Introduction
Bipolar disorder alias maniac depression is characterized by mood swings between lows( depression) and highs( mania), or a combination of these two at times. While depression is one of the most common features of this illness, maniac episodes are, usually, marked by a mix of irritability and anger, with or without euphoria. As such, the mood symptoms in the disorder may take four forms:
Mania: A period of persistently irritable mood accompanied by increased sense of self-esteem and optimism.
Depression: A period of unhappiness leading to changes in sleep, appetite, and indifference with the usual groove.
Mixed Mania: The stage when mania and depression coexist.
Hypomania: The state of persistently elevated mood marked by a higher level of functioning.
Three primary types of bipolar disorder include bipolar I, bipolar II, and bipolar NOS( Not Otherwise Specified). A patient feels repeated stages of severe mood swings bipolar I; the mood elevation in softer in bipolar II with mild episodes of hypomania and alternating periods of severe depression. If the symptoms cannot be clearly classified, they are referred to as bipolar NOS.
Theoretical Framework
Various theories that have been linked to bipolar disorder over time include psychodynamic, existential, biological and behavioral models. While biological models blamed the absence of certain monoamines, existentialism believed that the bipolar disorder is caused when a person is out of touch with himself/herself and the surrounding environment. Cognitive- behavioral model , as proposed by Aaron T. Beck, stated that some individuals possess problematic beliefs about themselves. They tend to experience bipolar symptoms when those beliefs get activated by life stressors. Though the disorder is multifactorial, and no theoretical explanation is absolute in itself, psychological behaviorism (PB) explain an important aspect, especially when scholars have endorsed that there is something beyond genes that causes the bipolar.
Saats, in his PB framework, has explained that organic and psychological factors of the past develop basic behavioral repertories (BBRs) that interact with concurrent organic and psychological factors to produce bipolar symptoms. BBRs have been divided into: emotional-motivational(e-m), sensory-motor(s-m), and language-cognitive(l-c). Saats argued that most of the human behaviors is regulated by these three BBR processes and individual differences in prompting BBRs are partly responsible for maniac episodes. For instance, vulnerable individuals may respond inappropriately to some psychological stimuli including dangerous situations.
Simply speaking, behaviorism presented a detailed hypothesis for bipolar resulting from the interplay of past psychological factors, concurrent psychological aspects, concurrent organic factors, e-m BBRs, s-m BBRs, and l-c BBRs. Some of its postulates include:
Past Psychological Factors: Bipolar individuals overcame stress by grandiose self-denial or self-labeling.
Concurrent Psychological Factors: Pleasing events and superficial successes like a win at gambling may catalyze euphoria and mania.
Concurrent Organic Factors: Medical issues including sleep deprivation may trigger bipolar symptoms.
Emotional-Motivational BBR: Vulnerable individuals exhibit excessive emotional responses to certain situations.
Sensory-Motor BBR: Bipolar individuals lack in social skills. Nevertheless, they have above-average skills for engaging in risky activities.
Language-Cognitive BBR: Bipolar people tend to employ self-labeling and denial for mood elevation. They reflect poor cognitive problem skills.
It is crucial to understanding the interactions between these factors to have a holistic understanding of bipolar. For instance, genetic factors may play a role in acquiring bipolar BBRs. It means that bipolar BBRs interact differently with situations of high emotions. Conversely, an individual with healthy BBRs simply avoid such situations. With this, many may think that genetic factors are the sole source of risk and neglect the importance of childhood learning. Though there is increasing evidence that genetic factors do not speak the whole story. For example, self-labeling and engagement in harmful activities cannot be explained without the notion of learning histories. It is important to discovering the learning type that interacts with genetics to increase the risk of bipolar. PB framework admits the existence of psychological factors and tends to fill the gap in the literature, to an extent. Further research in this area will explore more such factors thereby clarifying how psychology and genetics interact to cause bipolar. The importance given to psychological aspects of bipolar will lead to a holistic understanding of the disorder. Review to this theory suggests that more emphasis should be given to self-labeling, controlling euphoric responses to pleasing events, and adaptive use of educational, occupational, and recreational skills.
Empirical Evidence/Research
Bipolar is a complex multifactorial phenomenon with an ongoing research since several years. Nevertheless, most of the studies have emphasized the biological aspect while providing less importance on psychological features. Still, researchers support a psychology underlying bipolar though many consider this psychology as arising out of brain genetic/physical composition or functioning.
A recent research by Burdick et al.(2014) identified three neurocognitive subgroups including
a) a group with superior social cognition.
b) A group, otherwise normal, with impaired functioning in attention, verbal learning, and social cognition.
c) A global impairment group with deficiencies in many cognitive domains comparable to the deficits in schizophrenia.
