Understanding the Prevalence of Bipolar Disorder

Prevalence of Bipolar Disorder

Estimates of the bipolar prevalence vary widely. The results of a research piloted by Merikangas et al. (2011) reveals that bipolar affects up-to 5% of all patients in primary care. On the other hand, Ketter (2010) infer that the lifetime prevalence of bipolar type I is between 1% and 2% in the general population while that of bipolar type II is 2% and above in the general population. A cross-sectional survey by Cerimele et al. (2014) across 11 countries shows that the overall lifetime prevalence of both type I and type II bipolar is 2.4% with a higher prevalence of type II bipolar (0.4%) as compared to type I bipolar (0.6%). The lifetime prevalence of bipolar disorder in England is 2% but the study does not determine the differences by bipolar type (Culpepper 2014). According to DSM-5, the prevalence of bipolar is every 1 person in 100 since the age of 20 (American Psychiatric Association 2013). This information is crucial for those seeking healthcare dissertation help, as it underscores the significance of understanding bipolar disorder's prevalence in various populations.

Aetiology of Bipolar Disorder

Genetics, environmental factors, and gene-environment interactions are risk factors for bipolar disorder. Data from a twin study by Craddock and Sklar (2013) suggests monozygotic concordance of 40–70% and a lifetime risk in the immediate relatives of 5-10%, which is 7times higher than in men and women in the general population. On the other hand, Kerner (2014) infers that relatives to bipolar patients are at a higher risk of developing unipolar depression than bipolar disorders, which implies that genetic risk transcends diagnostic categories. Grozeva et al. (2010) reveal that bipolar patients are genetically susceptible to autism and schizophrenia. Studies on the aetiology of bipolar agree that bipolar disorders fail to follow the Mendelian inheritance pattern which means that individual genes are not strongly associated with development of bipolar (Kerner 2015). The bipolar genetic risk is partially influenced by multiple single nucleotide polymorphisms that are quite dominant in both men and women thus increasing the individual risk (Badner et al. 2012). Similarly, DSM-5 reveals that brain-derived neurotrophic factor (BDNF) SNPs are involved in the development of bipolar disorder (American Psychiatric Association 2013). Nonetheless, every single nucleotide polymorphism has a nearly insignificant effect in the development of bipolar.

Studies on gene-environment interactions and their influence in development of bipolar are very minimal. However, Grande et al. (2010) state that childhood abuse interacts with BDNF gene polymorphisms to considerably influences the development of bipolar. In the same vein, Oliveira et al. (2014) posit that the interaction between toll-like receptor 2 polymorphisms and stressful life events heighten the risk of developing bipolar. Similarly, Alemany et al. (2014) establish that COMT polymorphism interacts with the use cannabis in patients with psychotic symptoms to catalyse the risk of bipolar. In the case, Monty has experienced childhood abuse and has a long history of substance misuse factors that could have interacted with genes leading to development of bipolar.

Environmental factors have a substantial effect on development of bipolar disorder. According to Chudal et al. (2014), prenatal and perinatal factors implicates to the development of bipolar. Particularly, the authors state that prenatal viral infections are a risk factor for bipolar. Maternal influenza infection is among the proven risk factor for bipolar though with a very weak effect. The interaction between seropositivity for T.gondii infection and bipolar is quite a strong risk factor for bipolar (Del Grande et al. 2017). In agreement, Sutterland et al. (2015) state that T.gondii infection causes increases dopamine production thus leading to development of mental illnesses particularly bipolar.

Childhood maltreatment is a significant risk for development of bipolar in later life stages. Etain et al. (2010) state that emotional neglect and emotional abuse are the most two significant risk factors for later development of bipolar. On the contrary, Perroud et al. (2014) write that physical, emotional, and sexual abuse and childhood adversity are risk factors for bipolar. In the same vein, Etain et al. (2013) establish that traumatic events at childhood heighten the risk of later bipolar in that they increase the level of emotional dysregulation and affective instability. In the case, Monty was physically, sexually, and emotionally abused, which might have led to the development of bipolar. Monty was abused by both his father and the father’s wife a factor that could have increased his affective instability resulting to development of bipolar. Further, Monty lost her mother at a very tender age which is a psychological stressor capable of conferring the risk of bipolar.

