Explaining/Treating

• NEUROTRANSMITTER - Chemical substances that play an important role in the workings of the nervous system by transmitting nerve impulses across a synapse.
• GENETIC EXPLANATIONS - Genes make up chromosomes and consist of DNA which codes the physical features of an organism (such as eye colour, height) and psychological factors (such as mental disorders, intelligence). Genes are transmitted from parents to offspring.
• NEURAL EXPLANATIONS - The view that physical and psychological characteristics are determined by the behaviour of the nervous system, in particular the brain as well as individual neurons.
• Genes are often involved in individual vulnerability to OCD

  • Lewis (1936): out of his patients with OCD (37% had parents with OCD, 21% had siblings with OCD)
• Diathesis stress model:

  • Certain genes leave people more vulnerable and therefore more likely to develop a mental health disorder, but not certain
  • Environmental stress needed to trigger disorder
• DOPAMINE - pleasure neurotransmitter. Feelings of pleasure, and also addiction, movement and motivation. People repeat behaviours that lead to dopamine release.
• SEROTONIN - mood neurotransmitter. Contributes to well being and happiness; helps sleep cycle and digestive system regulation. Affected by exercise and light exposure.
• A possible candidate gene is the SERT gene which is involved in regulating serotonin, a neurotransmitter which facilitates message transfer across synapses. 

  • This creates lower levels of the neurotransmitter 
  • The study found a mutation of this gene in two unrelated families where six of the seven had OCD (Ozaki et al 2003)
• • Another possible candidate gene is the COMT gene
  • COMT is responsible for clearing dopamine from synapses
  • This variation produces lower activity of the COMT gene and higher levels of dopamine (Tukel et al 2013)
  • Dopamine affects motivation and drive
• • OCD is thought to be polygenic. 
  • This means that its development is not determined by a single gene but maybe as many as 230 genes (Taylor 2013)
  • This means that there is little predictive power from this explanation.
• • Different types of OCD: aetiologically heterogeneous
  • The origins (aetiology) may vary from one person with OCD to another (heterogeneous)
  • Also evidence to suggests different types of OCD may be the result of particular genetic variations, e.g. hoarding or religious obsession
• • Dopamine levels are thought to be abnormally high in people with OCD
  • Animal studies are used as evidence - high doses of drugs that enhance levels of dopamine induced stereotyped movements resembling the compulsive behaviours found in OCD patients (Szechtman et al 1998)
• • In contrast with dopamine, it is lower levels of serotonin associated with OCD
  • Anti-Suppressant drugs that increase serotonin levels have been shown to reduce OCD symptoms (Pigott et al 1990) whereas antidepressants that have less effect on serotonin do not reduce OCD symptoms (Jenicke 1992)
• • Researchers have implicated a part of the brain known as the basal ganglia
  • This area of the brain is responsible for innate psychomotor functions
  • Rapport and Wise proposed the hypersensitivity of the basal ganglia gives a rise to the repetitive motor behaviours seen in OCD
• • Other brain areas believed to be involved in OCD include the orbitofrontal cortex (OFC) and the thalamus.
  • The thalamus is a brain area whose functions include cleaning, checking and other safety behaviours.
  • The OFC sends signals to the thalamus about the things that are worrying, such as a potential germ hazard.
  • The caudate nucleus (located in the basal ganglia) normally suppresses signals from the OFC
  • When the caudate nucleus is damaged, it fails to suppress minor signals and the thalamus is alerted, which in turn sends signals back to the OFC
  • This acts as a ‘worry circuit’
• The Worry Circuit (with OCD)

