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.
Homeostatsis:The mechanisms by which biological variables are regulated within defined limits.This is the Idea
that the body is constantly striving to achieve an optimal physiological state (e.g. temperature/ satiety)
Negative feedback:Assumption that any given bodily variable has a set point (or range) and the actual value of
this variable is compared by the body to where it should be and adjusted accordingly.
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’: Activate when you are full to stop
Lateral hypothalamus- ‘feeding centre’: Active when you are hungry to start
More recent research has indicated, however, that there is a more complex system involving:
• ParaventricularHypolthalamus/ Nucleus- Increases eating behaviour
• Perifornical Area- Reduces eating behaviour
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 stimulates eating behaviour.
If injected into the perifornical area, NE reduces eating behaviour.
Leibowitz (1986) found that NE increases calorie intake, and increases the desire for carbohydrates
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, they will continue to consume large
amounts of food, even if they are already ill. This suggests that they may be being driven to eat by the hedonic/
pleasurable qualities of the food, rather than a physiological need to eat.
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 a reduction in appetite and satiation. It also suppresses weight gain.
2. Corticotropin-releasing hormone (CRH): This is a peptide which is produced in the paraventricular
CRH has been found to reduce food intake.
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
Influences the activity of the neurotransmitter Acetylcholine
Smokers generally weigh about seven pounds less than non-smokers (US Dept of Health and Human
Ogden and Fox (1994)- some dieters use smoking as a weight-loss strategy
Ogden (1994)- Smoking cessation may result in increased consumption of calories (particularly from sweet
2. Amphetamines-Amphetamines act on the catecholamines and some on serotonin pathway
Have been found to have an impact on subjective hunger and food intake (Silverstone and Kyriackides,
1982).Have been used legally and illegally by dieters to increase success of diets
3. Alcohol- Hollister (1991) found that alcohol influences eating behaviour in different ways
Looked at research into the effect of alcohol on eating behaviour and found that it sometimes increases
food intake and sometimes deceased food intake
Evaluation of neural explanations of eating behaviour:
Reflection of people’s experience:
People generally start eating when they are hungry
and stop eating when they become full
Insight into brain chemicals:
Practical applications: medical / neurological
treatments for eating disorders (e.g. obesity) could
be suggested if they increase/ decrease eating
Explanation of some differences:
Explains why some people with different disorders
or medical problems may eat more or less food
Lab based research (involving animals):
Although the research is controlled (IV and DV can
be controlled), much of the research has been
conducted on animals which reduces the
generalizability of the findings
Influence of social factors and social drives:
Doesn’t explain why people eat differently in
different situations, or why people eat in some
situations when there is no physiological drive to
Physiological drives can be overridden:
Other factors play a role in how much food a person
consumes (e.g. a desire to be thin will reduce the
amount of food an individual consumes). People
don’t just stop eating because they are full
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