People with a bipolar disorder experience both the lows of depression and the highs of mania. Many describe their life as an emotional roller coaster, as they shift back and forth between extreme moods. A number of sufferers eventually become suicidal. Their roller coaster ride also has a dramatic impact on relatives and friends (Barron et al., 2014; Lee et al., 2011; Lowe & Cohen, 2010).

Unlike people sunk in the gloom of depression, those in a state of mania typically experience dramatic and inappropriate rises in mood. The symptoms of mania span the same areas of functioning—emotional, motivational, behavioral, cognitive, and physical—as those of depression, but mania affects those areas in an opposite way.

A person in the throes of mania has active, powerful emotions in search of an outlet. The mood of euphoric joy and well-being is out of all proportion to the actual happenings in the person’s life. One person with mania explained, “I feel no sense of restriction or censorship whatsoever. I am afraid of nothing and no one” (Fieve, 1975, p. 68). Not every person with mania is a picture of happiness, however. Some instead become very irritable and angry, especially when others get in the way of their exaggerated ambitions.

In the motivational realm, people with mania seem to want constant excitement, involvement, and companionship. They enthusiastically seek out new friends and old, new interests and old, and have little awareness that their social style is overwhelming, domineering, and excessive.

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The behavior of people with mania is usually very active. They move quickly, as though there were not enough time to do everything they want to do. They may talk rapidly and loudly, their conversations filled with jokes and efforts to be clever or, conversely, with complaints and verbal outbursts. Flamboyance is not uncommon: dressing in flashy clothes, giving large sums of money to strangers, or even getting involved in dangerous activities.

In the cognitive realm, people with mania usually show poor judgment and planning, as if they feel too good or move too fast to consider possible pitfalls. Filled with optimism, they rarely listen when others try to slow them down, interrupt their buying sprees, or prevent them from investing money unwisely. They may also hold an inflated opinion of themselves, and sometimes their self-esteem approaches grandiosity. During severe episodes of mania, some have trouble remaining coherent or in touch with reality.

Finally, in the physical realm, people with mania feel remarkably energetic. They typically get little sleep yet feel and act wide awake (Armitage & Arnedt, 2011). Even if they miss a night or two of sleep, their energy level may remain high.

People are considered to be in a full manic episode when for at least 1 week they display an abnormally high or irritable mood, increased activity or energy, and at least three other symptoms of mania (see Table 7-5). The episode may even include psychotic features such as delusions or hallucinations. When the symptoms of mania are less severe (causing little impairment), the person is said to be having a hypomanic episode (APA, 2013).

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DSM-5 distinguishes two kinds of bipolar disorders—bipolar I and bipolar II. People with bipolar I disorder have full manic and major depressive episodes. Most of them experience an alternation of the episodes; for example, weeks of mania followed by a period of wellness, followed in turn by an episode of depression. Some, however, have mixed features, in which they display both manic and depressive symptoms within the same episode—for example, having racing thoughts amidst feelings of extreme sadness. In bipolar II disorder, hypomanic—that is, mildly manic—episodes alternate with major depressive episodes over the course of time. Some people with this pattern accomplish huge amounts of work during their mild manic periods (see PsychWatch below).

Without treatment, the mood episodes tend to recur for people with either type of bipolar disorder. If a person has four or more episodes within a one-year period, his or her disorder is considered to be rapid cycling. A woman describes her rapid cycling in the following excerpt, taken from a journal article she wrote anonymously several years ago.

Regardless of their particular pattern, people with a bipolar disorder tend to experience depression more than mania over the years (Advokat et al., 2014). In most cases, their depressive episodes occur three times as often as manic ones, and the depressive episodes also last longer.

Surveys from around the world indicate that between 1 and 2.6 percent of all adults are suffering from a bipolar disorder at any given time (Kessler et al., 2012; Merikangas et al., 2011). As many as 4 percent experience one of the bipolar disorders at some time in their life. Bipolar I disorder seems to be a bit more common than bipolar II disorder. The bipolar disorders are equally common in women and men. However, women may have more depressive episodes and more rapid cycling than men (Curtis, 2005; Papadimitriou et al., 2005). The disorders are more common among people with low incomes than those with higher incomes (Sareen et al., 2011).

Onset of bipolar disorder usually occurs between the ages of 15 and 44 years. In most untreated cases, the manic and depressive episodes eventually subside, only to recur at a later time. It also appears that over time, people with bipolar disorders develop more medical ailments than the rest of the population (Weiner, Warren, & Fiedorowitz, 2011).

Some people have numerous periods of hypomanic symptoms and mild depressive symptoms, a pattern that is called cyclothymic disorder in DSM-5. The symptoms of this milder form of bipolar disorder continue for two or more years, interrupted occasionally by normal moods that may last for only days or weeks. This disorder, like bipolar I and bipolar II disorders, usually begins in adolescence or early adulthood and is equally common among women and men. At least 0.4 percent of the population develops cyclothymic disorder. In some cases, the milder symptoms eventually blossom into a bipolar I or II disorder (Goto et al., 2011).

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Throughout the first half of the twentieth century, the search for the cause of bipolar disorders made little progress. Various explanations were proposed, but research did not support their validity. Psychodynamic theorists, for example, suggested that mania, like depression, emerges from the loss of a love object. Whereas some people introject the lost object and become depressed, others deny the loss and become manic. To avoid the terrifying conflicts generated by the loss, they escape into a dizzying round of activity (Lewin, 1950). Although case reports sometimes fit this explanation, only a few controlled studies have found a relationship between loss early or later in life and the onset of manic episodes (Post & Miklowitz, 2010; Tsuchiya et al., 2005).

