|PSY 101 Psychological Disorders II: Mood Disorders|
Central Issues: Disturbances in Emotion (Sadness or Melancholy vs. Elation & Excitement)
Some Recent Statistics
The Dual Face of Mood Disturbance
|Pole I: Depressive Episode
||Pole II: Manic Episode
|Motor & Physiological Symptoms||
1. Major Depressive Disorder (Unipolar Disorder)
- Marked by the symptoms listed above for a depressive episode
- Note that a unipolar mood disorder marked by a purely manic episode, that is, "pure mania", occurs so infrequently that most psychiatrists/clinical psychologists don't ever see it.
Onset & Course
- At any time, but particularly between 15 and 35 for first episode
- Depressive episodes tend to last for about 5 months
- While the majority of depressive episodes are resolved within 6 months, left untreated most people will re-experience another episode (> 75%).
NIMH suggests that up to 9.5% of Americans have a depressive disorder in any one year
Current lifetime risk in the US may be as high as 19% or more (Merikangas et al., 2011)
Some suggestions that, among younger people, the lifetime risk may turn out to be as high as 25-40%
Women are 2 times more likely to be diagnosed with depression as men.
2. Bipolar Disorder
Note that in DSM-5, Bipolar Disorder is treated as a separate disorder from Major Depression.
- Marked by an alternating patterns in which depressive episodes are preceded or followed by manic (or hypomanic or "mild" manic) episodes.
- NEW: In the last five to ten years, some researchers have begun to use a term called "bipolar spectrum disorder" which includes
- the traditional diagnostic category of bipolar disorder ("pure" bipolar disorder = Bipolar I [Depressive & Manic Episodes] and Bipolar II [Depressive & Hypomanic Episodes] disorder), and
- a new category of "subthreshold bipolar disorder", that is, a disorder in which an individual has some but not enough symptoms to actually qualify for a diagnosis of either Bipolar I or Bipolar II Disorders (Merikangas et al, 2007, 2011).
Onset & Course
- Usually develops in late adolescence and early adulthood: vulnerability is highest in the 20s.
- NEW: Often shows a "neuroprogressive" course, i.e., increasing frequency of manic episodes, decreased time between manic episodes, declining overall cognitive performance & functions (Sharma et al., 2016)
- NEW: Much less prevalent than depression: for "pure" bipolar disorder the annual prevalence is about 1% and a lifetime prevalence is about 2% (1% for Bipolar-I and 1% for Bipolar-II). However, for the expanded category of "bipolar spectrum disorders, the US rate is about 2.5% annually and about 4% lifetime prevalence. For unknown reasons the US appears to have one of the highest rates of "bipolar spectrum disorder" rates in world (Merikangas et al., 2011)
Etiology (Causes) of Mood DisordersGender differences in bipolar disorder are much smaller than in depression. For "pure" bipolar disorder, the rate between women and men is roughly 1:1 (equal). For bipolar spectrum disorder the rate between women and men is about 3:2 (50% greater in women).
- Strong evidence for genetic vulnerability in depression: Very high levels of concordance for the illness among identical twins (ca. 2/3 or 67%) compared to fraternal twins (15%)
- Bipolar disorder has an even higher genetic vulnerability than unipolar disorder (major depressive disorder).
- Early childhood loss, e.g., death of parent
- Negative cognitive style (see below)
- Childhood abuse: this might better be called a life stress, but since it usually doesn't immediately cause depression, but shows up later in adolescent/adult depression, it serves as a vulnerability.
Precipitating Factors: Stress
- Moderately strong degree of correspondence between stress and depression
- In 2003, researchers discovered that there is a significant relationship between a genetic vulnerability and stress leading to higher levels of depression. Specifically, on the 5-HTT (serotonin transporter gene) there are two variants (alleles) that we can inherit from our parents. Those who have two short (s/s) alleles are much more likely to become depressed than those who have two long (l/l) alleles when subject to multiple life stressors (Caspi et al, 2003).
- After 4 stressful life events (over 4 years), individuals with s/s alleles are 4 times more likely to have suicidal ideas or attempts than those with the l/l alleles: 16% vs. 4%.
A. Neurochemical & Biological Problems
- Neurotransmitters: Imbalances involving norepinepherine (NE) ↓ and serotonin (5-HT) ↓ are thought to be involved in depressive disorder.
- Newer medications for depression (SSRIs or "Selective Serotonin Reuptake Inhibitors" such as Prozac, Paxil, and Zoloft) increase the number of serotonin molecules in the brain by "plugging the drain" (that is, blocking the reuptake gates, see figure to right) which brings them back into the neuron. This has the effect of increasing the overall level of serotonin. They work particularly well for individuals with moderate to severe depression.
- NEW TO BOOK: However, the "serotonin hypothesis" is under significant attack as unpersuasive as the primary biological explanation for depression. Newer research suggests that nerve cell death in the hippocampus may be centrally involved in developing a depressive disorder. The mechanism for such death may involve the effects of stress and repeated exposure to corticosteroids (i.e., cortisol). It is notable that long-term antidepressant medications appears to promote new cell growth in the hippocampus.
- We have no generally-accepted theory to account for the manic phase of bipolar disorder
B. Cognitive Problems
- Martin Seligman's Theories of Learned Helplessness & Hopelessness
- Learned Helplessness: People explain setbacks & negative life events using a pessimistic explanatory style, i.e., they attribute the setbacks to causes which are personal (not situational), global, and permanent.
- Hopelessness Theory proposes that depression is a "final common pathway" in which the effects of a pessimistic explanatory style interact with other factors like high levels of stress, poor self-esteem, etc. to lead to hopelessness which, in turn, leads to depression.
- Susan Nolen-Hoeksema's 1991 study of depressed persons who ruminate over their situation appear to extend or deepen their depression
- Lauren Alloy et al. (1999): College students were evaluated for negative cognitive style without being actually depressed. Over subsequent 2.5 years, 17% of the "high-risk" students (high negative cognitive style) developed a major depressive disorder compared to only 1% of the "low-risk" students. Further, 39% of "high-risk" students overall had some minor depressive episodes compared to 6% of "low-risk" students.
C. Interpersonal Problems
- There is a significant degree of relationship between poor social skills and depression.
- Qualities like shyness, pessimism, and irritability tend to shut people off from other people who, lacking social support, are more prone to depression
Caspi, A., Sugden, K.,...& Poulton, R. (2003). Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Science, 301, 386-389.
Merikangas, K. R., et al. (2007). Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Archives of General Psychiatry, 64, 543-553.
Merikangas, K. R., et al. (2011). Prevalence and correlates of bipolar spectrum disorder in the World Mental Health Survey initiative. Archives of General Psychiatry, 68(2), 241-251. doi:10.1001/archgenpsychiatry.2011.12
Sharma, A. N., Fries, G. R., Galvez, J. F., et al (2016). Modeling mania in preclinical settings: A comprehensive review. Progress in Neuro-Pharmacology & Biological Psychiatry, 66, 22-34. doi: 10.1016/j.pnpbp.2015.11.001
This page was originally posted on 11/21/03 and last updated on December 4, 2016