Research has established as association between bipolar and substance misuse. Hjorthøj et al. (2015) write that bipolar is regularly comorbid with drug and substance misuse such as cannabis, cocaine, opioids, alcohol, and sedatives. In the case, Monty has for a long time misused substances including crack, alcohol, and heroin which began way before bipolar comorbidities. Therefore, we can infer that substance misuse has led to bipolar comorbidities for Monty.

Bipolar Differential Diagnosis

Bipolar differential diagnosis takes into consideration several conditions with manic-like symptoms as well as organic mood disorders. Research on the presentation of bipolar shows that depression is the most common symptom of bipolar thus imposes a weightier burden in relation to impact and duration than the manic symptoms. According to Connolly and Thase (2011), the severity of depressive symptoms in patients with bipolar type I and bipolar type II could be similar which means that bipolar type II is not milder than bipolar type I.

The first presentation of bipolar is either a depressive episode or a manic episode with subsequent presentations being characterised by repeated depressive or manic episodes. Between the presentations of episodes of bipolar, patients may continue to experience decreased functioning and abnormal brain functioning (Asherson et al. 2014). The duration, severity, polarity, and timing of frequent mood episodes vary between patients and episodes, which implies the presentation in one episode will not be the same as that in another episode or patient (Goldstein and Birmaher 2012).

Early and accurate diagnosis significantly lessens the burden of bipolar while improving long-term care outcomes (Phillips and Kupfer 2013). Nevertheless, establishing the diagnosis can be problematic due to difference in symptoms meaning patients can be subjected to alternative diagnoses. According to Zimmerman et al. (2010), bipolar patients that seek to primary care for the first time have an extensive array of mood-related symptoms such as mood swings, anxiety, irritability, depression, inability to concentrate and focus, fatigue, and difficulty in sleeping. These symptoms are common in patients with other mental illnesses, which underscores the need to consider other factors such as the patient’s social history, erratic occupational histories, and financial troubles among others. Perugi et al. (2015) write that diagnosing bipolar is a challenge given the varied symptoms and sequel thus a suspicion of high index is essential.

After diagnosis, people with bipolar can be treated using a combination of different treatments such as medicine to prevent episodes of mania and to treat main symptoms, recognising and learning how to respond to triggers, psychological treatment, and lifestyle changes (NHS 2019). Lithium is the most commonly used mood stabiliser in the UK and of a long-term treatment for mania episodes. Antipsychotics such as olanzapine, aripiprazole, quetiapine, and risperidone could also be prescribed to treat episodes of mania (NHS 2019). Psychiatric nurses are essentially important in helping bipolar patients recognise signs of episodes of mania thus helping prevent the episode from reoccurring. Other than medicine, psychological treatment including psychoeducation, family therapy, and cognitive behavioural therapy (CBT) is effective in treatment of bipolar.

Bipolar Co-morbidity

Bipolar patients are more prone to psychiatric illnesses, medical disorders and substance misuse leading to lower quality of life and reduced life expectancy. According to Kemp et al. (2010), more than 97% bipolar type I patients meet the concurrent psychiatric illness and the co-occurrence criteria to at least three disorders. In the case, Monty not only suffers bipolar but also paraphilic infantilism and paraphilic transvestism. Monty has a long history of substance abuse along with bipolar, which is a risk factor for paraphilia. According to Kafka (2012), it is common for people that misuse drugs and substances and with mood or anxiety disorders to have sexual performance difficulties given the effects of medication and the substance they abuse. This explains why Monty expresses his sexuality through paraphilic transvestism while reverting to paraphilic infantilism following drug abuse. On the other hand, Etain et al. (2013) write that childhood exposure to traumatic events is significant risk factor for bipolar. Monty had experienced childhood abuse resulting in self-medicating while regressing to an age prior to the sexual abuse, which provides him a ‘safe place’ in this case the girlfriend’s place.

