• Scientific Evidence
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Some studies have documented that people with bipolar disorder have an increased incidence of very stressful life events. There are a few problems with immediately assuming that increased life stress causes bipolar disorder, however.  For one thing, many of these studies collected their data using subject recall, and as such it’s very possible that subjects with bipolar disorder may be more prone to remember past life events as particularly stressful, either because they are viewed through the lens of their disease, or because of the natural need to find an explanation for the illness. For another thing, studies that examine stressful events or family environments of children generally study “high-risk” populations; that is, children of parents who have bipolar disorder. These children are hit with double potential risk factors – the risk of their inherited genetics, and the risk of being raised in a potentially more stressful family environment due to the illness of one or both parents. One explanation is that these two factors – genetics and life stress – feed off each other to produce bipolar disorder, but it may also be that genetics play a more prominent role, and that the life stress was not a key precipitating factor for the children who eventually go on to develop the disease themselves.

Another potential problem is that some studies only document stressful life events in the weeks immediately preceding a subject’s first hospitalization for mania. However, bipolar disorder may develop slowly over time, and an untreated individual may be more prone to experiencing negative and stressful life events as their mental health deteriorates. Thus, it would be expected that there would be an increase in such stressors immediately preceding a crisis (hospitalization) and the initiation of treatment.

Some of the specific risk factors that have been identified as possibly precipitating bipolar disorder (either the first episode, or the development of the disease) include:

• poor parent-child relationship (Tsuchiya 2003)
• early loss of a parent (Kessing et al 2004, Tsuchiya 2003, Agid et al 1999)
• death of a close relative, particularly by suicide (Kessing et al 2004)
• recent divorce, marriage, or unemployment (Kessing et al 2004).

One study in particular (Tsuchiya et al 2005) that examined 947 subjects with bipolar disorder and 47,350 age-matched healthy controls, estimated that “[t]hose having experienced maternal suicide at some point before reaching 10 years of age were seven times as likely to develop bipolar disorder.”

Again, it is very difficult to tease out whether these life events are causes or consequences of bipolar disorder, given that it is hard to know exactly how long a gap there was between the first manifestation of illness (affecting mood, attitude, and ultimately approach to life and life events) and first manic episode (and thus official diagnosis). Similarly, for risk factors such as maternal suicide, it is important to remember that suicide tends to run in families (see “Family genetic studies, suicide, and suicidal behavior”) and thus may have a genetic component to it as well. It may be that the genetics that make one more susceptible to suicidal tendencies also have an effect on the development of some affective disorder symptoms (for example, impulsivity or depression).

There is plenty of evidence, however, that environmental stress has a profound effect on the developing brain. Post et al (2001) examined the effects of maternal deprivation on very young rats. Those rats who were separated from their mothers for 24 hours during very early life had changes in their brains (as compared to control rats of the same age) that included decreased rate of neurogenesis, decreased BDNF (a growth factor that supports developing neurons), decrease in a critical enzyme for cellular learning and memory, and increased rate of neuronal apoptosis (cell death). Moreover, Post et al. found that separation stress had the same effects in adult rats, but the overall amount of stress needed to produce similar changes in the brain was much more than the amount of stress needed to affect the brains of young rats. Thus, there may be a critical period during early childhood (when the brain is developing very rapidly in response to its environment) in which children who are already susceptible to bipolar disorder may be more profoundly effected by negative stressors. Indeed, one study (Hillegers et al, 2004) of 140 children (all having at least one bipolar parent) found that “life event load” – that is, the number of stressful life events preceding the onset of bipolar disorder – increased the risk of mood disorder for the children while in their youth. The authors calculated that the effects of life event load on mood disorder risk decreased by 25% per year of life. Moreover, they determined that the effects of life events were independent from the number of relatives (other than parents) that were affected with bipolar disorder – suggesting that for susceptible children, life stress may play some sort of causal role independent of heavy genetic inheritance.

