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...