Depression: What 's Really Going On In The Brain
For this week's Mental Health Mondays blog, we're handing over to Neuroscience Student at King’s College London & Mental Health advocate, Ella Stanley to give her scientific perspective on what depression really is, it's potential physiological causes and how it can best be treated...
Over the last couple of years’ conversations around mental health have been gaining momentum. Research into the causes and treatment of various mental health conditions has also been growing subsequent to new funding and demand. Depression has become one of the leading areas of research with an estimated 350 million sufferers(1)and is the leading cause of disability worldwide according to the World Health Organisation. Most people understand depression as ‘low mood’, ‘extreme sadness’ or the inability to get out of bed and function optimally, all of which can be true however there is more to depression than just a bad bout of sadness…
What is depression?
The term depression is often used to describe exclusively unipolar depression, also known as a major depressive disorder and/or recurrent depressive disorder. During depressive periods sufferers can experience low mood, disturbed sleep, anxiety symptoms, changes in appetite, feelings of guilt and low self-worth. Globally, unipolar depression is the most widely spread depressive mood disorder, however, bipolar depression, commonly known as ‘bi-polar’ is also a depressive mood disorder. Bi-polar sufferers experience swings between depressive and elevated moods which can last for prolonged periods of time. During elevated, manic episodes’ individuals endure racing thoughts, over-activity, insomnia and an elevated or irritable mood.
What are the most popular theories of depression?
Many of us have come to think of depression as a result of a ‘chemical imbalance’ where levels of serotonin (our happy neurotransmitter) are significantly reduced. This idea stems from the monoamine hypothesis which deduced that the underlying pathophysiological basis of depression is a result of depleted levels of monoamine neurotransmitters(3), serotonin, dopamine and noradrenaline/norepinephrine within the central nervous system. This proposal is supported by the action of antidepressants, such as SSRI’s (selective serotonin reuptake inhibitors) which increase serotonin activity at the synapse and subsequently increase its transmission, elevating depressive moods.
Although the monoamine hypothesis of depression is the most widely accepted theory there are other theories gaining momentum. There have been numerous studies looking at the role of neurotrophic factors in the development of depressive disorders. Neurotrophic factors, especially the brain-derived neurotrophic factor (BDNF) are critical for the regulation, formation and plasticity of neuronal networks(2). Recent clinical trials looking into the role of BDNF and mood disorders have shown that serum and plasma BDNF levels may be reduced in untreated depressive patients.
This reduction in BDNF and subsequent neuronal plasticity can, however, be reduced or counteracted by the use of anti-depressants which suggests depression may be influenced by reduced neuronal plasticity, not just neurotransmission.
Although the development of depression is certainly influenced by biological and genetic factors there are also large environmental, lifestyle and social factors that should be considered too. It’s no secret that traumatic life events can trigger the onset or episode of depression. Essentially the stress caused by trauma, or just a fast-paced lifestyle can negatively impact neuronal plasticity and the transmission of our ‘happy’ neurotransmitters such as serotonin and dopamine.
How do we treat depression?
There are several different routes to consider when treating depressed individuals however the DCM-5 encourages the use of therapeutic techniques such as cognitive based therapy (CBT) and psychotherapy as the initial form of treatment especially in children or those with mild symptoms. For moderate to severe cases however it is recommended to combine talk therapy with the use of antidepressants.
There are new methods and drugs currently being explored within the research community, for example, ECT (electroconvulsive therapy) which triggers an epileptic seizure and can reverse the depressive state. The use of ECT in treating depression is being greatly explored subsequently to the faster onset compared to traditional anti-depressant medication. However, the use of ECT can occasionally cause long-term, debilitating memory loss and subsequently is only really used for research purposes or in severe, life-threatening cases.
In a nut-shell depression is a mood disorder that can affect anyone independent of age, gender, ethnicity and socio-economic background. Current research suggests that a number of genes may collectively influence the onset of depression which may lead to changes in the neurological architecture and neurotransmission. With that being said our lifestyle can act as a preventative tool to those who may be at ‘high risk’ or already suffering from mild depressive symptoms. Regular exercise, a balanced diet and social connection are often the pillars of a happy, healthy mind. Don’t be afraid to seek help or ask a friend, it really is important to be kind to your mind.
If you are experiencing any of the symptoms of depression try and book an appointment with your GP. If that feels a little daunting or you know someone struggling with depression, here are some links that may be helpful:
- World Health Organization. (2018). Depression. [online] Available at: http://www.who.int/news-room/fact-sheets/detail/depression [Accessed 6 Aug. 2018]
- Lee, B. and Kim, Y. (2010). The Roles of BDNF in the Pathophysiology of Major Depression and in Antidepressant Treatment. Psychiatry Investigation, 7(4), p.231.
- Heninger, G., Delgado, P. and Charney, D. (1996). The Revised Monoamine Theory of Depression: A Modulatory Role for Monoamines, Based on New Findings From Monoamine Depletion Experiments in Humans. Pharmacopsychiatry, 29(01), pp.2-11.