The Biomedical Model Of Depression

Depression is a mood disorder and the biomedical model portrays one way in which it can be understood. The biomedical model focuses on biological factors alone in an attempt to explain an illness or a disorder. It describes illnesses as disturbances within the human body that can be altered and corrected. Very unlike the biopsychosocial model, it doesn’t include other factors that may contribute to a disorder such as their psychological state or their social context. The biomedical model focuses on activities within the brain alone that can cause disorders like depression. In this assignment I will explain how biological processes in the brain can arguably be perceived to cause depression.
The prefrontal cortex is divided into two hemispheres.
There is a tiny gap between two neurons known as the synapse. Neurotransmitters cross the synapse from one neuron to another and attach onto the receptors of the receiving neuron. Neurotransmitters and receptors have a lock and key relationship; therefore, only specific neurotransmitters will fit into a certain receptor. It is suggested that depression can be caused by a chemical imbalance in the brain such as an imbalance of the neurotransmitters serotonin and dopamine. They have been identified as playing a primary role regulating emotions, regulating appetite, ability to sleep and so
Monoamines are group of neurotransmitters serotonin, noradrenaline, dopamine. It is suggested that people that suffer with depression have less of these neurotransmitters available to attach to the relevant receptor of the receiving neuron. Quite similar to that of the biomedical model this hypothesis believes that a solution to this imbalance would be to increase the number of the neurotransmitter in particular in the synapse so that there are more available to be able to attach onto the requiring receptor. This in turn would correct the mood disorder. Low levels of the neurotransmitters serotonin and dopamine are believed to play a key role in causing depression. Hirschfield 2000 cited in Datta (2010 p.59). claimed that low levels of these three monoamines can cause depression whilst increasing these levels will have the opposite effect and lift it . This is supported by Stanley and Mann; Yates et al cited in Datta (2010 p.61) who suggested that the post mortem results of those who were suffering with depression and had committed suicide had a ‘high number of serotonin receptors in the prefrontal