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 Rapid-cycling is used to describe having four or more mood episodes within a 12-month time period. Episodes need to last for a certain number of days to be considered a distinct episode. Some individuals experience changes in polarity within a single week or even a day. In this case, this may be called ultra- rapid cycling, which can be argued in psychiatry that this isn’t a valid or well-established phenomenon in bipolar disorder. Rapid-cycling can happen at any time in the course of the disease, however, it is more prevalent later on in life and in the duration of the disease. This classification can increase the risk of severe depression and suicide attempts (Bipolar Disorder, 2005).
+{{:cyclothymia_graph.png}}
+**Figure 1**: This image is used to outline and explain the major classifications for bipolar disorder.
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 === Bipolar I: Depression ===
 A.    “Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
 Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears tearful).
 Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
 Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day.
 Insomnia or hypersomnia nearly every day.
 Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).
 Fatigue or loss of energy nearly every day.
 Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
 Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
 Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
 B.     The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
 C.     The episode is not attributable to the physiological effects of a substance or another medical condition (DSM fifth edition, n.a).”
@@ Line 108: / Line 120: @@
 === Bipolar II: Hypomanic ===
 A.    “A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day.
 B.     During the period of mood disturbance and increased energy and activity, three (or more) of the following symptoms have persisted (four if the mood is only irritable), represent a noticeable change from usual behavior, and have been present to a significant degree:
 .      Inflated self-esteem or grandiosity.
 .      Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
 .      More talkative than usual or pressure to keep talking.
 .      Flight of ideas or subjective experience that thoughts are racing.
 .      Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed.
 .      Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation.
 .      Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).
 C.     The episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic.
 D.   The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by definition, manic.
 E. The episode is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, other treatment) or another medical condition (DSM fifth edition, n.a).”
@@ Line 124: / Line 147: @@
 === Bipolar II: Depression ===
 A.    “Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
 .      Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears tearful).
 .      Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
 .      Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day.
 .      Insomnia or hypersomnia nearly every day.
 .      Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).
 .      Fatigue or loss of energy nearly every day.
 .      Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
 .      Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
 .      Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, a suicide attempt, or a specific plan for committing suicide.
 B.     The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
 C.     The episode is not attributable to the physiological effects of a substance or another medical condition (DSM fifth edition, n.a).”
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 Experts explain that the high prevalence of BPD in the United states could be genetic or environmental. It may also be because different cultures deal and respond to mental illnesses differently. “Cultural awareness plays a big role in psychiatry. Some cultures have a huge reluctance to speak about psychiatric things.” Some cultures may not acknowledge mental illness as well as others. In the United States, individuals may be more prone to being diagnosed because they are more aware of the condition. Many low-income countries may have higher levels of stigma, resulting in fewer people speaking up about their symptoms (NewsMedical, 2011).
+{{:2011-06-bipolar-chart_tcm7-116499.jpg}}
+**Figure 2**: This image outlines the main results from the study done by Merikangas et al.
 ===== Societal Impact =====
@@ Line 148: / Line 185: @@
 === Family Impact ===
+. Emotional distress such as guilt, grief, and worry
+o Family members think they are the cause of the onset of BP in an individual
+· Disruption in regular routines
+o Because of an individuals extreme emotional phases, changes to daily activities may have to change to ensure to not cause more pressure or stress
+· Having to deal with bizarre or reckless behaviour
+· Financial stresses as a result of reduced income or spending sprees
+o Individuals may be reckless with their spending
+o May have extra costs for treatment and therapy
+· Strained marital or family relationships
+· Changes in family roles
+· Difficulty in maintaining relationships outside the family
+· Health problems as a result of stress (Mood Disorders Association, n.a)
 === Physiological Effects ===
+.During periods of mania or hypomania, psychological consequences to these phases include:
+.Auditory and visual hallucinations
+.Delusions, including delusions of grandeur and thoughts that objects are sending special messages
+.Intense anxiety, agitation, aggression, paranoia
+.Obsessive worried thoughts and feelings; feeling the need to check something
+.Feeling like life is spinning out of control
+.Heightened mood, exaggerated optimism and self-confidence
+.Racing thoughts; rapidly changing streams of thought; easily distractible (Tracy, 2016)
+During periods of depression, psychological effects of this phase include:
+.Prolonged sadness
+.Feeling helpless, hopeless and worthless; feelings of guilt
+.Pessimism, indifference; reoccurring thoughts of death and suicide
+.Inability to concentrate, indecisiveness
+.Inability to take pleasure in former interests (Tracy, 2016)
+.Physical effects of BP include the decrease of productivity during times of severe depression. BP can lead to an increase in productivity in times of the manic phase, however, these irregular behaviour leads to job loss.
