Hormonal control of eating | AQA A-Level Psychology Revision

Revision Notes
Aug 6
27 min read

Updated: 11 hours ago

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 60 minutes

Hormones provide the brain with information about immediate hunger and longer-term energy storage. These Hormonal control of eating A-Level Psychology revision notes focus on ghrelin, which increases hunger as a meal approaches, and leptin, which signals the amount of energy stored in body fat.

Neither hormone controls eating independently. Both communicate with the hypothalamus, allowing neural systems to integrate information from the stomach, bloodstream and fat stores. The current AQA specification explicitly requires the hypothalamus, ghrelin and leptin as neural and hormonal mechanisms involved in eating behaviour.

Learning Objectives 🎯

By the end of this revision page, you should be able to:

Explain how hormones influence eating behaviour.
Explain where ghrelin is released and how it stimulates hunger.
Explain how leptin communicates information about stored body fat.
Distinguish short-term and long-term hormonal control.
Explain how hormones interact with the hypothalamus.
Apply ghrelin and leptin to unfamiliar scenarios.
Evaluate hormonal explanations using research evidence and broader psychological issues.

Revision Notes 📚

Hormonal control of eating overview

A hormone is a chemical messenger released by a gland or body tissue and transported through the bloodstream to a target organ or tissue.

Hormonal control of eating involves communication between:

The stomach and digestive system.
Fat tissue.
The bloodstream.
The hypothalamus.
Wider neural systems.

The two hormones named in the AQA specification are:

Ghrelin
Leptin

Their basic functions can be remembered as:

Hormone	Main source	Main signal	Broad effect
Ghrelin	Stomach and digestive system	The body is ready for food	Increases hunger and eating
Leptin	Fat cells	Energy is stored in body fat	Increases satiety and reduces eating

AQA’s 2025 mark scheme describes ghrelin as being released when the stomach is empty and causing hunger, while leptin is produced when fat is stored and signals satiety.

Hormones and homeostasis

What is homeostasis?

Homeostasis is the regulation of the body’s internal conditions around a stable or preferred level.

For eating behaviour, the body attempts to maintain sufficient:

Immediately available energy.
Blood glucose.
Stored energy.
Body fat.

Hormones help this process by informing the hypothalamus about the body’s current condition.

Negative feedback

Eating regulation often follows a negative-feedback loop.

A negative-feedback response acts to reverse the change that triggered it.

For example:

available energy falls → hunger signals increase → eating occurs → energy becomes available → hunger signals fall

Similarly:

fat stores fall → leptin levels decrease → appetite increases → energy intake rises → fat stores may be restored

Hormones are therefore part of a regulatory system rather than independent causes of behaviour.

Hunger, appetite and satiety

Hunger

Hunger is a physiological state that motivates eating.

It may be influenced by:

Ghrelin.
Glucose availability.
An empty stomach.
Activity in the hypothalamus.

Appetite

Appetite is the desire to eat.

It can be influenced by physiological hunger, but also by:

Food appearance.
Smell.
Learning.
Social occasions.
Cultural expectations.
Habit.

A person can therefore have an appetite without having a significant energy deficit.

Satiety

Satiety is the state of fullness that inhibits eating.

It may involve:

Rising energy availability.
Digestive signals.
Leptin.
Other appetite-suppressing hormones.
Hypothalamic activity.

📌 Exam precision: Ghrelin is mainly associated with increasing hunger, while leptin is mainly associated with satiety and information about longer-term fat stores.

The role of ghrelin

What is ghrelin?

Ghrelin is a hormone involved in stimulating hunger and eating behaviour.

AQA’s specimen mark scheme states that ghrelin is released from the stomach and small intestine into the bloodstream in relation to food intake. Its levels are lowest after a meal and rise gradually before the next meal, increasing hunger and stimulating eating.

Where is ghrelin released?

Ghrelin is released mainly from the stomach, with AQA also accepting release from the small intestine.

Its release is related to:

Stomach emptiness.
Time since the previous meal.
Anticipation of eating.
Current food intake.

Ghrelin then travels through the bloodstream.

Ghrelin and the hypothalamus

Ghrelin travels to the brain and acts on the hypothalamus.

AQA directly assessed this relationship in June 2024. The correct statement was:

Ghrelin travels to the hypothalamus before eating.

The basic pathway is:

stomach becomes empty → ghrelin is released → ghrelin travels in the bloodstream → hypothalamus receives the signal → hunger increases → eating becomes more likely

Ghrelin levels across a meal

Ghrelin follows a meal-related pattern.

After a meal

The stomach contains food.
Ghrelin levels are relatively low.
Hunger is reduced.

Between meals

Food leaves the stomach.
Ghrelin levels gradually rise.
Hunger becomes more noticeable.

Before a meal

Ghrelin levels may be higher.
The hypothalamus receives a stronger hunger signal.
Food-seeking and eating become more likely.

Following food consumption

Ghrelin levels decline.
The hunger signal weakens.
Other satiety signals contribute to ending the meal.

Ghrelin as a short-term signal

Ghrelin is particularly important for the short-term control of eating.

It changes in relation to:

Individual meals.
Stomach emptiness.
The period since eating.

It helps explain:

Why hunger rises before meals.
Why people begin searching for food.
Why hunger often declines after eating.

It is less directly concerned with the total amount of body fat stored over months or years.

That longer-term role is more closely linked with leptin.

