Explaining OCD Flashcards
(17 cards)
Explanations of OCD
- Genetics
a. Polygenic
b. Genetic variations - Neural
a. Brain structures
b. Neurotransmitters
Genetics
- Polygenic
- Genetic variations
- Polygenic
- There is no single gene that causes OCD; however, it’s thought that a vulnerability or predisposition to OCD is inherited from parents.
- OCD seems to be polygenic, meaning that there are multiple genes involved in increasing the risk of developing the disorder.
- Taylor analysed findings of previous studies and found evidence that up to 230 different candidate genes may be involved in OCD.
- Genes that have been studied in relation to OCD include those associated with the action of dopamine as well as serotonin, both neurotransmitters believed to have a role in regulating mood and compulsive behaviours.
- Genetic variations
COMT: The COMT gene regulates the neurotransmitter dopamine. Although all genes come in different forms, one variation of the COMT gene results in higher levels of dopamine, which may contribute to compulsive behaviours. This variation is more common in patients with OCD, compared to people without OCD.
SERT: The SERT gene is linked to serotonin and affects the transport of this neurotransmitter. Transportation issues cause lower levels of serotonin to be active within the brain and are associated with OCD as well as depression. Ozaki et al. published results from a study of two unrelated families who both had mutations of the SERT gene. It coincided with 6 out of 7 of the family members having OCD.
Strength - Genetics
Point: One strength of the genetic explanation of OCD is the strong evidence base supporting the role of genetic factors in the disorder.
Evidence: Twin studies provide strong evidence for a genetic component. Gerald Nestadt et al. reviewed twin studies and found that 68% of monozygotic twins shared OCD, compared to 31% of dizygotic twins. Since monozygotic twins share 100% of their genes, whilst dizygotic twins only share about 50%, this higher concordance rate in monozygotic twins suggests a genetic influence.
Justification: The higher concordance rates in monozygotic twins compared to dizygotic twins indicates that genes play a significant role in OCD. If OCD were entirely due to environmental factors, we would expect concordance rates to be similar in monozygotic and dizygotic twins, which is not the case.
Implication: This strong evidence base highlights that the genetic explanation has high practical applications. Therefore, genetic research can contribute to the development of targeted drug treatments, such as SSRIs, that help regulate neurotransmitters involved in OCD.
Counterargument: However, a limitation of the genetic explanation of OCD is that it does not account for the fact that concordance rates are not 100% in monozygotic twins.
Evidence: Although Nestadt et al. found that 68% of monozygotic twins both had OCD, this still leaves 32% who did not share the disorder, despite having identical genetic make-up. Research from Kiara Cromer et al. even found that 54% of 265 of the OCD clients in their study had experienced a traumatic event in their past. Additionally, those who had suffered one or more traumas tended to have more severe OCD symptoms, suggesting that life experiences contribute to the onset and intensity of the disorder.
Justification: This discrepancy suggests that genetics alone cannot fully explain the onset of OCD. Environmental influences, such as stressful life events likely interact with genetic vulnerability to trigger symptoms of OCD. This idea is supported by the diathesis-stress model, which proposes that mental disorders are the result of an interaction between genetic predisposition and environmental stressors.
Implication: Therefore, the genetic explanation may be reductionist as it oversimplifies OCD by focusing solely on biological influences and ignoring the complex interplay of psychological and environmental factors. A more holistic approach may be needed to fully understand and treat the disorder.
Strength - Genetics
Point: Another strength of the genetic explanation of OCD comes from adoption studies which support the idea that OCD has a genetic basis.
Evidence: Adoption studies examine whether OCD risk is due to genetic inheritance or environmental factors. McKeon et al. conducted an adoption study on individuals with OCD. They compared the rates of OCD in adopted children with those in their biological families and adoptive families. The researchers identified that children with a biological parent who had OCD were more likely to develop OCD themselves, even if they were raised in an environment without the biological parent. Furthermore, children whose adoptive parents had OCD did not have the same increased risk.
Justification: This demonstrates that genetic inheritance significantly contributes to the likelihood of developing OCD. It rules out environmental influences as the sole cause by showing that genetic factors are passed on, even when the children are raised in different households.
Implication: As a result, this suggests that the genetic explanation of OCD has strong practical implications as it showcases the heritable nature of the disorder through identifying that individuals with a family history of OCD are still vulnerable to developing it regardless of the environment they were raised in. This makes this explanation useful in constructing preventative interventions and treatments in children with a family history of the disorder.
Strength - Genetics
Point: A further strength of the genetic explanation of OCD is that it is supported by findings from family studies.
Evidence: Marini and Stebnicki found that individuals with a first-degree relative, such as a parent or sibling, who suffers from OCD are four times more likely to develop the disorder compared to those without an affected relative.
