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In 2017, 17% of the adult population was prescribed antidepressants in the UK (Gov.UK, 2020). Antidepressants remain the first line of treatment for depression and can be an easily accessible, life-saving intervention.
Nevertheless, they have been surrounded by controversy in the psychological community. To understand the clinical benefits and risks associated with antidepressant treatment, we need to understand how they work.
Pharmacology is an intervention commonly used to treat depression, freepik.com/pch.vector
Moving along, we will draw the difference between antipsychotic and antidepressant medications.
Finally, we will evaluate pharmacological treatment for depression, considering antidepressant medication's effectiveness and antidepressant medication side effects.
Pharmacological treatment for depression relies on the assumption that depression is a biological disease or at least a disease with a significant biological component. Antidepressant treatment aims to relieve depressive symptoms by correcting biological abnormalities hypothesised to cause depression. The clinical use of antidepressants, which target specific neurotransmitters, resulted in the development of the monoamine theory of depression.
The monoamine theory is an example of a biological explanation. It proposes that depression is caused by an imbalance of monoamine neurotransmitters in the brain. In particular, much focus has been directed to serotonin, as its function overlaps with many depressive symptoms. Therefore, depleting serotonin is theorised to be responsible for the symptomatology of depression.
Monoamine neurotransmitters, hypothesised to play a role in depression, include serotonin, adrenaline, and noradrenaline. Serotonin is involved in the regulation of different biological functions as well as mood, while adrenaline and noradrenaline are involved in the fight-or-flight response to stress. These neurotransmitters essentially relay messages between neurons and are required to work correctly for human functioning.
The monoamine theory of depression supports the influence of nature (genetics) on psychological problems like depression.
This theory could explain why Selective Serotonin Reuptake Inhibitors (SSRIs) are effective at treating depression. SSRIs are a group of medications that act as serotonin agonists, which essentially means that it increases the availability and action of serotonin in the brain.
Neurons communicate by releasing neurotransmitters into the synapses between them. Usually, after a neurotransmitter has been released to excite the postsynaptic neuron, the neurotransmitter is reabsorbed back to the neuron that released it. SSRIs prevent serotonin from being reabsorbed, resulting in greater amounts of serotonin in the synapse.
Neuronal activity of specific neurotransmitters such as serotonin has been found to be affected in people with depression, freepik.com/goonerua
It can take up to six weeks after starting treatment for antidepressants to take effect. If a patient doesn't respond to a particular antidepressant, the doctor might decide to increase or change the medication dose.
The first antidepressant introduced to the clinical practice in the 1950s was Iproniazid, a monoamine oxidase inhibitor (MAOI) originally developed to treat tuberculosis. Due to its side effects, which included elevation in mood and arousal as well as improved sleep and appetite, it started to be prescribed to people with depressive symptoms.
Soon after, a tricyclic antidepressant (TCA) Imipramine was introduced. Imipramine was developed to treat psychotic symptoms. While it failed to show effectiveness as a schizophrenia treatment, it was reported to improve depressive symptoms for many people, with reportedly fewer side effects than iproniazid.
Early antidepressants were associated with significant side effects to minimise those SSRIs, and Serotonin and noradrenaline reuptake inhibitors (SNRIs) were developed in later decades, which affect the neurotransmitters associated with depression selectively. Studies have shown the new antidepressants to be more tolerable for patients and just as effective as the older ones (Anderson, 2001). Currently, these are also the first line of treatment for depression, with MAOIs and TCAs prescribed for depression resistant to treatment with SSRIs and SNRIs.
MAOIs - increase dopamine, adrenaline, noradrenaline and serotonin levels in the brain.
TCAs - act as serotonin and noradrenaline agonists but also block acetylcholine, muscarine and histamine receptors.
SSRIs - selective serotonin agonists.
SNRIs - serotonin and noradrenaline agonists.
Noradrenaline and Specific Serotoninergic Antidepressants (NASSAs) - increase the transmission of noradrenaline and serotonin.
SSRIs: fluoxetine, paroxetine, citalopram, escitalopram, sertraline and fluvoxamine.
SNRIs: duloxetine and venlafaxine.
NASSA: mirtazapine.
If depression is treatment-resistant, patients may be prescribed:
Antipsychotic medication influences the transmission of a monoamine neurotransmitter, dopamine. One theory of schizophrenia proposes that psychotic symptoms can be caused by increased dopamine transmission in the brain. Antipsychotic medication act by blocking dopamine receptors on the postsynaptic neuron, decreasing the amount of dopamine that can get to those receptors.