Ghrelin does not physically create food intake

It is inaccurate to say that ghrelin:

Forces the person to eat.
Physically moves food into the stomach.
Is released from fat cells.
Produces satiety.
Is at its highest immediately after eating.

Ghrelin creates a biological signal that increases the motivation to eat.

Whether eating actually occurs may also depend on:

Food availability.
Conscious decisions.
Social circumstances.
Dieting.
Cultural rules.
Stress.

Applying ghrelin

Scenario 1: hunger before lunch

Harper has not eaten since breakfast. Shortly before lunch, they experience strong hunger and begin thinking about food.

A hormonal explanation would suggest:

Harper’s stomach has become relatively empty.
Ghrelin levels have risen.
Ghrelin has travelled through the bloodstream to the hypothalamus.
Hunger-related neural activity has increased.
Harper is motivated to find and consume food.

Scenario 2: hunger falls after eating

After eating lunch, Zac reports that the intense hunger he experienced has disappeared.

A hormonal explanation would suggest:

Food has entered Zac’s digestive system.
Ghrelin levels fall following the meal.
The hunger signal to the hypothalamus weakens.
Satiety signals become relatively stronger.
Zac becomes less motivated to continue eating.

Scenario 3: food is unavailable

Aleesha feels hungry but cannot eat for another hour because she is sitting an examination.

Ghrelin may still:

Rise.
Signal the hypothalamus.
Produce hunger.

However, Aleesha’s behaviour is also affected by:

The examination rules.
Conscious control.
The lack of available food.

The example shows that hormonal signals influence rather than completely determine behaviour.

Evidence for ghrelin

Cummings’ research

AQA’s 2025 mark scheme identifies Cummings’ research linking levels of blood ghrelin with hunger as evidence for hormonal control.

The important conclusion is:

Changes in circulating ghrelin are associated with changes in hunger around meals.

This supports the proposed mechanism because:

Ghrelin rises when hunger is expected.
Ghrelin falls after food is consumed.
The timing of the hormone is consistent with a role in meal initiation.

Strength of the evidence

Measuring ghrelin in the bloodstream provides:

Quantitative data.
Objective biological measurements.
Comparisons before and after meals.
A testable link between physiology and reported hunger.

Limitation of the evidence

A relationship between ghrelin and hunger does not by itself prove that ghrelin is the sole cause.

Possible interpretations include:

Ghrelin increases hunger.
Other bodily changes increase both ghrelin and hunger.
Anticipating a normal mealtime affects both.
Hunger and ghrelin influence one another.

The evidence supports ghrelin’s involvement but not an isolated one-hormone explanation.

The role of leptin

What is leptin?

Leptin is a hormone or neuropeptide produced by fat cells.

Its level provides the brain with information about energy stored in body fat.

AQA’s 2025 mark scheme describes leptin as being produced when fat is stored and signalling satiety.

The broad pathway is:

fat is stored → leptin is released → leptin travels in the bloodstream → hypothalamus receives the signal → appetite is inhibited and satiety increases

Where is leptin produced?

Leptin is produced by adipose tissue, which is body-fat tissue.

This means that leptin is not primarily released from:

The empty stomach.
The liver.
The hypothalamus itself.

The amount of leptin generally provides information about longer-term energy reserves.

Leptin and stored energy

When fat stores are relatively high:

More leptin may be available.
The hypothalamus receives a signal that stored energy is sufficient.
Hunger may be reduced.
Satiety may increase.
Energy intake may decrease.

When fat stores fall:

Leptin levels may decline.
The hypothalamus receives less of the stored-energy signal.
Appetite may increase.
Satiety may weaken.
The person may become motivated to restore energy stores.

Leptin as a long-term signal

Leptin mainly contributes to the longer-term regulation of:

Stored energy.
Body fat.
Continuing appetite.
Body-weight stability.

This distinguishes it from ghrelin, which changes more directly around individual meals.

Ghrelin	Leptin
Shorter-term hunger signal	Longer-term energy-storage signal
Released mainly by the stomach	Released by fat cells
Rises as a meal approaches	Reflects stored body fat
Stimulates hunger	Signals satiety
Encourages meal initiation	Helps regulate intake over time

Leptin and lipostatic theory

What is lipostatic theory?

Lipostatic theory proposes that the body attempts to regulate stored body fat around a preferred or set level.

The hypothalamus monitors signals associated with body-fat levels.

Leptin is one of the signals through which fat tissue communicates with the hypothalamus.

The pathway can be represented as:

body-fat stores → leptin signal → hypothalamic response → adjustment of hunger and satiety

When body fat decreases

If a person loses body fat:

Fat stores become smaller.
Leptin levels fall.
The hypothalamus receives a weaker satiety signal.
Hunger may increase.
Food intake may rise.
The body is encouraged to restore energy stores.

When body fat increases

If body-fat stores increase:

Fat cells produce a stronger leptin signal.
The hypothalamus receives information that energy is stored.
Satiety may increase.
Appetite may decrease.
Food intake may be reduced.

This is a negative-feedback system because the response tends to oppose the original change.

Leptin and dieting

When a person loses a substantial amount of body fat:

Leptin signalling may fall.
Appetite may increase.
Food becomes more difficult to resist.
Maintaining the lower weight may become challenging.

AQA’s 2025 mark scheme recognises that fat levels change slowly and that lipostatic regulation can help explain why diets are sometimes difficult to maintain.