Justification: This increased prevalence among biologically related individuals provides strong support for the idea that OCD can run in families due to shared genetic makeup. First-degree relatives share approximately 50% of their genes, so a significantly higher risk in this group suggests that genetic factors may predispose individuals to OCD. While environmental influences can also play a role, the consistency of results across multiple family studies points to a strong genetic component.
Implication: These findings enhance the credibility of the genetic explanation by demonstrating a clear pattern of inheritance, therefore providing important real-world applications by helping identify individuals who are at greater genetic risk and allowing for earlier monitoring, support, and potentially prophylactic interventions before symptoms become severe.
Weakness - Genetics
Point: A limitation of the genetic explanation is that it only identifies vulnerability to OCD, not how symptoms develop. In contrast, the neural explanation provides a clearer mechanist viewpoint, linking brain dysfunction and neurotransmitter imbalances directly to OCD symptoms.
Evidence: Research conducted by Saxena and Rauch shows that individuals with OCD have abnormal functioning in brain areas such as the orbitofrontal cortex and basal ganglia, which are overactive and linked to compulsive behaviours. Additionally, Hu et al. found that low levels of serotonin have been associated with OCD, as serotonin regulates mood and impulse control.
Justification: Unlike the genetic explanation, which only suggests a genetic vulnerability, the neural explanation provides a clear understanding for how OCD develops. Furthermore the genetic model is too broad as OCD is polygenic, making it difficult to pinpoint specific genes involved in various cases of OCD. Conversely, neural explanations can be measured through brain scanning and imaging techniques by mapping the disorder to specific brain regions, making this method more beneficial and testable.
Implication: This highlights that the genetic explanation has limited practical applications because it focuses too rigorously on genetic predisposition which only identifies vulnerability to OCD instead of cause, which the neural explanation is more successful in demonstrating. This limits its usefulness in developing effective treatments because without understanding the underlying causes, interventions cannot be precisely implemented.
Neural
- Brain structures
- Neurotransmitters
- Brain structures
It is believed that several regions in the frontal lobes of the brain are implicated in OCD, these regions are all intertwined into a system called ‘the worry circuit’.
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The ‘worry circuit’
The ‘worry circuit’ is a group of brain areas involved in decision-making and emotional regulation, including the orbitofrontal cortex, basal ganglia, caudate nucleus, and thalamus. In people with OCD, this circuit is thought to be overactive, which can lead to persistent obsessive thoughts and compulsive behaviours.
The orbitofrontal cortex helps process sensory information, evaluate threats, and guide decisions. In OCD patients, PET scans show this area is more active than normal, which may cause the brain to overreact to minor threats, leading to intrusive thoughts.
The basal ganglia (especially the caudate nucleus) normally filters out minor or unnecessary worries from the orbitofrontal cortex. In OCD, this filter doesn’t work properly, so even small worries are passed on to the thalamus and then back to the orbitofrontal cortex—creating a repeating loop of worry. This may explain why obsessive thoughts keep coming back. Max et al. found that disconnecting the basal ganglia from the frontal cortex reduced OCD-like symptoms. Also, people with injuries to the basal ganglia sometimes develop OCD symptoms.
Compulsions are behaviours people use to try to stop the worry loop. These actions give temporary relief, but the circuit stays overactive, so the cycle continues.
Another brain area involved is the parahippocampal gyrus, which helps manage negative emotions. This area also functions abnormally in OCD, possibly contributing to the anxiety that drives obsessions and compulsions.
- Neurotransmitters
The role of neurotransmitters in OCD specifically involves the action of serotonin and dopamine.
Serotonin
- Serotonin is a neurotransmitter that helps in the transmission of signals in the brain. It is involved in emotional regulation and impulse control.
- Low levels of serotonin are thought to contribute to OCD symptoms. It is believed that when serotonin levels are insufficient or functioning improperly, it can lead to obsessive thoughts and compulsive behaviours, as serotonin plays a key role in controlling repetitive behaviours and reducing anxiety.
- Such low levels of serotonin occur when the process of reuptake of serotonin from the synapse occurs too quickly and it is the SERT gene responsible for serotonin transportation in the synapse.
Dopamine
- Dopamine is a neurotransmitter involved in reward, motivation and movement. It plays a key role in reinforcing behaviours and is often linked to pleasure and reward pathways in the brain.
- Abnormal dopamine levels in the brain may play a role in OCD. Increased dopamine activity in certain areas of the brain, e.g., the basal ganglia, have been linked to compulsive behaviours. This may explain the repetitive and ritualistic behaviours often seen in OCD. Such behaviours are seen as a ‘reward’ as they help compensate for the obsessive thoughts faced by OCD sufferers.
