Explaining OCD Flashcards
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. Additionally, family studies also support a genetic link. Marini and Stebnicki found that individuals with a first-degree relative (e.g., parent or sibling) with OCD were four times more likely to develop the disorder compared to those without an affective relative.
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. Similarly, the increased risk amongst first-degree relatives further supports the idea of hereditary vulnerability.
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.
Strength - Genetics
Point: Another strength of the genetic explanation of OCD is that adoption studies 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 shows that the OCD is not simply a result of environmental factors, such as family upbringing or learned behaviours like compulsions, but that genetic inheritance significantly contributes to the likelihood of developing the disorder. 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: This demonstrates 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 even if they are raised in a completely different environment. Additionally, understanding that OCD risk is heritable may help in early identification and preventative interventions, particularly in children with a family history of the disorder.
Weakness - Genetics
Point: One limitation of the genetic explanation of OCD is that it does not account for the influence of environmental factors on the likelihood of developing the disorder.
Evidence: While research supports the idea that genetic variation can increase vulnerability to OCD, there is strong evidence which suggests that environmental factors can trigger or worsen symptoms. Kiara Cromer et al. found that over half 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. Furthermore, the fact that concordance rates weren’t 100% amongst both monozygotic and dizygotic twins when studying the possibility of developing OCD (Gerald Nestadt) suggests that there is some environmental basis of OCD aside from genetic susceptibility.
Justification: Considering that traumatic events appear to increase both the likelihood and severity of OCD suggests that environmental factors play a crucial role alongside genetic influences. This aligns with the diathesis-stress model, which proposes that genetic vulnerability (diathesis) must interact with environmental stressors for a disorder to develop, henceforth OCD cannot be explained by genetics entirely.
Implication: This lowers the practical value of this explanation because it fails to recognise that there are other influences outside a genetic predisposition (environmental factors) which can impact one’s chances of developing OCD. Without this recognition, psychological interventions, such as Cognitive Behavioural Therapy, cannot be brought forth, in order to manage symptoms alongside providing biological treatments like SSRIs. Additionally, without this understanding, the role of traumas cannot be accounted for and therefore the likelihood of OCD developing amongst individuals cannot be reduced. This emphasises that a more holistic approach that considers both biological and environmental factors may be necessary for a comprehensive understanding and treatment of OCD.
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 serotonin levels have been associated with OCD, as serotonin regulates mood and impulse control. The effectiveness of SSRIs in treating OCD, which increases serotonin levels, further supports the neural explanation.
Justification: Unlike the genetic explanation, which only suggests a genetic vulnerability, the neural explanation provides a clear mechanism for how OCD develops. Furthermore the genetic model is too broad, as OCD is polygenic (Taylor), making it difficult to pinpoint specific causes. In contrast, neural explanations can be measured through brain scans and studies on neurotransmitters, making them more scientific and testable.
Implication: This highlights that the genetic explanation has limited practical applications because it focuses too rigorously on genetic predisposition and doesn’t consider alternative explanations. In contrast, the neural explanation is much more useful, as it provides a clear biological mechanism for OCD that can be tested using empirical methods. This has led to effective treatments, such as the use of SSRIs and neurosurgical interventions, which directly targets neural abnormalities. Therefore, the neural explanation not only offers a stronger scientific basis but also has greater real-world applications in treating OCD.
Neural
- Brain structures
- Neurotransmitters
- Brain structures
It is believed that several regions in the frontal lobes of the brain have abnormal brain circuits in patients with OCD. Two brain regions implicated specifically in OCD are: the basal ganglia and the orbitofrontal cortex.
(see image)
The basal ganglia
The basal ganglia is a cluster of neurons at the forebrain. It is involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD-like symptoms, following their recovery. Max et al. found that when the basal ganglia was disconnected from the frontal cortex during surgery, OCD-like symptoms had reduced, indicating that the basal ganglia has a role in OCD.
The orbitofrontal cortex
The orbitofrontal cortex is a brain region which converts sensory information into thoughts and actions. It is ultimately involved in decision-making, emotional responses and evaluating threats. PET scans have found an overactivity in the orbitofrontal cortex of patients with OCD. One suggestion is that the heightened activity in the orbitofrontal cortex increases the conversion of sensory information into actions, resulting in compulsions. Such overactivity may also lead to exaggerated fear or threat assessment, contributing to obsessive thoughts, as the brain constantly processes and interprets threats as more dangerous than they actually are.
The ‘worry circuit’
The ‘worry circuit’ is a set of brain structures in the orbitofrontal cortex of the brain. It involves the basal ganglia, the caudate nucleus and the thalamus. Communication between these structures appears to be overactive in people with OCD.