This does not mean:

Weight change is impossible.
Everyone responds identically.
Hormones completely remove conscious control.

It means that the body may produce biological pressures that oppose a continuing loss of stored energy.

Leptin deficiency

What happens when leptin cannot be produced?

If the body is unable to produce sufficient leptin:

The hypothalamus may fail to receive an accurate stored-energy signal.
The body may behave as though energy reserves are low.
Hunger may remain high.
Food intake may increase.
Weight gain may occur.

Licinio’s research

AQA’s 2025 mark scheme identifies Licinio’s research linking a genetic inability to secrete leptin with obesity.

This supports leptin’s role because:

A disruption in the hormone was associated with disrupted appetite or body-weight regulation.
The finding is consistent with leptin normally signalling that energy stores are available.
Without the signal, eating may remain elevated.

Limitation of leptin-deficiency evidence

A rare genetic inability to produce leptin does not show that every case of overeating or obesity has the same cause.

Body weight may also be affected by:

Other genes.
Wider neural mechanisms.
Learning.
Food availability.
Restraint and disinhibition.
Social and economic conditions.

Leptin deficiency provides strong evidence for the hormone’s importance but not a universal explanation of body weight.

Ghrelin and leptin compared

Feature	Ghrelin	Leptin
Main body source	Stomach and digestive system	Adipose tissue
Typical timing	Rises before eating	Reflects longer-term fat storage
Message	Food is needed	Energy is stored
Main effect	Increases hunger	Increases satiety
Behavioural outcome	Meal initiation becomes more likely	Continued eating becomes less likely
Primary timescale	Short-term	Longer-term
Neural target	Hypothalamus	Hypothalamus
AQA research example	Cummings	Licinio

The crucial distinction

Use this exam-safe summary:

Ghrelin goes up before eating and promotes hunger. Leptin is released by stored fat and promotes satiety.

AQA’s June 2025 examiner report noted that some students muddled ghrelin and leptin or failed to explain their precise mechanisms accurately.

Neural and hormonal interaction

Hormones do not act without the brain

Ghrelin and leptin circulate in the bloodstream, but their effects on eating depend partly on neural processing.

The hypothalamus:

Receives hormonal information.
Integrates several signals.
Coordinates hunger and satiety.
Influences food-seeking and meal termination.

The relationship is therefore:

body tissues release hormones → hormones carry information → hypothalamus interprets the information → neural activity influences eating behaviour

The hypothalamus as an integration centre

The hypothalamus receives information about:

Stomach emptiness.
Ghrelin.
Leptin.
Blood glucose.
Stored body fat.
Other digestive signals.

It then contributes to a coordinated response.

This extends the material in hypothalamic hunger and satiety mechanisms.

Interaction before a meal

A simplified pre-meal sequence is:

Time passes since the previous meal.
The stomach becomes emptier.
Ghrelin rises.
Ghrelin travels through the bloodstream.
The hypothalamus receives the hunger signal.
Hunger-related neural mechanisms become active.
Food-seeking and eating become more likely.

The June 2024 multiple-choice question directly confirmed that ghrelin travels to the hypothalamus before eating.

Interaction during and after a meal

As food is consumed:

The digestive system processes the meal.
Ghrelin levels decline.
Glucose availability changes.
Other satiety signals increase.
The hypothalamus integrates this information.
Hunger is inhibited.
Eating slows or stops.

Leptin contributes information about the body’s broader energy stores rather than acting only as a rapid signal that one meal has ended.

Interaction across days and weeks

Over longer periods:

Energy intake affects body-fat storage.
Fat cells alter leptin signalling.
The hypothalamus receives information about stored energy.
Appetite and satiety are adjusted.
Food intake may change.
Body stores may move towards a regulated level.

Ghrelin and leptin therefore operate on overlapping but different timescales.

Ghrelin, leptin and dual-control theory

The traditional dual-control account proposes:

The lateral hypothalamus contributes to hunger and meal initiation.
The ventromedial hypothalamus contributes to satiety and meal termination.

Hormonal signals provide information used within this neural system.

A simplified interaction is:

Signal	Hypothalamic function	Behaviour
Rising ghrelin	Hunger systems become more active	Eating begins
Falling ghrelin after a meal	Hunger signal weakens	Eating becomes less urgent
Leptin from stored fat	Satiety and energy-storage information	Appetite is inhibited
Reduced leptin after fat loss	Less satiety information	Hunger may increase

The older “two-centre” theory is useful for revision, although eating is better understood as involving an interacting network rather than two isolated switches.

Ghrelin and leptin do not simply cancel each other out

It may be tempting to think:

ghrelin increases eating + leptin decreases eating = one hormone wins

The interaction is more complex.

The final behaviour depends on:

The relative strength of several signals.
Current energy needs.
Fat stores.
Meal timing.
Learning.
Social context.
Cognitive restraint.
Food availability.

For example:

A person may have high ghrelin before a meal but decide not to eat because they are fasting.

Similarly:

A person may have substantial stored energy but continue eating because food is highly rewarding and socially available.

Other hormones in eating regulation

Ghrelin and leptin are the hormones specifically named in the AQA specification.

The June 2025 mark scheme also accepted supporting knowledge about:

Insulin.
Glucagon.
Cholecystokinin.

Insulin and glucagon

Insulin and glucagon help regulate blood-glucose levels.

