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| The role of anxiety in depression Anxiety The different types of Depression and Anxiety are classified separately by the DSM-IV-TR, with the exception of hypomania, which is included in the bipolar disorder category. Despite the different categories, depression and anxiety can indeed be co-occurring (occurring together, independently, and without mood congruence), or comorbid (occurring together, with overlapping symptoms, and with mood congruence). In an effort to bridge the gap between the DSM-IV-TR categories and what clinicians actually encounter, experts such as Herman Van Praag of Maastricht University have proposed ideas such as anxiety/aggression-driven depression . This idea refers to an anxiety/depression spectrum for these two disorders, which differs from the mainstream perspective of discrete diagnostic categories. Although there is no specific diagnostic category for the comorbidity of depression and anxiety in the DSM or ICD, the National Comorbidity Survey (US) reports that 58 percent of those with major depression also suffer from lifetime anxiety. Supporting this finding, two widely accepted clinical colloquialisms include * agitated depression - a state of depression that presents as anxiety and includes akathisia, suicide, insomnia (not early morning wakefulness), nonclinical (meaning "doesn't meet the standard for formal diagnosis") and nonspecific panic, and a general sense of dread. * akathitic depression - a state of depression that presents as anxiety or suicidality and includes akathisia but does not include symptoms of panic. It is also clear that even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. A pilot study by Ellen Frank et al., at the University of Pittsburgh, found that depressed or bipolar patients with lifetime panic symptoms experienced significant delays in their remission. These patients also had higher levels of residual impairment, or the ability to get back into the swing of things. On a similar note, Robert Sapolsky of Stanford University and others also argue that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically. To that point, a study by Heim and Nemeroff et al., of Emory University, found that depressed and anxious women with a history of childhood abuse recorded higher heart rates and the stress hormone ACTH when subjected to stressful situations. Hypomania Hypomania, as the name suggests, is a state of mind or behavior that is "below" (hypo) mania. In other words, a person in a hypomanic state often displays behavior that has all the earmarks of a full-blown mania (e.g., marked elevation of mood that is characterized by euphoria, over activity, disinhibition, impulsivity, a decreased need for sleep, hypersexuality), but these symptoms, though disruptive and seemingly out of character, are not so pronounced as to be considered a diagnosably manic episode. Another important point is that hypomania is a diagnostic category that includes both anxiety and depression. It often presents as a state of anxiety that occurs in the context of a clinical depression. Patients in a hypomanic state often describe a sense of extreme generalized or specific anxiety, recurring panic attacks, night terrors, guilt, and agency (as it pertains to codependence and counterdependence). All of this happens while they are in a state of retarded or somnolent depression. This is the type of depression in which a person is lethargic and unable to move through life. The terms retarded and somnolent are shorthand for states of depression that include lethargy, hypersomnia, a lack of motivation, a collapse of ADLs (activities of daily living), and social withdrawal. This is similar to the shorthand used to describe an "agitated" or "akathitic" depression. In considering the hypomania-depression connection, a distinction should be made between anxiety, panic, and stress. Anxiety is a physiological state that is caused by the sympathetic nervous system. Anxiety does not need an outside influence to occur. Panic is related to the "fight or flight" mechanism. It is a reaction, induced by an outside stimulus, and is a product of the sympathetic nervous system and the cerebral cortex. More plainly, panic is an anxiety state that we are thinking about. Finally, stress is a psychosocial reaction, influenced by how a person filters nonthreatening external events. This filtering is based on one's own ideas, assumptions, and expectations. Taken together, these ideas, assumptions, and expectations are called social constructionism. On a final note, researchers at the University of California, San Diego, under the guidance of Hagop Akiskal MD, have found convincing evidence for the co-occurrence of hypomanic symptoms associated with a diagnosis of depression where the diagnosis does not meet criteria for Bipolar Disorder. Symptoms under consideration, such as irritability, misdirected anger, and compulsivity, also may not present sufficiently to be considered a hypomanic episode, as described by a Bipolar II Disorder. As noted in the Frank study mentioned above, this particular course of the disease, with the breakthrough of anxiety, may have a significant impact on the overall course of the depression. This idea of co-occurring anxiety and depression is supported in a study by Giovanni Cassano MD of the University of Pisa and his collaborators on the Spectrum Project, who found a correlation between lifetime hypomanic and manic symptoms and the severity of the depression. "The presence of a significant number of manic/hypomanic items in patients with recurrent unipolar depression seems to challenge the traditional