Unipolar Depression

• Unipolar Depression (UD) is an affective (mood) disorder characterised by sadness, loss of interest or enjoyment and marked tiredness/fatigue.
• High dropout rates are costly for the NHS and make it difficult in research studies to assess the true effectiveness of the therapy.
• Both the DSM-5 and ICD-10 require symptoms to be present for at least weeks.
• Women are twice as vulnerable to UD, it affects ages 15-24 and 35-44 the most.
• 3.3% of the population is diagnosed with UD per week.
• Symptoms of UD include loss of energy, headaches, stomach upsets, poor personal hygiene, weight changes, sleep pattern disturbance, withdrawal from social life, constant depressed mood, feelings of worthlessness or guilt, hopelessness, loss of pleasure in life, and thoughts of death.
• The Monoamine Hypothesis suggests that depression is caused by depletion of monoamine neurotransmitters.
• Monoamines are a group of neurotransmitters that contain amino acids and regulate mood, including serotonin, noradrenaline and dopamine.
• These neurotransmitters were seen as good candidates because of their known roles in regulating the brain’s limbic system, which is the brain’s emotional centre.
• Low levels of serotonin prevents adequate control over other monoamine neurotransmitters and has a role in sleep, memory, mood and appetite.
• Noradrenaline is related to alertness and energy, low levels are linked to anxiety and the hypothalamus loses its ability to regulate cortisol (high levels = depressive symptoms).
• Dopamine provides attention and rewards, low levels linked to lack of pleasure.
• The Monoamine Hypothesis is supported by Haase and Brown (2015) and Delago (2000), who argue that monoamine deficiencies and drugs to replace these deficiencies are supporting evidence.
• The Monoamine Hypothesis is also supported by the different symptoms of UD, which can be explained by different monoamines.
• The Monoamine Hypothesis is also supported by different methods of scanning depressed patients, such as fMRI and PET scanning, which point to the monoamine hypothesis.
• The Monoamine Hypothesis is weakened by the fact that Selective Serotonin Reuptake Inhibitors (SSRIs) do not help everyone with depression, suggesting that the lack of serotonin is not a complete explanation.
• MRI scans show physical differences in the brain in people with depression, suggesting that drugs increasing serotonin levels affect depression because those heightened levels act to increase the hippocampal area.
• Cipriani et al (2018) reviewed studies of 21 antidepressants: 5 double blind studies of medicine, don’t know if a placebo or not, all found drugs were more effective than placebo.
• SSRIs have fewer side effects than the earlier antidepressants, but there are still adverse reactions like headaches, weight gain, lethargy, nausea and sexual problems.
• SNRIs recognise the role of noradrenaline in depression.
• Duloxetine, a 3rd generation antidepressant, inhibits the reuptake of both serotonin and noradrenaline (links to monoamine depletion).
• The serotonin repeatedly binds to the postsynaptic receptors to prolong the antidepressant effect.
• Beck’s Cognitive Therapy (CBT) uses assessments, education, and therapy sessions to challenge negative thoughts and help patients understand their symptoms.
• Irene Elkin (1989) found that CBT was just as effective in reducing symptoms as antidepressant medication or interpersonal therapy; all were more effective than a placebo pill.
• Improvement with 3rd generation antidepressants is less dangerous in overdose than with MAOIs.
• 3rd generation antidepressants, such as fluoxetine, inhibit the serotonin transporter in the presynaptic membrane and hence inhibit reuptake.
• Shea et al (1992) found that CBT effectiveness continued even after an 18 month follow up.
• SNRIs are also effective for people with anxiety disorders, such as OCD.
• Wiles et al (2016) found that when CBT was given, in addition to usual care that included antidepressants, it was effective in reducing depressive symptoms over the long term (average 46 months) for patients whose depression had not responded to medication alone.
• CBT requires a substantial commitment to session attendance and demanding homework tasks.
• Some may find it hard to adapt to the challenge to well established negative thought patterns.
• NaSSAs are antagonists (blockers) of particular serotonin and noradrenaline receptors involved in depression.
• Noradrenergic and specific Serotonergic Antidepressants (NaSSAs) inhibit the reuptake of serotonin and noradrenaline (both to a lesser extent than SNRIs) - links to the receptor sensitivity hypothesis.
• Both studies demonstrated that CBT was not a particularly useful therapy for severely depressed individuals.
• The Monoamine Hypothesis can be criticised for being reductionist, as it rather simplistically assumes low levels of individual neurotransmitters contribute to depression, when it is a complex matter.
• The Receptor Sensitivity Hypothesis argues that depression is caused by changes in the sensitivity of receptors.
• When there is a depletion of neurotransmitters in the body, the normal reaction is upregulation by increasing the sensitivity of receptors and producing more.
• In depression, serotonin and NA become even more sensitive (supersensitive) to reduced stimulation than normal.
• Post-mortem studies of patients who committed suicide show reduced levels of serotonin and an increased number of serotonin receptor sites, suggesting that the brain was starved of serotonin and adapted by increasing its serotonin receptors to process as much of it as possible.
• A particular gene called 5-HTT has been linked to regulating serotonin levels.