Their activity contributes to information about immediately available energy.

This information interacts with hypothalamic regulation.

Cholecystokinin

Cholecystokinin, usually abbreviated to CCK, is released from the digestive system and suppresses appetite.

AQA describes it as acting in opposition to ghrelin.

For examination purposes:

Ghrelin promotes hunger.
CCK contributes to appetite suppression.
Leptin communicates stored-energy information.

Ghrelin and leptin should remain the central focus because they are explicitly named in the specification.

Short-term and long-term control

Short-term hormonal control

Short-term control responds to individual meals.

It includes:

The stomach becoming empty.
Ghrelin rising.
Hunger increasing.
Ghrelin falling after eating.
Digestive satiety signals increasing.

Long-term hormonal control

Long-term control responds to energy stored in the body.

It includes:

Body-fat levels.
Leptin secretion.
Hypothalamic monitoring.
Adjustment of appetite over time.
Maintenance of a body-fat set point.

Short-term regulation	Long-term regulation
Organises individual meals	Regulates stored energy
Changes over hours	Changes over longer periods
Strongly linked with ghrelin	Strongly linked with leptin
Helps initiate eating	Helps regulate appetite and body weight
Responds to stomach emptiness	Responds to body-fat stores

A complete hormonal feedback cycle

Stage 1: energy is needed

The stomach becomes empty.
Ghrelin is released.
The hypothalamus receives a hunger signal.

Stage 2: hunger develops

Food-related motivation increases.
The person begins searching for food.

Stage 3: food is consumed

The digestive system becomes active.
Ghrelin falls.
Glucose and digestive signals change.

Stage 4: the meal ends

Hunger signals weaken.
Satiety signals become stronger.
Hypothalamic activity inhibits further eating.

Stage 5: energy is stored

Excess energy may be stored as body fat.
Fat tissue produces leptin.
The hypothalamus receives information about longer-term reserves.

Stage 6: future intake is adjusted

Higher stored-energy signals may reduce appetite.
Lower stored-energy signals may increase appetite.

This demonstrates why neural and hormonal mechanisms should not be taught as separate mini-explanations.

Hormonal control and food preference

Hormones mainly help explain:

When hunger begins.
How strongly food is wanted.
When eating stops.
How energy stores influence appetite.

They do not fully explain:

Why someone chooses one cuisine rather than another.
Why a child avoids unfamiliar vegetables.
Why a culture prefers a particular flavour.
Why one food has become associated with celebration.

Those choices are better explained through:

Hormonal state and food preference can interact.

For example:

Ghrelin may motivate a person to eat, while social learning determines which food they choose.

Hormonal control and restrained eating

A person may consciously attempt to ignore hormonal hunger signals.

For example:

Ghrelin rises.
The person feels hungry.
A dieting rule states that eating is not permitted.
The person delays food consumption.

This illustrates a conflict between:

Biological hunger.
Cognitive restraint.

Later, intense hunger may contribute to the breakdown of restraint.

This link is developed in restraint, disinhibition and the boundary model.

Applying both hormones

Scenario 1: pre-meal hunger and stored energy

Nia has not eaten for several hours and experiences strong hunger. She has recently lost a considerable amount of body fat.

A hormonal explanation could suggest:

The empty stomach has increased ghrelin.
Ghrelin travels to the hypothalamus and stimulates hunger.
The loss of fat has reduced leptin signalling.
The hypothalamus receives less information indicating stored energy.
Both short-term and long-term signals may therefore encourage eating.

Scenario 2: after a meal

Bailey eats a substantial meal and quickly loses interest in food.

A hormonal explanation could suggest:

Ghrelin falls after eating.
The hunger signal to the hypothalamus weakens.
Digestive and satiety signals become more influential.
Leptin continues to provide information about longer-term energy stores.
Neural mechanisms inhibit further eating.

Scenario 3: eating despite fullness

Anya has eaten a large meal but continues eating dessert with friends.

A hormonal account predicts that:

Ghrelin should have declined.
Satiety signals should be active.
Leptin continues to signal stored energy.

However, Anya may continue eating because of:

The pleasant taste.
Social modelling.
Cultural expectations.
Positive associations with dessert.

This demonstrates the limits of a purely homeostatic explanation.

Scenario 4: weight loss and hunger

After several weeks of dieting, Morgan reports feeling more hungry and finds the diet increasingly difficult to maintain.

A hormonal explanation could suggest:

Body-fat stores have decreased.
Leptin signalling has fallen.
The hypothalamus receives less satiety information.
Appetite increases in an attempt to restore energy stores.
Biological pressure makes continued restriction harder.

This is not proof that hormones are the only reason the diet is difficult. Restraint, food salience and disinhibition may also contribute.

Evaluating hormonal explanations

Strength: research supports ghrelin’s role

Cummings found an association between blood-ghrelin levels and hunger.

The timing of ghrelin around eating is consistent with the hormone acting as a meal-initiation signal.

Why this supports the explanation

Ghrelin is measurable.
Levels change in relation to meals.
Changes correspond with hunger.
The finding matches the predicted biological mechanism.

Limitation

The research establishes an association more confidently than a complete cause-and-effect relationship.

Meal expectation or another physiological process could affect both ghrelin and hunger.

Strength: leptin-deficiency evidence

Licinio’s research associated a genetic inability to secrete leptin with obesity.

