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Depressed By Default

Riki's picture


In my previous web paper, I contemplated the idea of a link between depression and the default mode network. I would like to explore the link between the two in this web paper.

            To review, the default mode network is the state the brain reverts to when external attention is not required. When consciously directed attention is active, the default mode network is less active and vice versa. Like many cognitive networks, the default mode network is composed of many different brain regions. One of these regions is known as the medial prefrontal cortex and it plays a role in imagination and self-referential thinking (1). Meanwhile the posterior cingulated cortex and the precuneus take part in memory “retrieval”, self-visualization, and self-description (1). The default mode network contributes to a sense of self. As a result, some neuroscientists believe the default mode network provides a state for internal exploration of the perceived external world (1). If this is the case, then I am not sure I see a difference between the I-function and the default mode network. Are they one and the same, or does the default mode network lie below the I-function in chain of command? Nevertheless, I can confidently say that the default mode network is involved with self-referential thinking.

            Depressed people are known to drown in intense ruminations. These ruminations require so much mental energy that little else gets accomplished, mentally or physically. A defining symptom of depression is a lack of energy. Perhaps it is not a lack of energy but rather a reallocation of energy to ruminations. Thinking along these lines is the analytic-rumination hypothesis of depression. Many researchers believe that depression must be an evolved adaptation mechanism since it is so common (2). It is thought that other symptoms of depression, such as anhedonia, loss of interest in food and sex, and social withdrawal, serve to keep the brain focused on ruminating (3, 2). The brain is able to devote nearly all of its attentional resources to ruminating when bereft of its usual distractions. It seems that a depressed person has no choice but to ruminate, given how difficult it is for them to concentrate on anything external. Researchers believe the focus for rumination stems from increased activity in the ventrolateral prefrontal cortex, deficits of which are associated with ADD (2). Proponents of this theory suggest that these focused ruminations serve to work through issues at the heart of the depression by allowing the person to untangle a complex problem into simpler pieces (2). Whether or not this is the purpose of the ruminations, neuroscientists are currently examining the relationship between attention and depression.

            If the default mode network is associated with self-referential thinking and depressed people are trapped in rumination, does this mean they are suffering from an impaired default mode network? “Normal”, non-depressed people show reduced activity in the default mode network while performing goal-directed tasks that do not require self-referential thinking (4). This suggests that self-referential thinking would distract and detract from overall task performance, which makes sense in light of my previous paper on brain farts/attentional lapses and the default mode network.

            Previous studies of depressed people have found structural and functional abnormalities in the regions of the default mode network and the limbic system, which is believed to be the “emotional” network (4). What are the connections between emotions and the default mode network? It is an understatement to say depressed people feel sad. They feel so sad it is painful. This intense emotion probably increases limbic system activity. The internal emotional states associated with depression might hijack the brain’s attention. As stated in my previous paper, the attentional network and the default mode network are constantly competing with each other for resources. If attentional networks are involved with more external tasks and the default mode network is associated with internal thinking, then maybe the internal emotions of depression inherently require more activity in the default mode network than the attentional networks. Since the default mode network must be activated by the demands of the limbic system, cognition must reflect the increased activity. Thus, a depressed person is forced to ruminate as a result of intense feelings. Ruminations are repetitive. Perhaps once a person begins the ruminative process as a result of feeling intense sadness, the balance between the attentional networks and the default mode network reaches a threshold whereby the attentional networks divert all attention to the default mode network’s self-referential ruminations. Once this threshold is reached, maybe it is incredibly difficult to reverse, like an action potential. At this point, the brain is stuck in a cycle of rumination and feelings of sadness.

Reversing the situation I proposed allows an explanation for why many philosophers become depressed. Philosophers are known to be great thinkers. Thinking is inherently an internal process. While a philosopher’s initial thought may result from an external stimulus, the cascade of thoughts rapidly turns inward. As I have now established, inward thinking is associated with the default mode network. Perhaps these thoughts spark emotions, or perhaps the limbic system is activated simply because the philosopher is ruminating. Philosopher David Hume, a champion of reason and rationality, once wrote in his “Letter to a Physician” that while his “reflections against death, and poverty, and shame, and pain, and all the other calamities of life” were useful when integrated with an active lifestyle, in “solitude they serve to little other purpose, than to waste the spirits” (6). Though philosophers try to rely on reason, they end up entangled in emotion.

If depressed people have structural and functional abnormalities in both the default mode network and the limbic system, how does one know whether the abnormalities are a cause or an effect of depression? It would be difficult to determine this in a study because researchers would have to image brains before, during, and after depression. Although depression has many precursors, it would still be impossible to know in advance whether or not a person who had never been depressed would become depressed.

            If increased activity in the limbic system is linked to increased activity in the default mode network, what are the implications for the analytic-rumination hypothesis and treatment of depression? The linked activities could very well support the analytic-rumination hypothesis. If the ruminations were necessary and beneficial for the sad feelings to lift, then it would be wise not to treat the depression with medication but rather to encourage and progress the ruminations with psychotherapy until the root is uncovered. But what about when a person’s depression is not caused by any apparent external event? What about the chronically depressed? Those who can’t escape depression because they are so depressed about being depressed? These situations hardly seem adaptive. If the ruminations and emotions are caught in an endless cycle, then some sort of interference may be necessary. Yvette Sheline, a neuroscientist researching the connection between the self-referential thinking of depression and the default mode network, is exploring the default mode networks of depressed people before pharmacotherapy and during the treatment (5). Results suggest that after taking antidepressants, subjects show more normally functioning default mode networks (5). Sheline will also test the effects of cognitive behavioral therapy on the default mode networks of depressed patients (5). She believes that the drugs or therapy (or both) might “reset the brain to function more normally” (5). I wonder, however, if she has considered the recent debate over the placebo effect’s role in treating depression (7). To summarize briefly, antidepressants are hardly more effective than placebos, and it is hypothesized that antidepressants’ main mechanism of action is through placebo effect. If this is the case, then it is not the treatment itself that “resets” the brain’s networks, but rather the idea of treatment that breaks the rumination cycle. It seems more fitting to me that an idea, not an external stimulus like exogenous chemicals, would be able to end the rumination-sadness cycle.

            No one really knows quite how an idea could break the cycle. Perhaps it is here that the I-function can be distinguished from the default mode network. Maybe the idea and process of treatment calls upon the executive powers of the I-function to separate itself from the default mode network. This new internal perspective could attenuate the default mode network, thus ending deep rumination. In turn, this change of thinking could alleviate some of the sad emotions. Once the cycle is broken, it is much easier to reach an optimal balance between all neural networks.





Works referenced:

  6. /exchange/davidhume
  7. /exchange/node/7497