In a nutshell, SSRIs are serotonin agonists. They make more serotonin available in the synapse, increasing serotonin transmission. Whereas antipsychotics are dopamine antagonists, they inhibit dopamine transmission by blocking the receptors dopamine should bind to.
Antidepressants clearly target depression symptoms. But does pharmacological treatment really address the underlying problems? How long-term are the effects of antidepressants? Are the side effects worth it? These are all important questions to consider when evaluating the use of antidepressant medication.
To test the efficacy of antidepressants, studies compare the change in the number and severity of depressive symptoms between a group given antidepressant treatment and a group treated with placebo. Meta-analyses of those trials can be used to confirm that antidepressants are more effective than a “sugar pill”.
Cipriani and colleagues (2018) conducted a meta-analysis of 522 published and unpublished trials investigating the efficacy of antidepressants after eight weeks of treatment. They found all antidepressants to be more effective than placebo. The highest effectiveness was found for a TCA – Amitriptyline, which was more than twice as effective as a placebo. This meta-analysis strongly supports the effectiveness of antidepressants in improving depressive symptoms.
However, other large-scale studies raise critical issues with long-term antidepressant treatment. An investigation followed 3,294 patients for nine years. It was found that antidepressant use was associated with greater symptom severity after nine years in patients who received antidepressant medication than in those who did not receive medication (Vittengl, 2017).
Is the research biased? Research on the effectiveness of antidepressants has been heavily criticised due to potential conflict of interest, as many studies are sponsored by companies manufacturing antidepressants.
The antidepressant drug market is predicted to rise to almost 16 billion dollars in 2023. This earning potential certainly casts doubt on the validity of findings produced by drug companies.
A common research method used to investigate the effectiveness of various medications to treat depression involves measuring and comparing depressive symptoms before and after receiving treatment, freepik.com/pch.vector
Newer antidepressants such as SSRIs or SNRIs are associated with less side effects in comparison to previously used antidepressants. Not everyone taking antidepressants will experience side effects. It is estimated that around 60% of people don't. Still, for a minority of patients, side effects can be severe and lead them to discontinue treatment.
Common side effects of SSRIs include agitation, anxiety, digestive issues, nausea, loss of appetite, insomnia, dizziness, loss of libido, blurred vision, headaches and erectile dysfunction.
It is also important to assess and monitor the suicide risk of young people that are prescribed antidepressants. This is because one of the adverse effects of those medications is a potential elevation in suicidality, especially in people under 25.
Pharmacological treatment for depression can be considered to be a reductionistic approach, which largely ignores psychological factors and reduces a complex condition to a biological problem. One way to make depression treatment more holistic and therefore potentially more effective is to offer people both pharmacological and psychological interventions, like Cognitive Behavioural Therapy.
A meta-analysis by Cuijpers and colleagues (2014) found combined treatment, consisting of CBT and antidepressants, to be twice as effective then using pharmacological treatment alone to treat depression, Obsessive Compulsive Disorder and Panic disorder.
These findings highlight the importance of holistic clinical interventions.
One major advantage of antidepressants is their availability and cost. Getting an antidepressant prescription from a GP is a much quicker process than accessing psychological therapies on the NHS. It is also much more affordable for people to take antidepressants than to pay for private therapy sessions. Overall, the accessibility of antidepressants makes them a crucial intervention for people in need of immediate and affordable treatment.
Antidepressant medications reduce depressive symptoms by affecting the transmission of neurotransmitters like serotonin in the brain.
A meta-analysis of Cipriani and colleagues (2018) found Amitriptyline, a tricyclic antidepressant, to have the highest effectiveness. However, tricyclic antidepressants are also associated with more side effects and are rarely used as a first-line treatment.
Antidepressant medication works by affecting the transmission of neurotransmitters in the brain. For example, SSRIs act by increasing the amount of serotonin in the synapses between neurons. Increased levels of serotonin is associated with fewer depressive symptoms.
Some of the newest antidepressants approved by the FDA include Brexanolone and Esketamine. Brexanolone acts to regulate hormones contributing to post-partum depression, while Esketamine is an anaesthetic drug recently introduced in the US to treat treatment-resistant depression.
Anxiety is often treated with antidepressants like SSRIs and SNRIs. Other treatments for anxiety include Pregabalin and benzodiazepines, both of which affect the GABA neurotransmitter. These medications are not all examples of antidepressants.
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