This supports leptin’s role because:

The body lacks an important stored-energy signal.
Hunger and intake may remain high.
Body-weight regulation becomes disrupted.

The finding has particular value because the proposed biological abnormality and behavioural outcome are theoretically connected.

Limitation: rare cases do not explain ordinary variation

A person unable to produce leptin represents an unusual biological condition.

Most people who gain weight are not necessarily unable to secrete leptin.

The finding therefore demonstrates that leptin can be causally important without showing that leptin deficiency explains every case of obesity.

Strength: objective measurement

Hormonal research can use:

Blood samples.
Measured hormone concentrations.
Recorded meal timing.
Quantified food consumption.
Body-fat measurements.

These produce quantitative data that are less dependent on personal interpretation than an interview alone.

This can increase:

Objectivity.
Reliability.
Replicability.
Scientific credibility.

Limitation of biological measurements

A hormone concentration does not reveal:

What the person is thinking.
Why they choose a particular food.
Whether they are following a cultural rule.
Whether they are consciously resisting hunger.
Whether the food is emotionally rewarding.

Hormonal and psychological measures may therefore need to be combined.

Strength: clear practical applications

Understanding hunger and satiety signals may contribute to treatments for:

Disrupted appetite.
Anorexia nervosa.
Obesity.
Difficulties regulating food intake.

The 2025 AQA mark scheme accepts implications for treating anorexia and obesity as relevant discussion.

For example:

Identifying an abnormal hormonal signal may guide biological treatment.
Monitoring appetite signals may improve understanding of weight changes.
Treatment may attempt to restore normal hunger or satiety communication.

Caution

A biological intervention may not address:

Cognitive distortions.
Family interaction.
Learned preferences.
Social pressures.
Food availability.

Practical application supports the importance of hormones but not hormonal exclusivity.

Strength: neural and hormonal integration is more complete

A major strength is that hormones are not treated as acting alone.

Ghrelin and leptin communicate with the hypothalamus.

This provides a coordinated explanation involving:

The body’s energy state.
Blood-borne chemical messages.
Brain processing.
Behavioural responses.

The interaction is more convincing than claiming that either:

The stomach controls eating alone.
The hypothalamus independently knows how much energy is stored.

Limitation: hormonal explanations are biologically reductionist

A hormonal explanation may reduce eating to:

Ghrelin concentrations.
Leptin concentrations.
Fat cells.
Hypothalamic responses.

This can overlook:

Food preference.
Culture.
Social influence.
Advertising.
Cognitive restraint.
Emotional eating.

Human eating takes place in a rich psychological and social context.

The account may explain biological hunger but not the complete decision to eat a particular food in a particular situation.

This connects with biological reductionism and levels of explanation.

Limitation: eating can occur without hunger

A person may eat despite low hunger because:

Food is highly palatable.
Friends are eating.
It is a celebration.
The food is associated with comfort.
A meal is part of a routine.
A culturally expected food is offered.

This challenges the claim that hormonal need is sufficient to explain every eating episode.

Hormones may still contribute, but non-homeostatic factors affect whether and what the person eats.

Limitation: people can resist hormonal signals

A person experiencing high hunger may choose not to eat because of:

Religious fasting.
Dieting.
Lack of food.
Work or school demands.
Personal goals.
Concern about body image.

This demonstrates that biological signals are not equivalent to unavoidable actions.

Hormones influence the motivational state, while cognitive and environmental factors influence the final behaviour.

Biological determinism

A strongly deterministic hormonal explanation might claim:

Hormone levels control whether a person eats.

This is too absolute.

People can respond differently to similar hunger signals.

A better conclusion is:

Ghrelin and leptin create biological pressures that influence the probability and strength of eating behaviour.

This position is closer to soft biological determinism.

It recognises causal influence without claiming that choice and experience are irrelevant.

Individual differences

People may differ in:

Ghrelin patterns.
Leptin production.
Sensitivity to hormonal signals.
Fat storage.
Learned responses to hunger.
Ability or willingness to delay eating.

This means that one hormonal pattern may not explain every individual’s behaviour.

For example:

Two people may have similar hunger but make different food choices.
The same person may respond differently depending on social context.
Hormonal signals may interact with genetic and neural differences.

Cause and effect

A researcher may find that:

Higher ghrelin is associated with hunger.
Lower leptin is associated with increased eating.
Abnormal hormone levels are associated with body-weight difficulties.

However, the direction can sometimes be complicated.

For example:

Hormonal changes may alter eating.
Eating and weight change may alter hormones.
A genetic factor may influence both.
Illness or medication may affect the relationship.

Longitudinal and experimental evidence strengthens causal conclusions, but no single design answers every question.

Hormonal research and animal studies

Some research into hunger and satiety mechanisms uses non-human animals.

Strengths

Animal studies can allow:

Greater control of diet.
Direct manipulation of biological mechanisms.
Accurate measurement of intake.
Investigation that would be unethical with humans.

Limitations

Human eating is affected by:

Language.
Culture.
Beliefs.
Dieting.
Social expectations.
Media.

Animal research may reveal basic hormonal mechanisms without explaining the full complexity of human eating behaviour.

The June 2025 examiner report notes that animal and lesion research were popular and often sophisticated evaluation points in the neural and hormonal essay.

Leptin and explanations of obesity

Abnormal leptin signalling may be relevant to genetic and neural explanations of obesity.