In normal functioning, the basal ganglia filters out minor worries coming from the orbitofrontal cortex. Inability to filter out small worries leads to overactivity therefore even small worries get transferred to the thalamus, which is then passed back to the orbitofrontal cortex, forming a loop. These are seen as the recurring obsessive thoughts in OCD sufferers.
Repetitive motor functions (compulsions) are an attempt to break this loop. While carrying out these compulsions may give temporary relief, the hyperactive basal ganglia will soon resume the worry circuit.
- Neurotransmitters
The role of neurotransmitters in OCD specifically involves the action of serotonin and dopamine.
Serotonin
- Serotonin is a neurotransmitter that plays a key role in regulating mood, anxiety and other behaviours. It helps the transmission of signals in the brain and 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 compulsive behaviours and obsessive thoughts, as serotonin plays a key role in controlling repetitive behaviours and reducing anxiety.
- Furthermore, a dysfunctional transmission of serotonin in the brain, particularly in areas like the orbitofrontal cortex and caudate nucleus, is thought to contribute to the development of OCD. This impairment in the transmission of serotonin could be due to serotonin being removed too quickly from the synapse before it has been able to transmit its signal into the postsynaptic neuron. Alternatively, serotonin reuptake may be happening too quickly and frequently in individuals with OCD, leading to reduced serotonin levels in the brain.
Dopamine
- Dopamine is a transmitter involved in reward, motivation and movement. It plays a 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, such as the basal ganglia and caudate nucleus, 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.
- 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, particularly, 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: The orbitofrontal cortex becomes hyperactive in individuals with OCD, leading to excessive worry about potential dangers and obsessive thoughts. Meanwhile, the basal ganglia, particularly the caudate nucleus, may fail to properly filter out these thoughts, resulting in repetitive compulsive behaviours. This dysfunction provides a clear neural explanation for why individuals with OCD experience a cycle of obsessions and compulsions.
Implication: This increases the practical application of the neural explanation as it reinforces the idea that OCD has a strong biological basis by observing its connection to specific brain areas.
Strength - Neural
Point: Another 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 biological link to OCD.
Justification: The fact that SSRIs, which increase serotonin levels, can reduce OCD symptoms strongly suggests that serotonin dysfunction is involved in the disorder. Furthermore, the presence of OCD symptoms in patients with Parkinson’s disease further supports the idea that biological factors, particularly those affecting neurotransmitters like serotonin and dopamine, play a critical role in the development of OCD.
Implication: This suggests a neurobiological basis of OCD by indicating its link to neurotransmitters, therefore increasing its practicality and contributing to the development of effective biological treatments, such as SSRIs and dopamine-modulating medications.
Weakness - Neural
Point: A limitation of the neural explanation of OCD is that there are issues with establishing causality.
Evidence: Research has shown that a significant proportion of individuals with OCD also suffer from clinical depression, a condition strongly associated with low serotonin levels. This suggests that serotonin dysfunction may not be specific to ODC but rather a general factor in mental health disorders.
Justification: If serotonin abnormalities are present in individuals with OCD and depression, it becomes difficult to determine whether low serotonin levels are a cause of OCD or simply a consequence of co-morbidity with depression. This challenges the idea that serotonin dysfunction is a unique causal factor in OCD, as it may just be a general marker of emotional distress rather than a distinct feature of the disorder itself.
Implication: This weakens the validity of the explanation as a link between serotonin and OCD may not be unique to the disorder. If serotonin imbalance in OCD is correlated with the disorder but not necessarily a cause, then treatments targeting it may not be addressing the underlying issue. Therefore, this raises doubts about serotonin-based treatments, such as SSRIs, as their effectiveness may stem from their impact on depression rather than OCD symptoms.
Weakness - Neural
Point: A limitation of the neural explanation of OCD is that it may only describe biological mechanisms involved rather than identifying the root cause of the disorder. In contrast, the genetic explanation offers a more fundamental account of why individuals develop OCD.
Evidence: Twin and family studies provide strong support for a genetic basis of OCD. Gerald Nestadt et al. found that 68% of monozygotic twins share OCD, compared to 31% of dizygotic twins, suggesting a significant genetic influence. Additionally, Marini and Stebnicki found that individuals with a first-degree relative with OCD were four times more likely to develop the disorder.
Justification: The genetic explanation suggests that OCD vulnerability is inherited, meaning that genetic predisposition may shape brain function, making it a stronger causal explanation than neural abnormalities alone. The neural explanation, on the other hand, struggles to establish causation, as abnormalities in serotonin levels or brain structures may be a consequence of OCD rather than a cause.
Implication: This highlights that the neural explanation has limited practical applications because neurobiological differences suggest a correlational relationship between neural features and OCD development. Henceforth, this limits its applicability to real-world situations as it is more likely to focus on symptoms rather than the root cause, which the genetic explanation may be more proficient in doing.