+The physical effects of BP include:
+.Increased physical and mental activity and energy; hyperactivity
+.Significant changes in appetite and sleep patterns
+.Trouble breathing
+.Racing speech
+.Social withdrawal
+.Loss of energy, persistent lethargy; aches and pains
+.Unexplained crying spells
+.Poor overall health
+.Weight gain; blood pressure and heart problems; diabetes (Tracy, 2016)
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 ===== Causes/Risk Factors =====
+The root cause of bipolar disorder is unknown, however, various risk factors can trigger the onset of the illness (Mayo Clinic Staff Print, 2017). One cause of bipolar disorder is due to biological differences (Mayo Clinic Staff Print, 2017). Those who are often affected by bipolar disorder have physical changes in their brains (Mayo Clinic Staff Print, 2017).
+The second cause is due to genetics, where individuals who have a first-degree relative affected by bipolar disorder are more susceptible to also suffer from bipolar disorder (Mayo Clinic Staff Print, 2017). Children who have one parent affected by the disorder have a 10-25% chance of developing of the disorder, while children with both parents affected by the disorder have a 10-50% chance of developing the disorder (Bipolar Disorder, n.d.). In the case of identical twins, there is a range of 40-70% chance of the other twin developing the disorder. The range is large due to the fact that genes are not the only contributing factor to the disorder, environment, and one’s lifestyle habits also contribute to the development of the disease (Bipolar Disorder, n.d.).
+In addition, one’s environment can trigger the onset of bipolar disorder. For example, stressful or traumatic events such as a death or loss of a loved one can trigger the onset of bipolar disorder. Research shows that about 50% of individuals suffering from bipolar disorder have a substance use problem (Bipolar Disorder, n.d.). Life style habits such as drug or alcohol abuse and lack of sleep may trigger bipolar disorder.
 ===== Symptoms =====
+Symptoms of bipolar disorder include high moods (mania) and low moods (depression). Bipolar 1 disorder is characterized by at least one manic episode, while hypomania is characterized by at least one episode of hypomania and a major depressive disorder. Hypomanic episodes are similar to manic episodes except that they do not entail psychosis, hospitalization or severe functional impairment.
+Mania and hypomania include three or more of the following symptoms: “abnormal upbeat, jumpy, or wired; increased activity, energy or agitation; exaggerated sense of well-being and self-confidence (euphoria); decreased need for sleep; unusual talkativeness; racing thoughts; distractibility; poor decision-making (Mayo Clinic Staff Print, 2017).”
+A major depressive episode includes five or more of these symptoms: “depressed mood; marked loss of interest; significant weight changes; insomnia or sleeping too much; restlessness; fatigue; feelings of worthlessness or excessive guilt; decreased ability to concentrate; indecisiveness; planning or attempting suicide (Mayo Clinic Staff Print, 2017).
+General symptoms of bipolar disorder include anxious distress, melancholy, psychosis, sleep dysregulation, increased prevalence of suicidal thoughts among others. However, bipolar disorder is often difficult to identify in children and teens (Mayo Clinic Staff Print, 2017). The most obvious symptom of bipolar disorder evident in children and teenagers may be severe mood swings, which are different from the usual (Mayo Clinic Staff Print, 2017). Some co-occurring conditions include: Anxiety disorders, eating disorders, attention-deficit/hyperactivity disorder (ADHD), alcohol or drug problems and physical health problems (Mayo Clinic Staff Print, 2017).
 ===== Pathophysiology =====
@@ Line 163: / Line 289: @@
 === Abnormalities in the synaptic and cellular plasticity ===
+A growing body of data suggests that BD arises from abnormalities in the synaptic and neuronal plasticity cascades, which leads to aberrant information processing in critical synapses and circuits. BD can be conceptualized as being a genetically influenced disorder of synapses and circuits, rather than simply having deficits or excesses in individual neurotransmitters  (Schloesser, Huang, Klein, & Manji, 2008).