- Additionally, hyperactivity of dopamine in the brain can lead to an overestimation of threat or risk, contributing to these obsessions and driving the need for compulsive rituals to reduce anxiety.
Strength - Neural
Point: A strength of the neural explanation of OCD is the supporting research on brain structures.
Evidence: Neuroimaging studies, such as that of Saxena and Rauch, have consistently shown that individuals with OCD have hyperactivity in their orbitofrontal cortex. Additionally, research by Pujol et al found that the basal ganglia, especially the caudate nucleus, which is involved in regulating movement and filtering out unnecessary thoughts, functions abnormally in OCD patients. These abnormalities are part of the ‘worry circuit’, which is thought to be dysfunctional in OCD sufferers.
Justification: These findings strengthen the neural explanation of OCD by showing a clear link between abnormal brain activity and the symptoms of the disorder. The consistent evidence from neuroimaging studies adds scientific credibility and objectivity, as it provides observable and measurable data.
Implication: This strengthens the practical value of the neural explanation, as identifying specific brain areas involved in OCD can lead to more targeted treatments, such as neurosurgery or drug therapies aimed at reducing activity in overactive regions, thereby improving symptoms and quality of life for sufferers.
Counterargument: A limitation of the neural explanation of OCD is that much of the supporting research is correlational rather than causal.
Evidence: Although neuroimaging studies, such as those by Saxena and Rauch, consistently find hyperactivity in brain areas like the orbitofrontal cortex and the basal ganglia in individuals with OCD, these findings only demonstrate an association. They do not establish whether the abnormal brain activity causes OCD or whether it is a consequence of having the disorder.
Justification: This weakens the explanatory power of the neural explanation as without clear evidence of causation, it is difficult to determine whether targeting these brain areas through treatment would effectively address the root cause of OCD. Other confounding factors may also contribute to both the symptoms and the observed brain abnormalities.
Implication: As a result, while the neural explanation is supported by objective imaging data, its practical application in treatment planning may be limited if it cannot reliably identify the underlying cause of OCD. This reduces confidence in the model’s ability to fully explain the disorder.
Strength - Neural
Point: A strength of the neural explanation of OCD is the existence of supporting evidence that links biological processes, such as neurotransmitter imbalances, to OCD symptoms.
Evidence: Research shows that antidepressants which specifically target serotonin, such as SSRIs, are effective in reducing OCD symptoms. Additionally, research by Nestadt et al. found that OCD symptoms are present in individuals with Parkinson’s disease, a neurodegenerative condition linked to dopamine imbalance, which also suggests a neural link to OCD.
Justification: This evidence supports the neural explanation by demonstrating a clear link between neurotransmitter imbalances and OCD symptoms. The effectiveness of SSRIs suggests that low serotonin contributes to the disorder, while the presence of OCD symptoms in people with Parkinson’s disease highlights the role of dopamine.
Implication: This adds to the credibility of the neural explanation of OCD, as it is backed by pharmacological and neurological evidence. This increases its practicality by contributing to effective biological treatments for OCD, such as SSRIs and dopamine-modulating medications.
Strength - Neural
Point: A strength of the neural explanation of OCD is the supporting research into the effectiveness of drug treatments that target neural mechanisms.
Evidence: A meta-analysis by Soomro et al. found that selective serotonin reuptake inhibitors (SSRIs) were significantly more effective than placebos in reducing OCD symptoms across multiple studies. SSRIs work by increasing levels of serotonin in the brain, which is believed to be abnormally low in OCD sufferers.
Justification: This supports the neural explanation by showing that manipulating neurotransmitter levels, particularly serotonin, can alleviate OCD symptoms. The consistency of the findings across many studies increases the reliability of the link between neural mechanisms and OCD.
Implication: This strengthens the practical value of the neural explanation, as it leads to effective, evidence-based drug treatments for managing OCD. It also highlights how understanding the neurological basis of the disorder can improve patient outcomes through targeted medical interventions.
Counterargument: However, a limitation of the neural explanation of OCD is that the effectiveness of drug treatments is not always consistent.
Evidence: Although SSRIs alter serotonin levels in the synapse within hours, they often take several weeks to reduce symptoms. Additionally, research shows that 40% to 60% of patients experience no or only partial symptom improvement.
Justification: This inconsistency suggests that while serotonin may play a role in OCD, it is unlikely to be the sole cause. If serotonin imbalance were the only explanation, we would expect quicker and more consistent treatment outcomes. It could even be that the low levels of serotonin are a consequence of comorbidity with depression considering that depression is one of the emotional characteristics of OCD.
Implication: This highlights that the neural explanation may be overly simplistic and reductionist, as it overlooks other potential contributing factors such as cognitive, environmental, or psychological influences that could be involved in the development and maintenance of OCD.