Conclusion

The aim of this paper was to discuss the prevalence, aetiology, differential diagnosis, and comorbidity of bipolar affective disorder. The paper reveals that bipolar lifetime prevalence in England is 2%and affects up-to 5% of patients in primary care. In addition, the paper establishes that there is a significant relationship between genetics, gene-environment interactions, and environmental factors and the development of bipolar. Further, bipolar presents in a variety of symptoms thus its differential diagnosis includes other conditions with manic-like symptoms. Additionally, depressive symptoms could have the same level of severity in patients with type I bipolar and those with type II bipolar making it problematic to distinguish between the two types of bipolar. Finally, individuals diagnosed with bipolar have high likelihood to develop medical, psychiatric, and substance misuse disorders including paraphilia as evident in Monty’s case.

Continue your exploration of Understanding the Pathophysiology of Sepsis Diagnosis with our related content.

References

Alemany, S., Arias, B., Fatjó‐Vilas, M., Villa, H., Moya, J., Ibanez, M.I., Ortet, G., Gastó, C. and Fananas, L., 2014. Psychosis‐inducing effects of cannabis are related to both childhood abuse and COMT genotypes. Acta Psychiatrica Scandinavica, 129(1), pp.54-62.

American Psychiatric Association, 2013. Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub.

Asherson, P., Young, A.H., Eich-Höchli, D., Moran, P., Porsdal, V. and Deberdt, W., 2014. Differential diagnosis, comorbidity, and treatment of attention-deficit/hyperactivity disorder in relation to bipolar disorder or borderline personality disorder in adults. Current medical research and opinion, 30(8), pp.1657-1672.

Badner, J.A., Koller, D., Foroud, T., Edenberg, H., Nurnberger Jr, J.I., Zandi, P.P., Willour, V.L., McMahon, F.J., Potash, J.B., Hamshere, M. and Grozeva, D., 2012. Genome-wide linkage analysis of 972 bipolar pedigrees using single-nucleotide polymorphisms. Molecular psychiatry, 17(8), p.818.

Cerimele, J.M., Chwastiak, L.A., Dodson, S. and Katon, W.J., 2014. The prevalence of bipolar disorder in general primary care samples: a systematic review. General hospital psychiatry, 36(1), pp.19-25.

Chudal, R., Sourander, A., Polo-Kantola, P., Hinkka-Yli-Salomäki, S., Lehti, V., Sucksdorff, D., Gissler, M. and Brown, A.S., 2014. Perinatal factors and the risk of bipolar disorder in Finland. Journal of affective disorders, 155, pp.75-80.

Connolly, K.R. and Thase, M.E., 2011. The clinical management of bipolar disorder: a review of evidence-based guidelines. The primary care companion for CNS disorders, 13(4).

Craddock, N. and Sklar, P., 2013. Genetics of bipolar disorder. The Lancet, 381(9878), pp.1654-1662.

Culpepper, L., 2014. The diagnosis and treatment of bipolar disorder: decision-making in primary care. The primary care companion for CNS disorders, 16(3).

Del Grande, C., Galli, L., Schiavi, E., Dell’Osso, L. and Bruschi, F., 2017. Is Toxoplasma gondii a trigger of bipolar disorder? Pathogens, 6(1), p.3.

Etain, B., Aas, M., Andreassen, O.A., Lorentzen, S., Dieset, I., Gard, S., Kahn, J.P., Bellivier, F., Leboyer, M., Melle, I. and Henry, C., 2013. Childhood trauma is associated with severe clinical characteristics of bipolar disorders. The Journal of clinical psychiatry, 74(10), pp.991-998.

Etain, B., Mathieu, F., Henry, C., Raust, A., Roy, I., Germain, A., Leboyer, M. and Bellivier, F., 2010. Preferential association between childhood emotional abuse and bipolar disorder. Journal of traumatic stress, 23(3), pp.376-383.

Goldstein, B.I. and Birmaher, B., 2012. Prevalence, Clinical Presentation, and Differential Diagnosis of Paediatric Bipolar Disorder. The Israel journal of psychiatry and related sciences, 49(1), p.3.