+Over the past 40 years, neurobiological studies of mood disorders have primarily focused on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer and antidepressant medications. The monoaminergic system consists of a network of limbic, striatal and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets, 2000). It is hypothesized that BD arises from the complex interaction of multiple susceptibility and protective genes and environmental factors. The phenotypic expression of the disease includes mood disturbance, as well as cognitive, motor, autonomic, endocrine and sleep or wake abnormalities (Schloesser et al., 2008).
+Figure 3 shows the pathophysiology of BD from different perspectives, and how these different systems are interlinked. For instance, there are different physiological levels at which the disease manifests: molecular, cellular, and behavioral. In addition, there are environmental factors which also contribute to the onset of BD (Schloesser et al., 2008). Once there is a dysfunction in one physiological level, it has been observed in the literature that there is a cascade of downstream events which are ultimately responsible for primary abnormalities in signaling pathways.
@@ Line 173: / Line 304: @@
 {{:screen_shot_2017-04-04_at_6.42.43_pm.png|}}
+Many signaling pathways play critical roles not only in synaptic plasticity, the cellular process that results in lasting changes in the efficacy of neurotransmission, but also in the long-term atrophic processes. Therefore, plasticity plays a role in the cascading effect for the pathophysiology of the disease (Schloesser et al., 2008).
+In healthy humans, there are numerous biological mechanisms which underlie neuroplasticity, a broader term that encapsulates changes in intracellular signaling cascades and gene regulation, modifications of synaptic number and strength, variations in neurotransmitter release, modeling of axonal and dendritic architecture, and in some areas of the CNS, the generation of new neurons. The remarkable plasticity of neuronal circuits is achieved through different biological means, including alterations in gene transcription and intracellular signaling cascades. These changes thereby modify diverse neuronal properties such as neurotransmitter release, synaptic function and even morphological characteristics of neurons. However, it has been shown that people with BD have abnormalities in cellular signaling cascades that regulate diverse physiologic functions, thereby causing tremendous medical comorbidity associated with BD (Figure 4) (Schloesser et al., 2008).
 **Figure 4**: Cellular signaling cascades that regulate diverse physiologic functions have shown to be disrupted in patients with BD. Retrieved from Schloesser et al., 2008.
@@ Line 179: / Line 314: @@
 === Structural Neuroimaging Findings ===
+Many forms of neural plasticity involve structural changes in the brain. Since neuroplasticity and cellular cascade changes play a role in BD, many studies to date have used neuroimaging and postmortem human brains to investigate the potential alterations in structural plasticity in mood disorders. Studies on people with BD using the aforementioned pathological techniques have revealed several functional and structural abnormalities in brain regions involved in the perception and control of mood states and emotions. These include the prefrontal cortex (PFC), amygdala, insula, hippocampus, anterior cingulate cortex, and ventral striatum (Figure 5). In addition, post-mortem morphometric brain studies in mood disorders have demonstrated that patients with mood disorders undergo cellular atrophy and/or loss (Table 1) (Schloesser et al., 2008).
 {{:screen_shot_2017-04-04_at_6.42.57_pm.png|}}
@@ Line 190: / Line 326: @@
 === Allostatic load in Bipolar Disorder ===
+Allostatic load (AL) is the bodily “wear and tear” that emerges due to the effects of chronic stress in general health. In patients with BD, AL offers an insight into why patients who undergo recurrent mood episodes are clinically perceived less resilient, and thereby, more susceptible to comorbid diseases. AL helps explain the stress- and episode-induced changes in the brain regions involved in the emotional circuitry, which then lead to dysfunctional processing of information. This in turn makes BD patients more vulnerable to environmental stressors, episodes and drug abuse (Kapczinski et al., 2008).
 === HPA axis and circadian rhythm disturbances ===
+The hypothalamic-pituitary axis (HPA) axis, is altered in mood disorders. Abnormalities in cortisol levels have been found in patients suffering from mood disorders. These changes in cortisol levels are central to the concept of AL (Kapczinski et al., 2008). A study by Cervantes et al. in 2001, showed that bipolar patients in different phases of the disease- depression, mania/ hypomania and remission, had higher levels of cortisol than healthy controls (Cervantes et al., 2001). It is postulated that the elevated cortisol levels may have important long-term consequences, such as neuroplastic alterations in the hippocampus, amygdala and prefrontal cortex. Elevated cortisol levels altering HPA axis also change several aspects of circadian rhythms, including sleep regulation, which then cause AL in BD. Further, many studies in the literature have shown the effects of sleep deprivation on the body, including impairment of brain function, increase inflammatory response, increase cortisol, insulin and blood glucose levels (Kapczinski et al., 2008).