  1. Worry detected by the OFC and message sent to the thalamus
  2. Caudate nucleus is unable to intercept the message, allowing it to pass unfiltered to the sensitive thalamus
  3. Thalamus picks up message and then sends message back to the OFC
  4. OFC then interprets the message and responds with drastic and compulsive behaviour to combat the worry, but only reinforces its purpose.
• One strength of the genetic explanation of OCD is strong support from other research, such as that from twin studies. Nestadt et al (2010) investigated identical twins and found that 68% of identical twins (MZ) shared OCD as opposed to 31% of non identical (DZ) twins. Alternative research conducted by Marini and Stebnicki (2012) found that someone with a family member diagnosed with OCD is around 4 x more likely to develop it as someone without.
• The biological explanation could be too reductionist as environmental factors have been shown to have an effect. Kiara Cromer 2007 conducted a study on 265 individuals with OCD and found that 54% of them had experienced a traumatic event in their past.
• Ahmari (2016) conducted a study on mice, hoping that it would reflect previously obtained results from other experiments (that the hyperactivity of genetically modified mice was down to heightened activity in the striatum), investigating whether neural connections are to blame for this localised hyperactivity. After placing a retrograde tracer into the striatum of control mice, they discovered that another area of the brain was sending messages, the secondary motor cortex. In the mouse model of OCD, these messages are heightened.
• There is supporting evidence. Serotonin antidepressants work to reduce the symptoms (see treatment segment of lesson), and Parkinson’s disease, a biological, degenerative disorder, shares some of its root symptoms with those of OCD. This supports the idea that OCD is a biological issue.
• The International OCD Foundation estimates that between 25 and 50% of all sufferers of OCD will also suffer from clinical depression (this theory is called comorbidity). As a result, and the links between serotonin levels and depression, the seeming biological causes of OCD may be for depression, as both normally coincide together.
• A second limitation is that it is hard to decipher causation and consequence. There is definitely a correlation between serotonin levels and OCD, but this isn’t necessarily neural abnormalities causing OCD, but it could be that OCD causes neural abnormalities.
• Serotonin is released from the presynaptic neuron. Travels across the synapse by diffusion. Binds to complementary receptors on the postsynaptic neuron. The neurotransmitters conveys the signal to the postsynaptic neuron. It is reabsorbed by the presynaptic neuron, broken down and reused. This is what the process should be like.
• SSRIs are an antidepressant drug that blocks the reabsorption of serotonin. 

  • Increases levels of serotonin in the synapse
  • Continues to stimulate the postsynaptic neuron
  • Compensated for whatever is wrong with OCD sufferers’ levels of serotonin.
• • Dosage may vary depending on which SSRI is prescribed
  • Typical dose of fluoxetine (Prozac) is 20mg a day, but may be increased
  • Available as capsules or liquids
  • Takes 3-4 months of daily use to have an impact on symptoms
• • Often used alongside CBT
  • Drugs reduce the emotional characteristics e.g. feelings of anxiety or depression
  • Then patients can engage with CBT techniques
  • In practice, some people respond better to CBT alone, whilst others have more benefit with the drug treatment
• TRICYCLICS

  • Older type of antidepressant e.g. clomipramine
  • Acts on various systems including serotonin, very similarly to SSRIs
  • More severe side effects are generally kept in reserve for people who don’t respond to SSRIs.
• SNRIs

  • Serotonin-noradrenaline Reuptake Inhibitors
  • More recently used 
  • Different class of antidepressants and also used as a second line of defence
  • SNRIs increase levels of serotonin as well as noradrenaline.
• G Mustafa Soomro et al 2009 reviewed 17 studies that compared SSRIs to placebos in the treatment of OCD. All 17 studies showed significantly better outcomes for SSRIs than placebos. Typically, symptoms reduce for around 70% of people. The other 30% can be treated with alternative treatments such as different drugs and CBT.
• HOWEVER, drugs may not be the optimum method of treatment: Skapinakis 2016, carried out a systematic review and found that cognitive and behavioural treatments might be more efficient in treating the majority.
• There are many serious side effects that could reduce the comfort in taking tablets. SSRIs, while not necessarily the worst example, have been associated with sexual dysfunction and weight gain as a result of carbohydrate craving and indigestion. The tricyclic clomipramine is particularly severe - 1 in 10 experience erection problems and weight gain - 1 in 100 become aggressive and experience heart-related problems.
• There is a lack of independent studies that aren’t backed by, or have motive to, the benefit of institutions. Goldacre 2013 theorised that much of the research conducted is biassed and used to uphold sales. Further, there are not so many studies that investigate drugs that aren’t sponsored, so whilst the available evidence suggests that drugs are effective, it could be deceptive and the truth could be shielded by the corporate marketing campaign.