explaining OCD

• Family studies indicate a genetic predisposition for OCD, candidate genes, like 5HT1-D beta, linked to serotonin regulation. While OCD is polygenic, involving multiple genetic variations, up to 230 genes may contribute, affecting neurotransmitter actions, particularly ser n dop. Both play a role in regulating mood. The heterogeneity of OCD's aetiology suggests different genetic influences & specific variations may lead to distinct OCD subtypes, like hoarding. According to the diathesis-stress model, genes create vulnerability & an environmental stressor is necessary to trigger the condition.
• Neurological explanations highlight serotonin's role in mood regulation; low serotonin levels may disrupt mood transmission, contributing to OCD symptoms. Additionally, impaired decision-making in OCD, notably in hoarding disorder, may stem from frontal lobe abnormalities, affecting logical thinking and emotional processing in regions like the left parahippocampal gyrus. These biological underpinnings underscore the complex interplay of genetics, neurotransmitters, and brain structures in OCD.
• Point: One strength of the genetic explanation for OCD is the strong evidence base.

  Evidence: Twin studies reviewed by Nestadt (2010) found a higher concordance rate for OCD in identical twins (68%) compared to non-identical twins (31%). 

  Explain: Family studies also show a fourfold increased risk of OCD in individuals with a family history of the disorder.

  Link: Therefore, this suggests that genetic factors play a crucial role in the development of OCD.
• Point: One limitation of the genetic model of OCD is the presence of environmental risk factors.

  Evidence: Cromer (2007) found that over half of OCD patients had experienced a traumatic event, and OCD severity was higher in those with trauma.

  Explain: This indicates that environmental factors, such as trauma, can trigger or worsen OCD symptoms.

  Link: Thus, genetic vulnerability alone does not fully explain the onset and severity of OCD symptoms.
• Point: One strength of the neural model of OCD is the existence of some supporting evidence.

  Evidence: Antidepressants targeting serotonin are effective in reducing OCD symptoms, suggesting a role for serotonin in OCD.

  Explain:  Additionally, OCD symptoms are present in conditions known to be biological in origin like Parkinson's disease, indicating a biological basis for OCD.

  Link: Therefore, this suggests that biological mechanisms play a significant role in OCD aetiology.
• Point: One limitation of the neural model is that the serotonin-OCD link may not be unique.

  Evidence: Many individuals with OCD also experience clinical depression, which also  involves disruptions in serotonin activity.

  Explain: This complicates the interpretation of serotonin's role in OCD, as it is unclear whether serotonin disruptions in OCD are simply a consequence of the depression.

  Link: Hence, serotonin may not be uniquely relevant to OCD symptoms, challenging the serotonin hypothesis in OCD pathology.