More recently, biological research has produced some promising clues. The biological insights have come from research into neurotransmitter activity, ion activity, brain structure, and genetic factors.

NeurotransmittersRemember from Chapter 3 that neurotransmitters released from neurons’ axon endings carry messages to the dendrites of neighboring neurons by binding to receptor sites there. As you read, different psychological disorders have been linked to the abnormal functioning of various neurotransmitters, including norepinephrine. Could overactivity of norepinephrine be related to mania? This was the expectation of clinicians back in the 1960s after investigators first found a relationship between low norepinephrine activity and unipolar depression (Schildkraut, 1965). One study did indeed find the norepinephrine activity of people with mania to be higher than that of depressed or control research participants (Post et al., 1980, 1978). In another study, patients with a bipolar disorder were given reserpine, the blood pressure drug known to reduce norepinephrine activity in the brain, and the manic symptoms of some subsided (Telner et al., 1986).

Because serotonin activity often parallels norepinephrine activity in unipolar depression, theorists at first expected that mania would also be related to high serotonin activity, but no such relationship has been found. Instead, research suggests that mania, like depression, may be linked to low serotonin activity (Hsu et al., 2014; Nugent et al., 2013). Perhaps low activity of serotonin, acting again as a neuromodulator, opens the door to a mood disorder and permits the activity of norepinephrine (or perhaps other neurotransmitters) to define the particular form the disorder will take. That is, low serotonin activity accompanied by low norepinephrine activity may lead to depression; low serotonin activity accompanied by high norepinephrine activity may lead to mania. In recent years, researchers have found that bipolar disorder may also be tied to the abnormal activity of other neurotransmitters, such as GABA, the brain chemical you read about in Chapter 5 (Benes, 2011; Walderhaug et al., 2011).

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Ion ActivityWhile neurotransmitters play a significant role in the communication between neurons, ions seem to play a critical role in relaying messages within a neuron. That is, ions help transmit messages down the neuron’s axon to the nerve endings. Positively charged sodium ions (Na⁺) sit on both sides of a neuron’s cell membrane. When the neuron is at rest, more sodium ions sit outside the membrane. When the neuron receives an incoming message at its receptor sites, pores in the cell membrane open, allowing the sodium ions to flow to the inside of the membrane, thus increasing the positive charge inside the neuron. This starts a wave of electrical activity that travels down the length of the neuron and results in its “firing.” After the neuron “fires,” potassium ions (K⁺) flow from the inside of the neuron across the cell membrane to the outside, helping to return the neuron to its original resting state (see Figure 7-4).

If messages are to be relayed effectively down the axon, the ions must be able to travel easily between the outside and the inside of the neural membrane. Some theorists believe that irregularities in the transport of these ions may cause neurons to fire too easily (resulting in mania) or to stubbornly resist firing (resulting in depression) (Manji & Zarate, 2011; Li & El-Mallakh, 2004). Not surprisingly, investigators have found membrane defects in the neurons of people suffering from bipolar disorder and have observed abnormal functioning in the proteins that help transport ions across a neuron’s membrane (Sassi & Soares, 2002).

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Brain StructureBrain imaging and postmortem studies have identified a number of abnormal brain structures in people with bipolar disorders (Eker et al., 2014; Chen et al., 2011; Savitz & Drevets, 2011). For example, the basal ganglia and cerebellum of these people tend to be smaller than those of other people, they have lower volumes of gray matter in the brain, and their dorsal raphe nucleus, striatum, amygdala, hippocampus, and prefrontal cortex have some structural abnormalities. It is not clear what role such structural abnormalities play in bipolar disorders. It may be that they help produce the neurotransmitter and ion abnormalities that you read about earlier. The dorsal raphe nucleus, for example, is one of the brain sites where serotonin is produced. Alternatively, the structural problems may simply be the result of the neurotransmitter or ion abnormalities or of the medications that many patients with bipolar disorders now take.

Genetic FactorsMany theorists believe that people inherit a biological predisposition to develop bipolar disorders (Wiste et al., 2014; Glahn & Burdick, 2011; Gershon & Nurnberger, 1995). Family pedigree studies support this idea. Identical twins of those with a bipolar disorder have a 40 percent likelihood of developing the same disorder, and fraternal twins, siblings, and other close relatives of such persons have a 5 to 10 percent likelihood, compared with the 1 to 2.6 percent prevalence rate in the general population.

Researchers have also conducted genetic linkage studies to identify possible patterns in the inheritance of bipolar disorders. They select large families that have had high rates of a disorder over several generations, observe the pattern of distribution of the disorder among family members, and determine whether it closely follows the distribution pattern of a known genetically transmitted family trait (called a genetic marker), such as color blindness, red hair, or a particular medical syndrome.

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After studying the records of Israeli, Belgian, Italian, and Finnish families that had high rates of bipolar disorders across several generations, several researchers seemed to have linked bipolar disorders to genes on the X chromosome (Ekholm et al., 2002; Mendlewicz et al., 1987, 1980). Other research teams, however, later used techniques from molecular biology to examine genetic patterns in large families, and they linked bipolar disorders to genes on chromosomes 1, 4, 6, 10, 11, 12, 13, 15, 18, 20, 21, and 22 (Green et al., 2013; Bigdeli et al., 2013; Wendland and McMahon, 2011). Such wide-ranging findings suggest that a number of genetic abnormalities probably combine to help bring about bipolar disorders.