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| An evolutionary psychology view is that moderate versions of compulsive behavior may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth, or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view OCD may be the extreme statistical "tail" of such behaviors possibly due to a high amount of predisposing genes.[31]
| | As a part of evolution, different species have grown to safeguard themselves by gathering/ hoarding food and constantly check for the threats around them. These [[evolutionary]] traits being passed on from generations may have a psychological cause for OCD. |
| | | <ref> Bracha, H. |
| Biological
| | (2006). "Human brain evolution and the "Neuroevolutionary Time-depth |
| | | Principle:" Implications for the Reclassification of |
| Main article: Biology of obsessive–compulsive disorder
| | fear-circuitry-related traits in DSM-V and for studying resilience to |
| | | warzone-related posttraumatic stress disorder". Progress in Neuro-Psychopharmacology and Biological Psychiatry 30 (5): 827–853. doi:10.1016/j.pnpbp.2006.01.008. PMID 16563589.</ref> |
| OCD has been linked to abnormalities with the neurotransmitter serotonin, although it could be either a cause or an effect of these abnormalities. Serotonin is thought to have a role in regulating anxiety. To send chemical messages from one neuron to another, serotonin must bind to the receptor sites located on the neighboring nerve cell. It is hypothesized that the serotonin receptors of OCD sufferers may be relatively understimulated. This suggestion is consistent with the observation that many OCD patients benefit from the use of selective serotonin reuptake inhibitors (SSRIs), a class of antidepressant medications that allow for more serotonin to be readily available to other nerve cells.[32]
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| A possible genetic mutation may contribute to OCD. A mutation has been found in the human serotonin transporter gene, hSERT, in unrelated families with OCD.[33] Moreover, data from identical twins supports the existence of a "heritable factor for neurotic anxiety".[34] Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases where OCD develops during childhood, there is a much stronger familial link in the disorder than cases in which OCD develops later in adulthood. In general, genetic factors account for 45-65% of OCD symptoms in children diagnosed with the disorder.[35] Environmental factors also play a role in how these anxiety symptoms are expressed; various studies on this topic are in progress and the presence of a genetic link is not yet definitely established.
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| People with OCD evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, while decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri.[36][37] These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular / caudate nuclei, while also decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri.[37] Orbitofrontal cortex overactivity is attenuated in patients who have successfully responded to SSRI medication, a result believed to be caused by increased stimulation of serotonin receptors 5-HT2A and 5-HT2C.[38] The striatum, linked to planning and the initiation of appropriate actions, has also been implicated; mice genetically engineered with a striatal abnormality exhibit OCD-like behavior, grooming themselves three times as frequently as ordinary mice.[39] Recent evidence supports the possibility of a heritable predisposition for neurological development favoring OCD.[40]
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| Rapid onset of OCD in children and adolescents may be caused by a syndrome conntected to Group A streptococcal infections (PANDAS)[41][42] or caused by immunologic reactions to other pathogens (PANS).[43]
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| Neurotransmitters role
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| Main article: Etiology of obsessive-compulsive disorder
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| Researchers have yet to pinpoint the exact cause of OCD, but brain differences, genetic influences, and environmental factors are being studied. Brain scans of people with OCD have shown that they have different patterns of brain activity than people without OCD and that different functioning of circuitry within a certain part of the brain, the striatum, may cause the disorder. Differences in other parts of the brain and neurotransmitter dysregulation, especially serotonin and dopamine, may also contribute to OCD.[44] Independent studies have consistently found unusual dopamine and serotonin activity in various regions of the brain in individuals with OCD. These can be defined as dopaminergic hyperfunction in the prefrontal cortex and serotonergic hypofunction in the basal ganglia.[45][46][47] Glutamate dysregulation has also been the subject of recent research,[48][49] although its role in the disorder's etiology is not yet clear.
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| ==References== | | ==References== |