Biological explanations of eating behaviour
Neural mechanisms and eating behaviour
From a biological perspective, eating behaviour is usually referred to as ingestive behaviour which serves to
maintain homeostasis via negative feedback.
For example the 'lipostatic hypothesis' and the 'gluclosatic hypothesis' which suggest that when our fat stores
are depleated or blood gluglose levels are low, we feel hungry, which makes us eat
Resent evidence has indicated that a number of neural mechanisms are associated with eating; for example,
the hypothalamus (including the paraventrial hypothalamus and the perifornical area) and neurotrasmitters
(catecholamines, serotonin and peptides).
Research into the role of neural areas associated with eating behaviour has indicated that the hypothalamus
plays a significant role.
Early research suggested that the hypothalamus was central to food intake:
Medial hypothalamus- ‘satiety centre’:
Lateral hypothalamus- ‘feeding centre’:
More recent research has indicated, however, that there is a more complex system involving:
• Paraventricular Hypolthalamus/ Nucleus-
• Perifornical Area-
Central to both the simple and more complex models are a number of neurotransmitters which are regarded as
key to our understanding of the neurological basis of eating behaviour. These neurotransmitter pathways are
situated in the central nervous system and the peripheral nervous system. These neurotransmitters are the
catecholamines, serotonin and peptides.
Neurotransmitters that increase food intake:
1. Norepinephrine (NE): This neurotransmitter is a catecholamine, and has been found to influence eating
behaviour if injected into areas of the hypothalamus.
If injected into the paraventricular nucleus, NE
If injected into the perifornical area, NE
Leibowitz (1986) found that NE
2. Neuropeptide Y: This neurotransmitter is a peptide, which is found in high concentrations in the
paraventricular nucleus and the perifornical area.
Research has found that when rats are injected with Neuropeptide Y,
Leibowitz (1986) found that Neuropeptide Y increases the preference and desire for carbohydrates.
3. Galanin: This neurotransmitter is particularly found in the paraventricular hypothalamus
Leibowitz (1986) injected Galanin into rats and found that it increased food intake and caused a preference for
fats rather than carbohydrates.
Neurotransmitters that decrease food intake:
Rowland et al (1996) found that a number of neurotransmitters decrease food intake:
1. Cholecystokinin (CCK): This is a peptide which is released into the blood stream during meals
If injected into rats, CCK causes
2. Corticotropin-releasing hormone (CRH): This is a peptide which is produced in the paraventricular
CRH has been found to
3. Serotonin (5HT): Has been linked to suppressed appetite and reduced food intake. This could explain why
patients with depression have a suppressed appetite and often lose weight, as they have higher levels of
serotonin than is considered normal.
Neurotransmitters, therefore, seem to function by either increasing or decreasing food intake. The role of
neurotransmitters has also been investigated through research on the impact of drugs on eating behaviour.
The impact of drugs on eating behaviour:
If we understand the ways in which particular drugs make us want to eat more or less, and also how these
drugs affect our brains, we can begin to comprehend how the chemicals in our brains influence what, how and
when we eat and stop eating.
1. Nicotine- Has been found to decrease food intake
2. Amphetamines-Amphetamines act on the catecholamines and some on serotonin pathway
3. Alcohol- Hollister (1991) found that alcohol influences eating behaviour in different ways
Evaluation of neural explanations of eating behaviour:
Reflection of people’s experience: Insight into brain chemicals:
Explanation of some differences: Lab based research (involving animals):
Influence of social factors and social drives: Physiological drives can be overridden:
It has been suggested that the catecholamine, serotonin and peptide pathways influence eating behaviour in
the following ways:
The serotonin pathway: Influence feelings of fullness (satiety) during a meal, causing the person to stop
Catecholamines: Influence satiety between meals, thereby triggering hunger and determining the intervals
Peptides: Influence the reward and pleasurable (sometimes referred to as ‘hedonic’) properties of food
(Blundell et al, 1989).
This approach is reductionist because it assumes that all aspects of eating behaviour
can be explained by biology (neurological factors)
This approach argues from the nature perspective, as it assumes that eating
behaviour is influenced by biological mechanisms rather than social or
This approach argues that eating behaviour is determined by physiological factors,
meaning that the individuals eating behaviour is controlled by factors other than
their own free will (in this sense it is deterministic)
This approach is parsimonious as it explains eating behaviour from one point of view
and ignores other possibilities such as psychological or environmental factors