secreted by the stomach lining when it is empty. It travels to the hypothalamus to stimulate the orexigenic pathway, signaling that the body requires immediate energy intake.
Leptin: A long-term signaling hormone produced by adipose (fat) cells. As fat stores increase, leptin levels rise, acting on the hypothalamus to suppress appetite and increase energy expenditure.
Cholecystokinin (CCK): A hormone released by the small intestine during digestion that acts as a short-term satiety signal, reducing meal size by signaling the brain via the vagus nerve.

4. Key Distinctions: Short-term vs. Long-term Regulation

5. Exam Strategy & Tips

6. Common Pitfalls & Misconceptions