In order to properly and thoroughly assess the potential risk factor of bipolar affective disorder (BAD), it is important to overview and analyze the current literature on the given subject. The research studies conducted on BAD can be categorized into two major subcategories regarding their approach to the issue. Some studies address bipolar affective disorder by assessing their biological and pharmacological features, whereas other researchers conduct experiments in order to learn more about BAD’s hereditary and environmental risk factors. Therefore, the given literature review will be organized in a similar fashion, because it is important to overview current treatment approaches and biomarkers, and preventative prognosis.
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The studies presented in the given review will be grouped into themes, such as pharmacology and biology, and environmental and hereditary risk factors. The first study addresses the fact that lithium can be used as a long-term treatment approach for bipolar affective disorder. Methods for treating bipolar disorder are aimed at treating the manic, hypomanic, and depressive symptoms of the disorder, as well as maintaining treatment by reducing or preventing cyclicity. Lithium has long been considered the standard treatment for the bipolar disorder based on several early clinical studies, which have since been often criticized for the methodology.
Nevertheless, no doubt lithium is an effective remedy for mania, but less effective in treating depression. In addition, patients treated with lithium may show some symptoms of the disease, the sudden end of treatment can cause a manic episode, and after that, not all patients will tolerate such treatment. However, there is no clear demonstration of lithium biochemical function and how it suppresses the major BAD symptoms.
It is stated that lithium can be suppressing the factor of excessive activity in the regulatory networks, which increases a person’s stress resilience (Alda, 2015). The overall complication and the lack of sufficient information on BAD are due to the fact that it is challenging to clinically distinguish unipolar depression from the disorder.
In addition, there are no strong biomarkers, and the only method to detect bipolar affective disorder is to conduct a longitudinal assessment of hypomanic episodes (Grande, Berk, Birmaher, & Vieta, 2016). The current situation on the issue of BAD is manifested in the fact that both scientific and clinical fields are more aware of the given disorder and address it separately from unipolar depression. However, historically, the majority of instances of BAD were simply diagnosed and recognized as a form of unipolar depression because both possess similar symptoms. The identification of biomarkers is one of the most important tasks of medicine.
The biological markers may contribute to a new approach to diagnosis, a better understanding of pathogenesis. This also includes pathophysiological mechanisms, the prognosis of disease progression, monitoring of its course, and prediction of outcome.
The study of biomarkers will make it possible to detect targets for drug treatment, which can contribute to the creation of new drugs with desired properties and may lead to the development of new therapeutic approaches. Biomarker research has achieved certain results in various areas of clinical medicine, such as cardiovascular disease, liver disease, and several others. However, in psychiatry to date, not a single potential biomarker has been found that would be introduced into clinical practice.
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Currently, biological psychiatry is focused on the use of all available modern approaches and methods that would identify biological markers. These approaches include epigenetics, genomics, proteomics, lipidomics, and metabolomics. The goal of such approaches is the identification of new sensitive and specific biomarkers. In this regard, the use of a systematic approach methodology can lead to progress in biological psychiatry.
The systematic approach, unlike the reductionist one, indicates the very complex nature of mental disorders, since such disorders are characterized by multifactorial genetic and environmental relationships along with the dynamics of protein disorders that cause both cellular and structural changes at the neuronal level. Therefore, the assessment of mental disorders cannot be carried out only, for example, at a behavioral or cellular level, but should be considered in the aggregate of various components of such diseases.
Nevertheless, despite the lack of sufficient data, there are valid and plausible biological hypotheses regarding the bipolar affective disorder. Neuroimaging reveals that there is a significant reduction of the gray matter in the brain alongside with a progressive decrease of cerebellar, fusiform, and hippocampal gray matter. In addition, the genetic approach identified that there is a major risk factor in one’s genome because twins develop BAD in 85% of cases (Sigitova, Fišar, Hroudová, Cikánková, & Raboch, 2017). The genetic risk contributes to the development of the bipolar affective disorder in polygenetic fashion. This means that a set of genes’ collective expression and regulation leads to an increase in the probability of developing BAD.
In regards to neurotransmitters, it is stated that the disturbance in monoamine neurotransmission can be linked with bipolar affective disorder symptoms. Neurotrophic growth factors can also be a major contributor to BAD because activity disturbances of these elements, such as nerve growth factor (NGF), can be detrimental to one’s neuroplasticity, which is observed in BAD patients. In addition, it is suggested that neuroinflammation and oxidative stress can play a role in advancing bipolar affective disorder (Sigitova et al., 2017). Thus, there are a number of underlying biological biomarkers and few treatment strategies.
Moreover, it is critically important to address potential environmental and hereditary risk factors. The former might include factors such as trauma, infections, birth complications, maternal smoking, climate, social support, and life events. However, the majority of studies indicate that traumatic life events and childhood traumas are the most prevalent risk factor from an environmental standpoint.
There is strong evidence on the link between childhood tragedies and the development of the bipolar affective disorder. In addition, life events play a big role in contributing to BAD, and these events are comprised of sudden changes in the environment or excessively positive or negative connotations in one’s life. All these factors increase a person’s chance of suffering from bipolar affective disorder (Aldinger & Schulze, 2016). In the cohort longitudinal study, which aimed to create a risk calculator, it is shown that it is possible to confidently predict if people with BAD will have offspring with BAD in five years (Hafeman et al., 2017). This research suggests that there is a strong hereditary risk factor, which can be a major determining factor of bipolar affective disorder.
In conclusion, it should be noted that most of the given studies are bound by the limited amount of data available in regards to BAD. The researchers aim to find critical features of bipolar affective disorder, such as biomarkers, hereditary and environmental risks, and biochemistry behind lithium treatments, but most of these ideas are mainly scientific assumptions. Thus, there is a great need for experimental evidence with a full picture of both the biological and psychological mechanisms behind BAD. However, the most valid answer for the current research base of BAD is the fact that hereditary burden is the key risk factor, which is supplemented by environmental disturbances. In addition, biomarkers and the overall biological changes are intricate changes that were predetermined by one’s genes or environment.
Alda, M. (2015). Lithium in the treatment of bipolar disorder: Pharmacology and pharmacogenetics. Molecular Psychiatry, 20(6), 661-670. Web.
Aldinger, F., & Schulze, T. (2016). Environmental factors, life events, and trauma in the course of bipolar disorder. Psychiatry and Clinical Neurosciences, 71(1), 6-17. Web.
Grande, I., Berk, M., Birmaher, B., & Vieta, E. (2016). Bipolar disorder. The Lancet, 387(10027), 1561-1572. Web.
Hafeman, D., Merranko, J., Goldstein, T., Axelson, D., Goldstein, B., & Monk, K., … Birmaher, B. (2017). Assessment of a person-level risk calculator to predict new-onset bipolar spectrum disorder in youth at familial risk. JAMA Psychiatry, 74(8), 841. Web.
Sigitova, E., Fišar, Z., Hroudová, J., Cikánková, T., & Raboch, J. (2017). Biological hypotheses and biomarkers of bipolar disorder. Psychiatry and Clinical Neurosciences, 71(2), 77-103. Web.