The Correlation between Obsessive-Compulsive Disorder (OCD) and Environmental Factors
Literature Review
Many researchers have focused on investigating on the obsessive- compulsive disorder (OCD) where majority claim that OCD is a psychiatric condition that needs to be addressed professionally or by well-trained physicians. Failure to respond to the condition at its early stages can lead to chronic function impairment or what is referred to as the abnormal functioning of the brain (Mian et al., 2010). The other important issue relating to the OCD is the environmental factors, as literature shows that environmental elements, such as trauma and infection, are etiological components of OCD within the life of many people globally.
Bokor and Anderson (2014) posit that malfunctions of the cortico-striato-thalamo-cortical circuit in the brain can lead to obsessions (which are intrusive and repetitive thoughts) and compulsions (which are repetitive behaviors that an individual performs in response to obsessions). The authors also claim that problems with brain signaling can also affect obsessive and compulsive human behaviors. Specifically, they list serotonin, dopamine, and glutamate as the neurotransmitters that are implicated in OCD. According to Hesse et al. (2005), the availability of dopamine transporters in the striatum and the availability of serotonin transporters in the thalamus, hypothalamus, midbrain, and brainstem can affect the severity of obsessive and compulsive behaviors in patients with OCD. Additionally, Welch et al. (2007) argue that defects in the cortico-striatal circuitry contributes to the main symptoms of OCD: obsessions (which they define as persistent intrusive thoughts) and compulsions (which they define as repetitive actions).
Foroughipour et al. (2012) note that the brain has a direct influence on the spreading of OCD, particularly when cortical-cortical and cortical is involved. Their research outlines that OCD is an illness that occurs due to the disturbance of the functional connection within the cortical-cortical and cortical and the brain. On the other hand, Mian et al. (2010) assert that the pathophysiological foundation of OCD is directly involved in the function of the Calcutta State Transport Corporation (CSTC) brain, especially when the CSTC is functioning abnormally. In this context, their research indicates that when the brain is not functioning correctly, this loops to the formation of OCD. Mian et al. (2010) have also expressed that the dysregulation of the human’s nervous system such as dopamine and serotonin plays a significant role in the formation of OCD.
Advancements in brain imaging technology, such as the SPECT system used by Hesse et al. (2005) have made it possible to determine whether there is an association between human behavior and structural and functional features of the brain, such as the presence of neurotransmitter proteins. Moreover, genetic manipulation technologies have made it possible to conduct behavioral studies in mice, like the one conducted by Welch et al. (2007). The ability to delete proteins in mice has made it possible to find out how their absence affects behavior in mice, which have many of the same neural circuits as humans. Also, the development of technology in which lentiviruses are used to selectively express proteins makes it possible to conduct rescue experiments to determine whether introducing the protein in mutant mice can restore normal behavior.
Views on the pathophysiology have changed drastically over time. In the 17th century, OCD behaviors were not attributed to brain physiology at all, but rather to “religious melancholy.” A more modern understanding of OCD began to develop in the 19th century, when obsessions and compulsions were seen as part of mental illnesses. These concepts evolved over the course of the 20th century based on the theories of influential psychologists like Sigmund Freud. However, it was not until the end of the 20th century and the start of the 21st century that scientists have been able to use advances in the fields of pharmacology, neuroanatomy, and neurophysiology to understand which neural structures and processes are implicated in OCD (Stanford Medicine, 2017). For example, structural and functional imaging techniques made it possible to identify the anatomical features of the brain are implicated in OCD pathophysiology, as well as the neurotransmitters involved in the disease. Pharmacological studies have also provided insight into OCD-related neurotransmitters (Bokor & Anderson, 2014).
Based on previous studies, it can be concluded that the pathophysiology of OCD involves dysfunction of the cortico-striato-thalamo-cortical neural circuit and problems with the transport of serotonin, dopamine, and glutamate neurotransmitters. Understanding brain regions impaired in OCD, such as brainstem, thalamus, amygdala, striatum, orbito-frontal cortex, basal ganglia, and anterior cingulate cortex, is critical in the treatment process. Therefore, given the complexity of OCD, finding new treatment procedures requires more research.
While some studies such as Bokor and Anderson (2014) have used a literature review format, some studies have conducted actual primary research. Hesse et al. (2005) conducted a cohort study (also known as a prospective observational study), in which individuals with a condition (in this case, OCD) are compared with those who are not affected by the condition. This design allowed them to compare the brains of individuals with OCD to those of individuals without OCD. In Welch et al. (2007), the researchers designed multiple experiments. The first part of the study was an observational study of the behaviors of mutant mice. They then used a randomized control trial to intervene in randomly selected mice to treat them with lentivirus (enabling selective expression of Sapap3 in the striatum) or SSRIs to find out how they were affected by these treatments. The researchers designed these experiments this way to learn as much as possible about the relationship between cortico-striatal synapses and OCD.
As a literature review, Bokor and Anderson did not need any participants, hence, no ethical issues with regards to notifying participants on the nature of the research. For Hesse et al. (2005), the study was conducted on human subjects; therefore, it was necessary for the researchers to address ethical issues. Specifically, the study was approved by the ethics committee of the University of Leipzig (where the study was conducted), and all participants gave written informed consent before participating in the study. This adequately addressed potential ethical issues since it demonstrates that the authors fulfilled the ethics guidelines of the university. Welch et al. (2007) do not mention how they addressed potential ethical issues involved in using animals for a research study. However, since the study was published in the high-impact journal Nature, a peer-review journal, the study must have followed the required ethical procedures. However, they should have outlined what they did within the paper to verify that the animals were treated ethically throughout the study.