Another study (Petti et al 2004) surveyed the parents of affective and non-affective children. Some family groups had a history of bipolar illness in other relatives, but in others the children were the first identified diagnosis. The authors reported that parents of children with bipolar disorder recalled more negative life events for their affected children when compared with the reports of parents of non-affected children, regardless of whether or not there was a history of bipolar disorder in other family members. This may provide evidence for the role of life stress as independent from amount of genetic susceptibility, although negative life event recall was not confined to a period of time before the diagnosis. Thus, the symptoms of bipolar disorder might well predispose affected children to experience more negative life events.

Still other studies have examined the effects of life stress on bipolar relapse rather than bipolar onset. Miklowitz et al (1988) found that family stress is a predictor of relapse rates for people with bipolar disorder. Others (Johnson et al 2000; Post et al 2001) have suggested that perhaps stressful life events provoke an earlier (and therefore more severe) onset and course in already susceptible individuals.  Possible reasons why stress might provoke relapse include simple explanations (stressful events cause changes and interruptions in sleep cycles, which is a known precipitator of manic episodes for bipolar patients), as well as more complex ones (stress may have a neurochemical effect in the brain that directly effects neuron and neurotransmitter functioning). For more on these links, see pp. 103-104 in “Surviving Manic Depression” by Dr. E Fuller Torrey.

Helpful Actions:

The causal relationship between life stressors and bipolar disorder, for all the reasons mentioned above, remains suggestive but inconclusive. However, independent of whether life stress causes bipolar onset, it may be very important for individuals who know they are susceptible to minimize their life stress as much as possible, to avoid the possibility of an earlier onset and/or a more severe course of illness. Studies (Kendler 2000, Post 2001) have indicated that the more episodes an individual experiences, the greater the chance of future relapse, and the shorter the wellness interval between episodes.

If you know you are genetically susceptible to bipolar disorder, or if you already have a diagnosis of bipolar or another affective disorder, try your best to know what causes you stress in your life and minimize your exposure to those events as much as possible. You can also work with your psychiatrist, a mental health therapist, or a workbook to find healthy ways to manage day-to-day stress.

You may find it helpful to make an actual written plan for stress management. Dr. James T Stout, author of “Rebuilding Your Life: Bipolar Disorder” and a bipolar disorder sufferer himself, estimated that “at least 75% of my mood disruptions were caused by stress...I re-learned that prevention was the key to remaining stable” (240). Dr. Stout implemented the following three steps for his own coping strategy:

1. Recognize and admit – either to self or someone else – when you are feeling any form of stress
2. Identify the specific triggering person, place, or emotion (you may want to write these triggers down in a notebook or journal).
3. Take immediate action to defuse the stress

Information resources on identifying and managing stress:

• Stress: Coping with everyday problems (from NMHA)
• The Principles of Stress
• Tips and Techniques for Managing Stress
• Stress: The Silent Killer
• Learning to Cope with Stress - Measuring Your Stress Load
• America's Most (and Least) Stressful Cities

Books that may be helpful in stress relief:

• Relaxation & Stress Reduction Workbook
• The Anxiety & Phobia Workbook
• Don't Sweat the Small Stuff- and It's All Small Stuff

Scientific Studies:

• Parental death and bipolar disorder: a robust association was found in early maternal suicide. J Affect Disord. 2005 Jun;86(2-3):151-9.
• Impact of stressful life events, familial loading and their interaction on the onset of mood disorders: study in a high-risk cohort of adolescent offspring of parents with bipolar disorder. Br J Psychiatry. 2004 Aug;185:97-101.
• Major stressful life events and other risk factors for first admission with mania. Bipolar Disord. 2004 Apr;6(2):122-9.
• Psychosocial variables in children and teens of extended families identified through bipolar affective disorder probands. Bipolar Disord. 2004 Apr;6(2):106-14.
• Risk factors in relation to an emergence of bipolar disorder: a systematic review. Bipolar Disord. 2003 Aug;5(4):231-42. Review.
• Developmental vulnerabilities to the onset and course of bipolar disorder. Dev Psychopathol. 2001 Summer;13(3):581-98. Review
• Age of onset in affective disorder: its correlation with hereditary and psychosocial factors. J Affect Disord. 2000 Aug;59(2):139-48.
• Family factors and the course of bipolar affective disorder. Arch Gen Psychiatry. 1988 Mar;45(3):225-31