However, it is inaccurate to conclude:

“Obesity is caused by low leptin.”

Possible biological pathways differ between people.

Obesity may involve:

Hormonal factors.
Genetic predisposition.
Neural reward mechanisms.
Food availability.
Restrained and disinhibited eating.
Environmental influences.

Leptin is one part of a broader biological account.

Hormonal control and anorexia nervosa

Hormonal levels may change when a person consumes very little food or loses substantial body fat.

However, altered hormone levels might be:

A cause of disrupted eating.
A consequence of starvation or weight loss.
Both part of a continuing cycle.

This direction-of-causality issue is important when considering genetic and neural explanations of anorexia nervosa.

A hormone abnormality identified after severe weight loss does not automatically show what originally caused the condition.

Research methods used to investigate hormones

Blood tests

Researchers may take blood samples:

Before a meal.
Immediately after a meal.
At regular intervals.

They can measure changes in:

Ghrelin.
Leptin.
Glucose.
Other biological signals.

Repeated-measures design

The same participant can be measured at several points.

Strength

Participant variables are controlled because each person is compared with themselves.

Limitation

Repeated blood tests or awareness of meal timing may alter stress, appetite or behaviour.

Correlational design

Researchers may correlate:

Ghrelin with hunger ratings.
Leptin with body-fat measurements.
Hormone levels with food consumption.

Strength

Naturally occurring biological relationships can be investigated ethically.

Limitation

Correlation does not establish causality.

Operationalising hunger

Hunger might be measured using:

A rating scale.
Time until eating begins.
Quantity consumed.
Food choice.

Each measure captures a different aspect.

A person may report strong hunger but eat very little because they are restraining intake.

Using several measures improves validity.

A hypothetical hormonal investigation

Researchers measure ghrelin immediately before lunch and ask participants to rate hunger from 0 to 10.

Co-variables

Ghrelin concentration.
Hunger rating.

Predicted relationship

The hormonal explanation predicts a positive correlation:

higher ghrelin → higher hunger rating

Possible conclusion

A significant positive correlation would support an association between ghrelin and subjective hunger.

Limitation

The researchers could not conclude that ghrelin alone caused the hunger.

Meal expectation, habitual lunchtime or another biological variable might influence both.

Applying hormonal research data

Suppose researchers obtain the following results:

Time	Mean ghrelin level	Mean hunger rating
Immediately after breakfast	20 units	2
Before lunch	52 units	8
After lunch	24 units	3

The data show that:

Ghrelin and hunger are lowest after meals.
Both are higher before lunch.
The pattern is consistent with ghrelin contributing to hunger and meal initiation.

However, the table alone does not establish:

Statistical significance.
Individual variation.
Cause and effect.
Whether another variable changed simultaneously.

How to answer a ghrelin question

For a two-mark question, use two clear stages:

Source and transport
Pattern and behavioural effect

A full answer could be:

“Ghrelin is released mainly by the stomach into the bloodstream. Its level is low after eating and rises before a meal, signalling the hypothalamus and increasing hunger and eating.”

This follows the specimen mark scheme’s required elements.

How to answer a leptin question

Use:

source → stored-energy signal → hypothalamus → effect on eating

For example:

“Leptin is released by fat cells in relation to stored body fat. It travels to the hypothalamus and signals that energy reserves are available, increasing satiety and reducing appetite.”

How to explain interaction

A weak interaction answer states:

“Ghrelin and leptin both work with the hypothalamus.”

A stronger answer explains:

“An empty stomach releases ghrelin, which travels through the blood to the hypothalamus and increases hunger. Fat cells release leptin, which provides the hypothalamus with information about longer-term energy stores and promotes satiety. The hypothalamus integrates these opposing signals to regulate the initiation and termination of eating.”

Structuring an eight-mark evaluation

A hormonal evaluation might use three developed paragraphs.

Paragraph 1: ghrelin evidence

Cummings.
Ghrelin levels and hunger.
Objective biological measurement.
Correlation and causality.

Paragraph 2: leptin evidence

Licinio.
Genetic inability to secrete leptin.
Association with obesity.
Rare case or limited generalisation.

Paragraph 3: broader explanation

Neural and hormonal integration.
Biological reductionism.
Eating without hunger.
Learning and cultural influences.

Structuring a 16-mark essay

The June 2025 examination asked:

Discuss the role of neural and hormonal mechanisms involved in the control of eating behaviour.

The mark allocation was:

AO1: 6 marks
AO3: 10 marks

A strong essay should therefore include detailed discussion as well as description.

Paragraph 1: homeostasis

Define homeostatic regulation.
Explain negative feedback.
Introduce the hypothalamus.

Paragraph 2: neural mechanisms

Lateral hypothalamus.
Ventromedial hypothalamus.
Glucose-related signals.
Hunger and satiety.

Paragraph 3: ghrelin

Released by the empty stomach.
Rises before eating.
Travels to the hypothalamus.
Stimulates hunger.

Paragraph 4: leptin

Produced by fat cells.
Communicates stored-energy information.
Signals satiety.
Links with lipostatic regulation.

Paragraph 5: interaction

Hormones provide information.
Hypothalamus integrates it.
Short-term and long-term regulation.
Avoid treating the mechanisms separately.

Paragraph 6: evidence

Cummings and ghrelin.
Licinio and leptin.
Explain implications and limitations.