Grande, I., Fries, G.R., Kunz, M. and Kapczinski, F., 2010. The role of BDNF as a mediator of neuroplasticity in bipolar disorder. Psychiatry investigation, 7(4), p.243.

Grozeva, D., Kirov, G., Ivanov, D., Jones, I.R., Jones, L., Green, E.K., St Clair, D.M., Young, A.H., Ferrier, N., Farmer, A.E. and McGuffin, P., 2010. Rare copy number variants: a point of rarity in genetic risk for bipolar disorder and schizophrenia. Archives of general psychiatry, 67(4), pp.318-327.

Hjorthøj, C., Østergaard, M.L.D., Benros, M.E., Toftdahl, N.G., Erlangsen, A., Andersen, J.T. and Nordentoft, M., 2015. Association between alcohol and substance use disorders and all-cause and cause-specific mortality in schizophrenia, bipolar disorder, and unipolar depression: a nationwide, prospective, register-based study. The Lancet Psychiatry, 2(9), pp.801-808.

Kafka, M., 2012. Axis I psychiatric disorders, paraphilic sexual offending and implications for pharmacological treatment. The Israel journal of psychiatry and related sciences, 49(4), p.255.

Kemp, D.E., Gao, K., Chan, P.K., Ganocy, S.J., Findling, R.L. and Calabrese, J.R., 2010. Medical comorbidity in bipolar disorder: relationship between illnesses of the endocrine/metabolic system and treatment outcome. Bipolar disorders, 12(4), pp.404-413.

Kerner, B., 2014. Genetics of bipolar disorder. The application of clinical genetics, 7, p.33.

Kerner, B., 2015. Toward a deeper understanding of the genetics of bipolar disorder. Frontiers in psychiatry, 6, p.105.

Ketter, T.A., 2010. Diagnostic features, prevalence, and impact of bipolar disorder. J Clin Psychiatry, 71(6), p.e14.

Merikangas, K.R., Jin, R., He, J.P., Kessler, R.C., Lee, S., Sampson, N.A., Viana, M.C., Andrade, L.H., Hu, C., Karam, E.G. and Ladea, M., 2011. Prevalence and correlates of bipolar spectrum disorder in the world mental health survey initiative. Archives of general psychiatry, 68(3), pp.241-251.

NHS 2019. Treatment: Bipolar disorder. [Online] Available at

Oliveira, J., Hamdani, N., Busson, M., Etain, B., Bennabi, M., Amokrane, K., Boukouaci, W., Fortier, C., Marzais, F., Bengoufa, D. and Bellivier, F., 2014. Association between toll-like receptor 2 gene diversity and early-onset bipolar disorder. Journal of affective disorders, 165, pp.135-141.

Perroud, N., Dayer, A., Piguet, C., Nallet, A., Favre, S., Malafosse, A. and Aubry, J.M., 2014. Childhood maltreatment and methylation of the glucocorticoid receptor gene NR3C1 in bipolar disorder. The British Journal of Psychiatry, 204(1), pp.30-35.

Perugi, G., Angst, J., Azorin, J.M., Bowden, C.L., Mosolov, S., Reis, J., Vieta, E. and Young, A.H., 2015. Mixed features in patients with a major depressive episode: the BRIDGE-II-MIX study. The Journal of clinical psychiatry, 76(3), pp.e351-8.

Phillips, M.L. and Kupfer, D.J., 2013. Bipolar disorder diagnosis: challenges and future directions. The Lancet, 381(9878), pp.1663-1671.

Sutterland, A.L., Fond, G., Kuin, A., Koeter, M.W.J., Lutter, R., Van Gool, T., Yolken, R., Szoke, A., Leboyer, M. and De Haan, L., 2015. Beyond the association. T oxoplasma gondii in schizophrenia, bipolar disorder, and addiction: systematic review and meta‐analysis. Acta Psychiatrica Scandinavica, 132(3), pp.161-179.

Zimmerman, M., Ruggero, C.J., Chelminski, I. and Young, D., 2010. Psychiatric diagnoses in patients previously overdiagnosed with bipolar disorder. The Journal of clinical psychiatry.