Depression: Causes or Effects?
Depression: Causes or Effects?
Depression supplies a distinct depiction of the brain equals behavior theory. The physiological characteristics that taint the diseased brain directly impact the thoughts and behaviors of the millions of sufferers. The genesis of this dehabilitating problem is both mysterious and complicated and I am not offering any sort of revelation in stating that it is a multi-factorial manifestation involving both biological and environmental components. The end product of these variable factors do, however, provide some common biochemical alterations in the brain that lend insight into understanding the reality and possible treatment of the disease.
So, in the spirit of "working backwards," I will explore this end product. Perhaps the most popularized end-product of depression is the monoamine depletion or disturbance that is commonly detected in depressed persons. Serotonin, norepinephrine, and dopamine have been identified as the main culprits, serotonin and norepinephrine being the most suspect. "Among the findings linking impoverished synaptic norepinephrine levels to depression is the discovery in may studies that indirect markers of norepinephrine levels in the brain-levels of its metabolites, or by-products, in more accessible material (urine and cerebrospinal fluid)-are often low in depressed individuals. In addition, postmortem studies have revealed increased densities of certain norepinephrine receptors in the cortex of depressed suicide victims" (indicating compensatory up-regulation) (1).
It is not surprising that deficits in serotonin circuits are also seen in depressed patients, as these depletions may interact with and indeed be responsible for falls in norepinephrine levels (a phenomenon called the permissive hypothesis). Sluggish serotonin secretion may also account for the emotional, appetite, libido, and sleep disturbances associated with depression (1).
Hormonal abnormalities may also characterize the depressed brain. The most pervasive irregularity lies in the hypothalamic-pituitary-adrenal (HPA) axis, the system that manages the body's response to stress. When a threat to physical or psychological well-being is detected, the hypothalamus increases production of corticotropin-releasing factor (CRF), which, in turn, induces the pituitary to secrete adrenocorticotropic hormone (ACTH). ACTH then instructs the adrenal glands to release cortisol. Chronic activation of the HPA axis may result in illness and depression. In fact, hyperactivity in the HPA axis is the most replicated finding in all of biological psychiatry (1).
I have been referring to these conditions as "end-products" but they could, just as easily, be viewed as causes and not consequences of depression. Perhaps I have not been working backwards at all but have instead been addressing the origins of this disease. It all depends on why people get depressed in the first place. Seeing as how preventative medicine is almost always the best medicine, the "why" of this issue becomes quite critical. Unfortunately, the why of depression seems to be even more elusive than the how.
There is, of course, the stress dimension, which was made very relevant by the HPA axis discovery. But what about individuals who encounter depressive episodes with no history of stress or trauma? And why do some people endure extreme stressors with no such unpleasant repercussions? In other words, what renders individuals relatively vulnerable or relatively invulnerable to the pathogenic effects of environmental stress?
This is where "propensities" come in. A propensity, to me, sounded at first like some intangible, dormant potential that resided somewhere in the many folds of the brain, just waiting to be triggered by a sad or stressful event. I have since come to view a propensity as something a bit more concrete. Perhaps it is a property of one's genes. As it is often observed that depression runs in families, a search for some sort of genetic glitch seemed to be in order. Researchers have linked chromosomes eleven, eighteen, and twenty-one with a vulnerability to bipolar disorder. They have also suggested a gene somewhere on the X chromosome may be responsible (1).
Another possibility is that this predisposition element is simply personality. (I'm not sure where exactly personality is, floating around somewhere with the I-function I suppose, but I'm assuming that is does not originate entirely from genes since identical twins typically have very different personalities). Certain personality traits, for instance, are predictive of bouts of depression. Introverts, perfectionists, and over-achievers are all more prone to depression. Interestingly, artists and highly creative people are also more likely to struggle with depression. In fact, one of the "antecedents to problem behavior" is a tremendously active and independent fantasy life (2). In addition, highly independent people with a low dependency on others and aggressive people who exhibit hostility are at an increased risk of suffering a depressive relapse (3). Are the parts of the brain that manifest the specified personality traits therefore the trigger points where "depressive tendencies" dwell?
And are the emotional symptoms of depression therefore a function of personality or abnormality? "[Depression] is characterized by a pervasive sense of dejection, cheerlessness, and unhappiness. These gloomy and joyless individuals feel inadequate and worthless. Their low self-esteem is displayed as being critical, self-blaming and derogatory. They brood, worry, are judgmental of others and are prone to periods of guilt and remorse" (4). What exactly is making these individuals so miserable? Is their disease invading their personality or is their personality inviting their disease? Or is it both? While it may be impossible to pinpoint what determines the impending doom of depression or the biological basis of individual differences, the biochemical and dispositional commonalities offer hope in providing treatment and prevention for this problem that appears to permeate every facet of one's being.
In conclusion, I would like to again demonstrate how the phenomenon of depression supports the brain equals behavior assertion. While the overlapping of cause and effect is certainly confusing and somewhat counterintuitive, remembering that brain and behavior are one and the same helps clear things up. If the brain does indeed equal behavior, than this, of course, requires that behavior equals the brain. A simple point, granted, but it does explain why behaviors (perhaps instigated by stressful environmental "input") have the potential to physically change the brain. Likewise, as stated before, if the cause of depression is sometimes just an inherently sick brain, then it is understandable why some people have intense episodes of depression with no apparent environmental trigger. And if you cannot have a brain without behavior and you cannot have behavior without a brain, it would make sense that the two must interact, both serving as causes and effects working to perpetuate the vicious cycle of depression.
Comments made prior to 2007
I am a counsellor working with women who are survivors
of long term childhood sexual abuse and domestic violence. Many (most)
of my clients are on medication and have been diagnosed with a mental
illness primarily bi-polar or just depresion. I know there is a link
between trauma & mental illness but I am just wondering if there
has been research done specifically on the possible link between
chemicals that are released during trauma that is ongoing over many
years & the later diagnosis of a mental illness. I find it
interesting that it is after the fact that women are diagnosed. I
question why that is and am curious again if this is so because with
the trauma situation ending (say a woman leaves her abusive partner)
there is again a change in chemicals in the brain. I strongly believe
that the normal responses of sadness to the remembering of childhood
abuse are being 'pathologised' by doctors and reframed as 'depression
or bi-polar' rather than a normal respose of sadness.
In this article the writer does link chemicals with stress but I am wondering if she/he did any further research on the link to trauma? I would be grateful for any info of web sites or articles etc. you may have ... Sandra Stubbs, 1 April 2004