 === Amygdala and emotional processing ===
+Chronic stress is known to induce hyperactivation of the amygdala, enhancing amygdala-dependent unlearned fear, fear conditioning and aggression. Patients with BD appear to have abnormalities in the emotional processing involving the amygdala circuitry. Functional neuroimaging studies have shown increased activity of the amygdala during acute mood episodes. Amygdala-related circuits seem to be overactive, but dysfunctional in patients with BD. Such malfunctioning is postulated to render BD patients more vulnerable to stress and thereby, leading to increased AL (Kapczinski et al., 2008).
 === Prefrontal cortex and coping ===
+The prefrontal cortex (PFC) is a key brain region involved in the regulation of emotional behaviour, executive function and fear extinction. This area is sensitive to the remodeling effects of stress. Several studies have shown structural and functional frontal lobe abnormalities (reduction in size) in BD, including the anterior cingulate and subnegual PFC. These are consistent with the cognitive deficits found in BD (Kapczinski et al., 2008).
+Figure 6 encapsulates the brain rewiring that happens after recurrent stress and mood episodes in BD patients. Neural substrate reactivity is altered in BD patients, leading to cell endangerment, pro-apoptotic cascades, thereby leading to altered size of brain parts involved in emotional processing and coping. Such brain rewiring is related to increased emotionality and poor coping which render subjects more vulnerable to life stress (Kapczinski et al., 2008).
 {{:screen_shot_2017-04-04_at_6.43.19_pm.png|}}
@@ Line 334: / Line 478: @@
 . Bipolar and Related Disorders. (n.a). Retrieved March 25, 2017, from http://dsm.psychiatryonline.org/doi/10.1176/appi.books.9780890425596.dsm03
-. CAMH: Antipsychotic Medication. (2017). Camh.ca. Retrieved 24 March 2017, from http://www.camh.ca/en/hospital/health_information/a_z_mental_health_and_addiction_information/antipsychotic_medication/Pages/antipsychotic_medication.aspx
+.Bipolar Disorder: Who's at Risk? (n.d.). Retrieved March 22, 2017, from http://www.webmd.com/bipolar-disorder/guide/bipolar-disorder-whos-at-risk#2
-. Centre for Addiction and Mental Health. (n.d.). Treatments for bipolar disorder. Retrieved March 29, 2017, from http://www.camh.ca/en/education/about/camh_publications/info_guides/bipolar-info-guide/Pages/Treatments-for-bipolar-disorder.aspx#psych
+. CAMH: Antipsychotic Medication. (2017). Camh.ca. Retrieved 24 March 2017, from http://www.camh.ca/en/hospital/health_information/a_z_mental_health_and_addiction_information/antipsychotic_medication/Pages/antipsychotic_medication.aspx
-. Colom, F., Vieta. E., Martinez-Aran, A., Reinares, M., Goikolea, JM., Benabarre, A., Torrent, C., Comes, M., Corbella, B., Parramon, G., & Corominas, J. (2003). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of General Psychiatry, 60, (4), 402-4027. http://10.1001/archpsyc.60.4.402
+. Centre for Addiction and Mental Health. (n.d.). Treatments for bipolar disorder. Retrieved March 29, 2017, from http://www.camh.ca/en/education/about/camh_publications/info_guides/bipolar-info-guide/Pages/Treatments-for-bipolar-disorder.aspx#psych
-. Geddes, J., & Miklowitz, D. (2017). Treatment of bipolar disorder. The Lancet. Retrieved 23 March 2017, from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60857-0/abstract
+. Colom, F., Vieta. E., Martinez-Aran, A., Reinares, M., Goikolea, JM., Benabarre, A., Torrent, C., Comes, M., Corbella, B., Parramon, G., & Corominas, J. (2003). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of General Psychiatry, 60, (4), 402-4027. http://10.1001/archpsyc.60.4.402
-. Kapczinski, F., Vieta, E., Andreazza, A. C., Frey, B. N., Gomes, F. A., Tramontina, J., ... & Post, R. M. (2008). Allostatic load in bipolar disorder: implications for pathophysiology and treatment. Neuroscience & Biobehavioral Reviews, 32(4), 675-692.