Paragraph 7: neural evidence

Lesion studies.
Human case evidence.
Problems generalising animal research.

Paragraph 8: broader evaluation

Reductionism.
Determinism.
Learning and social influences.
Practical implications for eating and weight difficulties.
Multi-level conclusion.

Examiner-focused advice 💡

The June 2025 examiner report found that successful responses often included impressive technical detail and referred accurately to both neural and hormonal mechanisms. Some students, however, confused ghrelin and leptin and muddled the exact mechanisms.

To avoid this:

Always state the source of each hormone.
State when its level changes.
Explain its effect on hunger or satiety.
Link it explicitly with the hypothalamus.
Distinguish immediate meal control from longer-term fat storage.

Overall conclusion

Hormonal control of eating depends on communication between the body and the brain.

Ghrelin is released mainly by the stomach as it becomes empty.
Ghrelin travels through the bloodstream to the hypothalamus.
Its level rises before meals and increases hunger.
Its level falls after food is consumed.

In contrast:

Leptin is released by fat cells.
It provides information about longer-term energy stores.
It signals the hypothalamus and contributes to satiety.
Reduced leptin signalling may encourage eating when fat stores fall.

The hormonal system works with the hypothalamus rather than separately from it:

peripheral hormone signal → hypothalamic integration → hunger or satiety → eating begins or ends

Research involving ghrelin and leptin supports their biological importance. However, hormonal explanations cannot fully account for eating influenced by culture, learning, pleasure, conscious restraint or social situations.

The strongest conclusion is:

Ghrelin and leptin are important interacting signals within a wider neural, hormonal, cognitive and environmental system controlling eating behaviour.

Hints from the Examiner Reports 💡

Examiner hint: Do not reverse ghrelin and leptin.

Use:

Ghrelin: stomach, before eating, hunger.
Leptin: fat cells, stored energy, satiety.

AQA’s 2025 examiner report specifically identified confusion between the two hormones as a weakness.

Examiner hint: State the mechanism, not just the outcome.

Weak:

“Ghrelin makes you hungry.”

Stronger:

“As the stomach becomes empty, ghrelin is released into the bloodstream and travels to the hypothalamus, where it increases hunger and stimulates eating.”

Examiner hint: AQA has directly tested the ghrelin pathway.

The June 2024 correct answer was that ghrelin travels to the hypothalamus before eating.

Examiner hint: Leptin is not released by the stomach.

It is produced by fat tissue and communicates information about stored energy.

Examiner hint: Link hormones and neural mechanisms.

Do not write:

One disconnected paragraph about the hypothalamus.
One disconnected paragraph about ghrelin.
One disconnected paragraph about leptin.

Explain how the hormones send information to the hypothalamus.

Examiner hint: Use Cummings and Licinio analytically.

Do not write only:

“Cummings supports ghrelin.”

Explain the finding and why it supports the proposed mechanism.

Examiner hint: Distinguish association from causation.

A correlation between ghrelin and hunger supports involvement but does not prove that ghrelin acts alone.

Examiner hint: Keep the 16-mark weighting in mind.

The June 2025 neural and hormonal question awarded:

6 marks for AO1.
10 marks for AO3.

Evaluation should therefore be detailed and evidence based.

Examiner hint: Do not forget both elements of the essay title.

A neural and hormonal question requires:

Neural control.
Hormonal control.
Their interaction.

AQA’s specimen mark scheme states that ghrelin is lowest after a meal and rises gradually before another meal.

How to improve:

Remember:

ghrelin grows as the stomach empties

finding → link to hormone → theoretical implication → limitation

Exam-Style Questions ✍️

Questions

1. What is meant by a hormone?

[2 marks]

Answer

Award up to two marks:

A hormone is a chemical messenger.
It is released by a gland or body tissue and transported in the bloodstream to a target organ or tissue.

2. Briefly outline the role of ghrelin in the control of eating behaviour.

[2 marks]

Answer

Award up to two marks:

Ghrelin is released mainly by the stomach into the bloodstream.
Its level is lowest after a meal and rises before eating.
It travels to the hypothalamus, increasing hunger and stimulating eating.

3. Explain the role of leptin in the control of eating behaviour.

[4 marks]

Answer

Award up to four marks:

Leptin is produced by fat cells or adipose tissue.
Its level communicates information about stored body fat.
Leptin travels through the bloodstream to the hypothalamus.
It signals that energy reserves are available.
This increases satiety or reduces appetite and food consumption.

4. Explain one difference between ghrelin and leptin.

[3 marks]

Answer

Award up to three marks for one developed difference.

Possible answer:

Ghrelin is released mainly by the stomach, whereas leptin is released by fat cells.
Ghrelin rises before eating and stimulates hunger.
Leptin reflects longer-term fat stores and promotes satiety.

5. Explain how ghrelin interacts with the hypothalamus.

[4 marks]

Answer

Award up to four marks:

The stomach becomes empty.
Ghrelin is released into the bloodstream.
Ghrelin travels to the hypothalamus.
Hunger-related neural activity increases.
Food-seeking and meal initiation become more likely.

6. Explain how leptin interacts with neural mechanisms involved in eating.

[4 marks]

Answer

Award up to four marks:

Fat cells release leptin in relation to stored energy.
Leptin travels through the bloodstream.
The hypothalamus receives the stored-energy signal.
Neural satiety mechanisms become more active.
Appetite and food intake may decrease.