unipolar-bipolar dichotomy." These authors, along with many other researchers, argue in support of a revision of the approach to psychiatric diagnosis into what is being called the mood spectrum, so as to "[make] more accurate diagnostic evaluation[s]." This approach, although controversial, has begun to be given consideration by many behavioral health professionals. Causes of depression No specific cause for depression has been identified, but a number of factors are believed to be involved. * Heredity – The tendency to develop depression may be inherited; there is some evidence that this disorder may run in families. A 2004 press release from the National Institute of Mental Health declares "major depression is thought to be 40-70 percent heritable, but likely involves an interaction of several genes with environmental events." Brain chemicals called neurotransmitters allow electrical signals to move from the axon of one nerve cell to the neuron of another. A shortage of neurotransmitters impairs brain communication. * Physiology – There may be changes or imbalances in chemicals that transmit information in the brain, called neurotransmitters. Many modern antidepressant drugs increase levels of certain neurotransmitters, such as serotonin and norepinephrine. Although the causal relationship is unclear, it is known that antidepressant medications can relieve certain symptoms of depression, although critics point out that the relationship between serotonin, SSRIs, and depression usually is typically greatly oversimplified when presented to the public (see here). Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus. This horseshoe-shaped structure is a center for both mood and memory. Loss of neurons in the hippocampus is found in depression and correllates with impaired memory and dysthemic mood. The hippocampus regains mass when exposed to treatments that increase brain serotonin, and when regrown, mood and memory tend to be restored. * Seasonal affective disorder (SAD) is a type of depressive disorder that occurs in the winter when daylight hours are short. It is believed that the body's production of melatonin, which is produced at higher levels in the dark, plays a major part in the onset of SAD and that many sufferers respond well to bright light therapy, also known as phototherapy. * Psychological factors – Low self-esteem and self-defeating or distorted thinking are connected with depression. Although it is not clear which is the cause and which is the effect, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem. Psychological factors related to depression include the complex development of one's personality and how one has learned to cope with external environmental factors such as stress. * Early experiences – Events such as the death of a parent, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse can also increase the likelihood of depression later in life. Post-traumatic stress disorder (PTSD) includes depression as one of its major symptoms. * Life experiences – Job loss, poverty, financial difficulties, gambling addiction, long periods of unemployment, the loss of a spouse or other family member, divorce or the end of a committed relationship, involuntary celibacy, or other traumatic events may trigger depression. Long-term stress at home, work, or school can also be involved. Bullying in late adolescence is also thought to be a contributing factor. * Medical conditions – Certain illnesses, including cardiovascular disease, hepatitis, mononucleosis, hypothyroidism, and organic brain damage caused by degenerative conditions such as Parkinson disease, Multiple Sclerosis or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as birth control pills and steroids. Gender dysphoria can also cause depression. * Diet – The increase in depression in industrialised societies has been linked to diet, particularly to reduced levels of omega-3 fatty acids in intensively farmed food and processed foods. This link has been at least partly validated by studies using dietary supplements in schools and by a double-blind test in a prison. An excess of omega-6 fatty acids in the diet was shown to cause depression in rats]. * Alcohol and other drugs – Alcohol can have a negative effect on mood, and misuse of alcohol, benzodiazepine-based tranquilizers, and sleeping medications can all play a major role in the length and severity of depression. The link between frequent cannabis use and depression is also widely documented, although the direction of causality remains in question; Dr. Salynn Boyles writes, ". . . research has linked pot smoking with depression and schizophrenia . . . daily use [of marijuana] was associated with a five-fold increase in later depression and anxiety among young women. But depression and anxiety were not predictive of later marijuana use." * Postpartum depression (also known as postnatal depression) – Dr. Ruta M Nonacs writes that while many women experience some mood changes after giving birth, "10-15% of women experience a more disabling and persistent form of mood disturbance (eg, postpartum depression, postpartum psychosis)." When it occurs, the onset typically is within three months after delivery, and it may last for several months. About two new mothers out of a thousand experience the more serious depressive disorder Postnatal Psychosis which includes hallucinations and/or delusions. * Living with a depressed person – Those living with someone suffering from depression experience increased anxiety and life disruption, increasing the possibility of also becoming depressed. * Evolutionary biological hypotheses of depression – Evolutionary analyses usually