Over the course of history, issues of ethics in biopsychology have grown more prominent. In the past, researchers were less concerned about the physical and mental welfare of research subjects. Today, studies that involve human and/or animal subjects must undergo strict scrutiny before they are approved by universities and governmental bodies. Researchers must be able to demonstrate that a study will not cause significant harm and that it has a clear purpose.
Research Design
Future research studies can more closely investigate the relationship between neurotransmitter transport and OCD. Specifically, Hesse et al recommend studies with radiotracers that are more selective for dopamine and serotonin transporters. Further research is also needed to better understand the role of glutamatergic neurotransmission relates to OCD.
The correlation between OCD and environmental factors is not captured in the reviewed studies. This is a fundamental element which is not fully delved into by the researchers in their respective studies. As such, it is prudent to note that environmental factors are “of substantial importance in the likelihood to obtain and persist or remit concerning OCD symptomology” (Cath et al., 2008, p.109). Major events or even stressful events can bring about OCD or even aggravate OCD related symptoms; with common occurrences in an individual’s day-to-day life. OCD can easily be triggered, and hence studies in the said areas must be investigated. In the recent decade, studies have also established links between OCD and socioeconomic elements. Many individuals that have lower socioeconomic standards are at high risk of developing OCD. Therefore, the research question for this study is what structural and functional changes in neural circuitry are present in individuals with OCD, as compared to healthy individuals?
Weich et al. (2007) use the genetic deletion of Sapapa3 in mice to investigate OCD in mice. The study highly relies on structural, electrophysiological and biochemical studies to highlight the link between genetic defects and OCD. They fail to incorporate the environmental element in the studies to comprehend whether indeed there is any correlation to the aggravation of the disorder in the mice. Bokor and Anderson (2014 focus on the neurotransmitters and their involvement in OCD related behaviors. They, however, thrive in a gray area when it comes to environmental factors as stressors and how they impact on neural activity. Hesse et al. (2005) focus on the dopamine transporters and how their availability in the striatum as well as the availability of the serotonin transporters in the hypothalamus, thalamus, brainstem and mid brain. Largely lacking in the study is the influences wielded by environmental factors or stressors which have been known to enhance OCD. Environmental factors continue to push the production of neurochemicals which have a direct correlation to OCD.
This study will use a cohort study design and have two groups of participants, one with OCD and another without. The researcher will collect data on the life events, birth complications, lifestyle, health, family structure, and psychopathology of 50 participants with 25 among them with OCD. This approach was successful in Hess et al. (2005). Cassie et al. (2008) used a similar approach but chose to use 25 pairs of twins. However, getting a pair of 25 twins would be a major challenge for this study, hence not a good alternative. The researcher will then analyze different environmental factors that the participants face based on collected data.
Hess et al. (2005), the researcher will inform participants of the experiments and purpose of the study. Moreover, the researcher will seek the consent of the participants before conducting the research. Since the researcher will use data from a hospital like Cassie et al. (2008), it will be important to get authorization from the chosen facility’s ethics committee and uphold all research ethics.
Cassie et al. (2005) notes in her research that examining environmental factors that may associated with obsessive compulsive behavior requires requires a direct contact with participants. Therefore, by ensuring that this study informs participants of the objectives and nature of the study, the research will ensure their protections and seek their consent in analyzing the environmental factors associated with OCD.
References
Bokor, G. & Anderson, P.D. (2014). Obsessive-compulsive disorder. Journal of Pharmacy Practice 27(2), 116-130.
Cath, D. C., van Grootheest, D. S., Willemsen, G., van Oppen, P., & Boomsma, D. I. (2008). Environmental Factors in Obsessive-Compulsive Behavior: Evidence from Discordant and Concordant Monozygotic Twins. Behavior Genetics, 38(2), 108–120. http://doi.org/10.1007/s10519-007-9185-9
Foroughipour, M., Behdani, F., Hebrani, P., Marvast, M. N., Esmatinia, F., & Akhavanrezayat, A. (2012). Frequency of obsessive-compulsive disorder in patients with multiple sclerosis: A cross-sectional study. Journal of research in medical sciences: the official journal of Isfahan University of Medical Sciences, 17(3), 248-253.
Hesse, S., Müller, U., Lincke, T., Barthel, H., Villmann, T., Angermeyer, M. C., … & Stengler-Wenzke, K. (2005). Serotonin and dopamine transporter imaging in patients with obsessive–compulsive disorder. Psychiatry Research: Neuroimaging, 140(1), 63-72.
Mian, M. K., Campos, M., Sheth, S. A., & Eskandar, E. N. (2010). Deep brain stimulation for obsessive-compulsive disorder: past, present, and future. Neurosurgical focus, 29(2), 10-18.
Stanford Medicine. (2017). History. Stanford Medicine. Retrieved from http://ocd.stanford.edu/treatment/history.html
Welch, J. M., Lu, J., Rodriguiz, R. M., Trotta, N. C., Peca, J., Ding, J. D., … & Dudek, S. M. (2007). Cortico-striatal synaptic defects and OCD-like behaviors in SAPAP3 mutant mice. Nature, 448(7156), 894-900.