+. Geddes, J., & Miklowitz, D. (2017). Treatment of bipolar disorder. The Lancet. Retrieved 23 March 2017, from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60857-0/abstract
-. Mayo Clinic. (2017). Bipolar Disorder. [online] Available at: http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/diagnosis-treatment/treatment/txc-20308001 [Accessed 25 Mar. 2017].
+. Kapczinski, F., Vieta, E., Andreazza, A. C., Frey, B. N., Gomes, F. A., Tramontina, J., ... & Post, R. M. (2008). Allostatic load in bipolar disorder: implications for pathophysiology and treatment. Neuroscience & Biobehavioral Reviews, 32(4), 675-692.
-. National Collaborating Centre for Mental Health (UK). (2006). Bipolar disorder: The management of bipolar disorder in adults, children and adolescents, in primary and secondary care. Leicester, UK: British Psychological Society.
+. Mayo Clinic. (2017). Bipolar Disorder. [online] Available at: http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/diagnosis-treatment/treatment/txc-20308001 [Accessed 25 Mar. 2017].
-. Post, R., Altshuler, L., Leverich, G., Frye, M., Nolen, W., & Kupka, R. et al. (2006). Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. The British Journal Of Psychiatry, 189(2), 124-131. http://dx.doi.org/10.1192/bjp.bp.105.013045
+. Mayo Clinic Staff Print. (2017, February 15). Symptoms and causes. Retrieved March 21, 2017, from http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/symptoms-causes/dxc-20307970
-. Prevalence of bipolar disorder. (2011, March 07). Retrieved March 25, 2017, from http://www.news-medical.net/news/20110307/Prevalence-of-bipolar-disorder.aspx
+. National Collaborating Centre for Mental Health (UK). (2006). Bipolar disorder: The management of bipolar disorder in adults, children and adolescents, in primary and secondary care. Leicester, UK: British Psychological Society.
-. Schloesser, R. J., Huang, J., Klein, P. S., & Manji, H. K. (2008). Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology, 33(1), 110-133.
+. Post, R., Altshuler, L., Leverich, G., Frye, M., Nolen, W., & Kupka, R. et al. (2006). Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. The British Journal Of Psychiatry, 189(2), 124-131. http://dx.doi.org/10.1192/bjp.bp.105.013045
-. Severus, E., Taylor, M., Sauer, C., Pfennig, A., Ritter, P., Bauer, M., & Geddes, J. (2014). Lithium for prevention of mood episodes in bipolar disorders: systematic review and meta-analysis. International Journal Of Bipolar Disorders, 2(1). http://dx.doi.org/10.1186/s40345-014-0015-8
+. Prevalence of bipolar disorder. (2011, March 07). Retrieved March 25, 2017, from http://www.news-medical.net/news/20110307/Prevalence-of-bipolar-disorder.aspx
-. Smith, D., Jones, I., & Simpson, S. (2010). Psychoeducation for bipolar disorder. Advances in Psychiatric Treatment, 16 (2), 147-154. http://10.1192/apt.bp.108.006403
+. Schloesser, R. J., Huang, J., Klein, P. S., & Manji, H. K. (2008). Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology, 33(1), 110-133.
-. Tracy, N. (2016, June). Effects of Bipolar Disorder - Bipolar Information - Bipolar Disorder. Retrieved March 26, 2017, from http://www.healthyplace.com/bipolar-disorder/bipolar-information/effects-of-bipolar-disorder/
+. Severus, E., Taylor, M., Sauer, C., Pfennig, A., Ritter, P., Bauer, M., & Geddes, J. (2014). Lithium for prevention of mood episodes in bipolar disorders: systematic review and meta-analysis. International Journal Of Bipolar Disorders, 2(1). http://dx.doi.org/10.1186/s40345-014-0015-8
+. Smith, D., Jones, I., & Simpson, S. (2010). Psychoeducation for bipolar disorder. Advances in Psychiatric Treatment, 16 (2), 147-154. http://10.1192/apt.bp.108.006403
+. Tracy, N. (2016, June). Effects of Bipolar Disorder - Bipolar Information - Bipolar Disorder. Retrieved March 26, 2017, from http://www.healthyplace.com/bipolar-disorder/bipolar-information/effects-of-bipolar-disorder/
+.Written by Jaime HerndonMedically Reviewed by. (n.d.). Risk Factors for Bipolar Disorder. Retrieved March 21, 2017, from http://www.healthline.com/health/bipolar-disorder/bipolar-risk-factors#Possibleriskfactors3

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