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Discuss one biological explanation of eating behaviour (25)
What we eat, when we eat and our perception of food is our eating behaviour. Hunger and the motivation to eat is
triggered by both environmental and biological cues when our stomach is empty & we need energy. Satiation is when we
are no longer feeling hungry, but instead full. Neural explanation to eating behaviour focuses on the part of the
hypothalamus responsible for regulating our food intake and homeostasis. In this essay, I shall be discussing the role of
the Lateral Nucelus (LN) and the Ventromedial Hypothalamus (VMN) in terms of explaining controlled eating.
The way in which neural mechanisms control our eating behaviour is through homeostasis. The part of the brain in which
is responsible for homeostasis is the hypothalamus. Homeostasis meaning keeping things in our body constant and
balanced, in terms of eating behaviour, it regulates our food intake maintaining equilibrium. The lateral and ventromedial
hypothalamuses are the two areas of the hypothalamus that are involved with regulating our consumption. When our
energy runs low our motivation to eat increases. Our lateral hypothalamus is responsible for alerting us to eat, firing
neurons which evoke feelings of hunger when it the receptors in the LN detect a drop in our glucose levels. Damage
caused to the lateral hypothalamus causes aphagia (also affects thirst and sex), failure to eat whilst stimulation elicits
feeding behaviour. Research conducted by Winn et al show support the theory that damage to our LN can alter our eating
patterns. They administered both large and small doses of the toxin NMDA to make lesions on the lateral hypothalamus
of rats and compared the results to a control group. Those who had small doses did not show any differences, after a
recovery period, to their eating behaviour, whilst those who received large doses showed longterm eating deficits. It was
concluded that damage made to the LN impaired feeding responses.
Criticisms to this study are that the results cannot be extrapolated to humans as it was an animal study. Also, it
wasn't a study focused on the relationship between the LN and controlled eating therefore it may then render the finding
unreliable as the necessary variable may not have been controlled. However, it has established that the LN is not
the only factor involved with alerting us to eat.
Once our glucose levels have reached a certain level, our ventromedial hypothalamus detects the increase in our blood
and acts to suppress our hunger. Electrical stimulation to the VMN has shown reduced eating behaviours however
malfunctions in this part of the hypothalamus may result in obesity, as shown by Baylis' experiment. Two lesions were
made in the VMN of 5 female rats and 8 male rats, results were compared to the agematched control group. Results
showed that the rats overate due to hyperphagia and it was concluded that the VMN plays a role in satiation.
However, again this was an animal experiment so it lacks external validity and it was also unethical. Lesions made to
the VMN could've also affected its surrounding therefore other factors could've contributed to altered eating habits of
the rats. There was a sample bias as only one breed of rats was used and they were a small sample.
To say that our eating behaviour is down to our neural mechanisms render the explanation reductionist as it doesn't
account for other approaches such as psychological or social learning explanations. Our experiences, culture, interests
or how we're nurtured are not taken into account as this approach looks at the nature side, through focusing on the LN &
VMN, of the nurture nature debate. Biological factors can also be overridden by the desire to lose weight, availability
of food, dislike of certain foods... many other things can influence hunger, for example when we think we need food,
but biologically we don't, or stressed, some of us tend to confuse anxiety with hunger, depending on the individual's
emotional intelligence (individual differences). Other areas of the brain are involved in the neural control of cognitive
factors, such as the amygdala which has been linked to our preference to eat foods we are familiar with. Rolls & Rolls
found through removing the amygdala of rats, they then ate familiar and novel foods indiscriminately, whilst amygdala
intact rats stuck to familiar foods. The inferior prefrontal cortex is linked to food smells and damage to this can result in
decreased consumption as smell influences taste.
In conclusion, there are numerous biological factors linked to eating behaviour and it is supported with years of scientific
research. However, most research conducted has been on rats making it difficult to extrapolate the findings to humans,
also it could be argued that some have been unethical. Eating behaviour is too complex to explain through neural
mechanisms alone as it human behaviour is often a complex interaction of social learning, biological and psychological
factors. In order to shed a light on the explanations behind eating behaviour, more research is needed.