With bipolar is a bitter fact and enduring condition for a significant population globally, researchers have attempted to define a homogeneous subgroup to identify some common genetic biomarkers . It is expected to delineate more tailored and efficacious treatment regimes. Age of developing bipolar disorder has been considered as valid characteristics of similar subgroups. Researchers have also tried to identify the specific features of juvenile bipolar. Findings reveal that bipolar is significantly associated with a comorbid prior suicide attempt, alcohol abuse, rapid cycling, and other such habits. Despite these findings, there have been found variations in childhood bipolar based on geographical areas. Proposed rationales include varying levels of psychological stress in childhood and migration patterns; no single theory is said to possess greater validity than the other.
A recent study published in the journal of bipolar disorder does admit the influence of life events in the onset of bipolar. The study, in line with behaviorism framework, spotlighted how genetic/non-biological traits interact with environmental stressors to trigger the disorder. The study identified that number and threats of life events influence first and recurrent admission in bipolar patients.
Succinctly, there is a lot of published literature on the subject of bipolar. While researchers are unanimous in accepting its ill-effects, there is a gap in identifying the causes of the illness. As Saats has pointed out, there is still a scope of digging into psychological and learning aspects along with identifying genetic factors. If a person is unable to respond normal to some situations, it may be because of the learning deficit or past learning experiences, not specifically genetic factors. It is not required to link all the causes to genetic spectrum, and there is the need to have an integrated approach towards bipolar encompassing all physical, biological, and psychological dimensions.
Various studies have demonstrated the high heritability of the disorder. Still, scholars have pinpointed genetic interaction with environmental factors especially in the case of childhood trauma. There have been growing suggestions on further exploring the interaction between susceptible genes and environmental factors. More research in this regard is expected to unearth some more dimensions that will prove helpful in treating the illness.
Conclusion
Bipolar is a fact; still there is a debate on whether it is a psychological or neurological diseases. Further, views are divided if it suddenly starts in adulthood or appears in childhood. Stephen A. Diamond, a Psychology Scholar, has aptly spotlighted that bipolar occurs over time. "It is not a bomb waiting to go off at some genetically predetermined moment". Succinctly, the relation between nature( biology) and nurture( psychology) is murkier with respect to bipolar.
As discussed by PB framework and highlighted by other studies also, emphasizing on the underlying psychology will help finding integrated solutions for treatment/therapy of the bipolar disorder. As behaviorism has suggested, depression is catalyzed by the lack of personal skills to handle environmental stressors. Peter Lewinsohn, in the mid-1970s, argued that depression is learned; so, it can be unlearned too. Bipolar is not all about genes; there is something beyond that; something related to cognition and learning.
It does not mean to say that there is no role of biological and genetic factors but the fact the need to emphasized is that it can be learned to tackle unpleasing situations. As such, medicine and psychology need to be conflated to have a holistic approach towards bipolar and associated mental health issues.
Summary
Bipolar is a brain disorder characterized by the episodes of mania and depression. Researchers, though, are unanimous of its existence; they are divided on its causes, and other relate aspects. Some view it as a neurological issue while some take it as a psychological problem. Psychological Behaviorism has explained it the result of the interplay between various past and concurrent organic and psychological factors.
In this regard, PB framework seems suitable as it emphasizes on the psychological aspect while leaving room for genetics also. As a matter of fact, it is hard to divide bipolar between psychology and biology. Rather, a synthesis between these two streams will lead to more integrated and effective solutions in terms of diagnostic and treatment.
References
Burdick, K., Russo, M., Franguo, S., Mahon, K., & Braga, R. (2014). Empirical Evidence for Discrete Neurocognitive Subgroups in Bipolar Disorder: Clinical Implications. Psychology Medicine , 3083-96.
Clark, D. A., & Beck, A. T. (2011). Cognitive Therapy of Anxiety Disorders: Science and Practice. Guilford Press.
GreenHill, L. L. (2012). Bipolar Disorder: Parents' Medication Guide for Bipolar Disorder in Children and Adolescents. ParentsMedGuide.org.
Holtzman, J. N., Lolich, M., & Ketter, T. A. (2015). Clinical Characteristics of Bipolar Disorder: A Comparative Study Between Argentina and the United States. The journal of Bipolar Disorder .
Kemner, S. M., Bootsman, F., & Vonk, R. (2015). The Influence of Life Events on First and Recurrent Admissions in Bipolar Disorder. International Journal of Bipolar Disorder .
Kesebir, S., Unubol, B., & Yaylaci, E. (2015, December). Impact of Childhood Trauma and Affective Temperament on Resilience in Bipolar Disorder. International Journal of Bipolar Disorders .
Leonard, B., & Jovinelly, J. (2012). Bipolar Disorder. New York: The Rosen Publishing Group.
Riedel, H. P., Heiby, E. M., & Kopetskie, S. (2001). Psychological Behaviorism Theory of Bipolar Disorder. The Psychological Record , 507-32.
Stephen, D. A. (2012). Bipolar Disorder Debate: Myths of Mental Illness. Psychology Today .