7. Rowan has not eaten for several hours. Shortly before dinner, Rowan reports intense hunger.

Explain Rowan’s experience using your knowledge of ghrelin.

[4 marks]

Answer

Award up to four marks:

Rowan’s stomach is relatively empty after several hours without food.
Ghrelin levels have risen.
Ghrelin travels through the blood to the hypothalamus.
The hypothalamus responds by increasing hunger-related activity.
Rowan becomes strongly motivated to eat dinner.

8. After losing a substantial amount of body fat, Billie finds that hunger becomes increasingly difficult to manage.

Explain Billie’s experience using your knowledge of leptin.

[4 marks]

Answer

Award up to four marks:

Billie’s body-fat stores have decreased.
Fat cells therefore provide a reduced leptin signal.
The hypothalamus receives less information indicating that energy is stored.
Satiety may weaken and appetite may increase.
This response may encourage Billie to restore lost energy stores.

9. Explain one difference between short-term and long-term hormonal control of eating.

[4 marks]

Answer

Award up to four marks:

Short-term hormonal control regulates individual meals.
Ghrelin rises as the stomach empties and stimulates hunger.
Its level falls after eating.
Long-term control reflects stored energy.
Leptin is released by fat cells and communicates information about body-fat reserves.
It contributes to continuing regulation of appetite and body weight.

10. Explain how neural and hormonal mechanisms interact to initiate and terminate eating.

[6 marks]

Answer

Award up to six marks:

Eating is regulated homeostatically.
An empty stomach releases ghrelin.
Ghrelin travels to the hypothalamus and increases hunger.
Hunger-related neural systems encourage food-seeking and meal initiation.
Following food intake, ghrelin declines and satiety signals increase.
Leptin from fat tissue informs the hypothalamus about stored energy.
The hypothalamus integrates these signals.
Hunger is inhibited and eating slows or stops.

11. Briefly outline one study relating to ghrelin and evaluate what the study tells psychologists about eating behaviour.

[4 marks]

Answer

Award up to two marks for outline and two marks for evaluation.

Possible answer:

Cummings found that blood-ghrelin levels were associated with hunger around meals.
Ghrelin was higher when hunger was greater and lower after food consumption.
This supports the hormone’s proposed role in stimulating hunger.
However, an association between ghrelin and hunger does not prove that ghrelin alone caused the change, because meal expectation or another physiological process may affect both.

12. Briefly outline one study relating to leptin and evaluate what the study tells psychologists about eating behaviour.

[4 marks]

Answer

Award up to two marks for outline and two marks for evaluation.

Possible answer:

Licinio identified an association between a genetic inability to secrete leptin and obesity.
This supports the idea that leptin normally communicates information about stored energy and helps suppress appetite.
Disrupted leptin signalling may result in continued hunger and weight gain.
However, this unusual form of leptin deficiency cannot explain every instance of obesity.

13. Researchers measured mean ghrelin levels and mean hunger ratings before and after a meal.

Measurement	Before meal	After meal
Mean ghrelin level	48 units	24 units
Mean hunger rating	8	3

a) Calculate the percentage decrease in mean ghrelin after the meal.

[2 marks]

Answer

50%

b) Explain one conclusion and one limitation of these findings.

[4 marks]

Answer

Award up to four marks.

Possible conclusion:

Mean ghrelin and mean hunger were both lower after the meal.
This is consistent with ghrelin contributing to hunger before eating and declining once food has been consumed.

Possible limitation:

No inferential-test result is provided, so statistical significance cannot be claimed.
Means conceal individual differences.
A pre-meal and post-meal comparison does not prove that ghrelin caused the hunger change.
Other digestive or psychological factors may have changed at the same time.

14. Explain one strength and one limitation of hormonal explanations of eating behaviour.

[6 marks]

Answer

Award up to three marks for a developed strength and three marks for a developed limitation.

Possible strength:

Hormonal explanations are supported by biological evidence. Cummings linked circulating ghrelin with hunger, while Licinio linked disrupted leptin secretion with obesity. The findings are consistent with specific hormones having predictable effects on appetite and stored-energy regulation.

Possible limitation:

The account is biologically reductionist. People may continue eating when ghrelin is low because of pleasure, social occasions or learned preferences, so hormone levels cannot explain the complete complexity of human eating.

Alternative creditworthy points include:

Objective measurement.
Practical applications.
Cause-and-effect problems.
Individual differences.
Animal generalisation.
Biological determinism.
Interaction with neural systems.

15. Evaluate hormonal mechanisms involved in eating behaviour.

[8 marks]

Answer

A strong answer should include:

Cummings’ evidence connecting ghrelin and hunger.
Licinio’s evidence connecting leptin deficiency and obesity.
Objective measurement of hormone concentrations.
Biological plausibility.
Practical implications for eating and weight difficulties.
Hormonal signals interacting with the hypothalamus.
Correlation not proving causation.
Rare leptin deficiency not explaining ordinary obesity universally.
Individual differences.
Biological reductionism.
Biological determinism.
Eating without physiological hunger.
Conscious resistance to hunger.
Learning, social and cultural influences.
Hormonal changes potentially being consequences as well as causes of altered eating.
A multi-level explanation being more complete.

16. Discuss the role of neural and hormonal mechanisms involved in the control of eating behaviour.

[16 marks]