consider possible functions for depressed mood as well as clinical depression. * o The psychic pain hypothesis: psychic pain, such as depression, is analogous to physical pain. The function of physical pain is to inform the organism that it is suffering damage, to motivate it to withdraw from the source of damage, and to learn to avoid such damage-causing circumstances in the future. Analogously, depression informs the sufferer that current circumstances, such as the loss of a mate, are imposing a threat to biological fitness, it motivates the sufferer to cease activities that led to the costly situation, if possible, and it causes him or her to learn to avoid similar circumstances in the future. Proponents of this view tend to focus on low mood, and regard clinical depression as a dysfunctional extreme of low mood. See, e.g., Nesse 2000 and Keller and Nesse 2005; see also Hagen and Barrett n.d.. * o Rank theory: If an individual is involved in a lengthy fight for dominance in a social group and is clearly losing, depression causes the individual to back down and accept the submissive role. In doing so, the individual is protected from unnecessary harm. In this way, depression helps maintain a social hierarchy. This theory is a special case of a more general theory derived from the psychic pain hypothesis: that the cognitive response that produces modern-day depression evolved as a mechanism that allows people to assess whether they are in pursuit of an unreachable goal, and if they are, to motivate them to desist. See, e.g., Nesse 2000. * o Honest signalling theory: When social partners have conflicts of interest, 'cheap' signals of need, such as crying, might not be believed. Biologists and economists have proposed that signals with inherent costs can credibly signal information when there are conflicts of interest. The symptoms of major depression, such as loss of interest in virtually all activities and suicidality, are inherently costly, but, as costly signaling theory requires, the costs differ for individuals in different states. For individuals who are not genuinely in need, the fitness cost of major depression is very high because it threatens the flow of fitness benefits. For individuals who are in genuine need, however, the fitness cost of major depression is low because the individual is not generating many fitness benefits. Thus, only an individual in genuine need can afford to suffer major depression. Major depression therefore serves as an honest, or credible, signal of need. See, e.g., Hagen 2003, Watson and Andrews 2002. * o Social navigation or niche change theory: The social navigation, bargaining, or niche change hypothesis suggests that depression, operationally defined as a combination of prolonged anhedonia and psychomotor retardation or agitation, provides a focused sober perspective on socially imposed constraints hindering a person’s pursuit of major fitness enhancing projects. Simultaneously, publicly displayed symptoms, which reduce the depressive's ability to conduct basic life activities, serve as a social signal of need; the signal's costliness for the depressive certifies its honesty. Finally, for social partners who find it uneconomical to respond helpfully to an honest signal of need, the same depressive symptoms also have the potential to extort relevant concessions and compromises. Depression’s extortionary power comes from the fact that it retards the flow of just those goods and services such partners have come to expect from the depressive under status quo socioeconomic arrangements. Thus depression may be a social adaptation especially useful in motivating a variety of social partners, all at once, to help the depressive initiate major fitness-enhancing changes in their socioeconomic life. There are extraordinarily diverse circumstances under which this may become necessary in human social life, ranging from loss of rank or a key social ally which makes the current social niche uneconomic to having a set of creative new ideas about how to make a livelihood which begs for a new niche. The social navigation hypothesis emphasizes that an individual can become tightly ensnared in an overly restrictive matrix of social exchange contracts, and that this situation sometimes necessitates a radical contractual upheaval that is beyond conventional methods of negotiation. Regarding the treatment of depression, this hypothesis calls into question any assumptions by the clinician that the typical cause of depression is related to maladaptive perverted thinking processes or other purely endogenous sources. The social navigation hypothesis calls instead for a penetrating analysis of the depressive’s talents and dreams, identification of relevant social constraints (especially those with a relatively diffuse non-point source within the social network of the depressive), and practical social problem-solving therapy designed to relax those constraints enough to allow the depressive to move forward with their life under an improved set of social contracts. Bargaining theory: This theory is similar to the honest signaling, niche change, and social navigation theory. It basically adds one additional element to honest signaling theory. The fitness of social partners is generally correlated. When a wife suffers depression and reduces her investment in offspring, for example, the husband's fitness is also put at risk. Thus, not only do the symptoms of major depression serve as costly and therefore honest signals of need, they also compel social partners to respond to that need in order to prevent their own fitness from being reduced. See, e.g., Hagen 1999, Hagen 2003. |