This segment seeks to distinguish chronic fatigue syndrome (CFS) from depression, a psychiatric/psychological condition that many physicians and researching bodies have alleged CFS to be.
While CFS and depression do have similarities, the weight of the dissimilarities is far greater. These distinctions are discussed far less frequently however, and thus the notion that CFS and depression are "one in the same" is perpetuated. This segment will now illuminate all notable similarities and differences between the two.
Similarities between CFS and depression:
1) CFS and depression overlap.
This overlap is explainable in one of two ways. First, many sufferers of CFS add depression as a secondary symptom of their extant pain, fatigue, and resultant disability. Secondly, some CFS sufferers entered into the condition with pre-existing symptoms of depression. In either scenario, it is predictable that there will be a crossover of virtually all symptoms.
2) Both conditions cause the sufferer to feel sick or unwell.
Each condition typically expresses cytokine-induced sickness behavior. In this situation, pro-inflammatory cytokines operating in the brain manifest a motivational state that physically supports recovery. This state is associated with a general feeling of fatigue/malaise and a decrease in the motivation to participate in daily activities including a reduced social motivation, decreased hygienic behavior, decreased sexual libido, etc (Kelley, et. al., 2003). These behavioral alterations will commonly produce changes in bodyweight as well.
3) Both conditions induce disrupted sleep and rest patterns.
Although a state of "recovery" is being supported, both CFS and depression typically induce patterns of less restful sleep (often despite sleeping/resting more than usual). This results in the perpetuation of lethargic behavior under the hood of cytokine-induced sickness behavior, adding further difficulty with cognitive tasks (including concentration and decision making).
4) Both conditions are associated with an egocentrism of symptoms.
In both populations, there is an increased sense of awareness (egocentrism) of their symptoms. This ensures that none of these altered behaviors (or symptomatic manifestations of that behavior) go unnoticed. Moreover, this egocentrism of symptoms in both conditions often results in an increased sensation of pain, frequently myalgic in nature, as well as an increased vulnerability to other minor illness symptoms.
5) Both conditions experience brain alterations.
Both CFS and depression generate imbalances in brain neurotransmitters. Though neurotransmitters are difficult to measure*, dopamine and norepinephrine levels appear to be routinely low in both populations (Kurup & Kurup, 2003).
Given the propagation of these similarities, it seems logical to propose that the origin of CFS must be psychological. Certainly the lack of a single identifiable medical etiology has not helped convince the public otherwise. However, when the entirety of research is considered, biological markers are uncovered that support the contrary: that CFS is physiologically rooted and thus distinct from depression.
Differences between CFS and depression:
1) The majority of CFS patients are not depressed.
This clearly makes it challenging to connect the two. However, this is complicated by the fact that cognitive behavioral therapy has demonstrated to be beneficial in both CFS and depressed groups as a whole.
2) CFS has somatic symptoms.
Unique symptoms that categorize a diagnosis of CFS exist, as CFS causes at least four of the following: sore throat, tender lymph nodes, muscle pain, multi-joint pain without swelling/redness, headaches of a new type, pattern or severity, un-refreshing sleep, and/or discomfort for at least twenty-four hours after physical exertion (Fukuda, et. al., 1994). Other common symptoms of CFS that are not common in depression include dizziness, impaired balance/coordination, nausea, cognitive dysfunction and mental fog. Further non-physiological differences include self esteem disparities (lower self esteem in those with depression), a feeling of hopelessness in depressed populations (uncommon in CFS sufferers), and interest in social and physical activity independent of participation (CFS populations have interest in pursuing activity but rarely overcome the adversity of their fatigue to do so).
3) Brain neurotransmitters are different.
The similarities the two conditions share in neurotransmitter imbalances are also matched by patterns of divergence. The general trend of serotonin levels is to be increased in CFS patients while decreased in those suffering from depression (Kurup & Kurup, 2003). This helps lend an explanation to why anti-depressant use (as well as alcohol) often exacerbates symptoms in CFS sufferers while improving the condition of depression. Furthermore, exercise, being associated with an elevation in serotonin levels has equally divergent effects on each population. In depression, exercise provides a therapeutic response while in CFS, exercise causes a post-exertional malaise that can last for several days to weeks. This difference in exercise response is motivating to those suffering from depression and devastating to those with CFS, creating a disinclination of further activity and a consequent cycle of de-conditioning. Moreover, recovery from physical exertion is extensive in CFS and normal in depression.
Further dissimilarities exist in brain chemistry as well. Clinical brain scans have revealed significant differences, especially in the response to exercise, offering explanation to the pattern of exercise-induced cognitive dysfunction in CFS populations that doesn't appear in those with depression. This offers further explanation for the exacerbation of CFS symptoms (particularly muscle weakness, cardiac arrhythmias, and sleep disturbances) upon the introduction of most antidepressants.
4) Clear immunological differences exist.
Though cytokine-induced sickness behavior exists in both populations, the cytokine abnormalities in CFS routinely differ from those seen in depression. Tumor necrosis factor alpha and beta are more characteristic of CFS (and not depression) in cytokine panels. In addition to circulating cytokine differences, several other immunological abnormalities exist in CFS that are not apparent in depression. These include activated T lymphocytes, low natural killer cell toxicity, and impaired function of the 2-5A immune pathway via isoform imbalances of RNase L (Suhadolnik, Reichenbach, Gabriel & Gaughan, 2004).
Biochemical differences in blood cell data have been seen in CFS and depression in terms of IFN-Alpha expression, sodium, liver enzymes, glucose, and reduced chloride levels and platelet count.
5) Neuro-endocrinological differences exist.
Endocrine differences between the two conditions are most clearly seen in adrenal function. The adrenal glands are triggered by corticotropin releasing hormone, released by the pituitary gland under control of the hypothalamus. In CFS, adrenal function is typically reduced, causing low levels of cortisol to be in the bloodstream. Contrarily, about half of those suffering from depression have excess cortisol in the blood. It is believed that anxiety (often accompanying depression) influences the hypothalamus, which in turn causes continuous production of corticotropin releasing hormone by the pituitary gland regardless of extant cortisol levels in the blood.
Further, there is a difference in autonomic tone between the two conditions. Where depression tends to have little influence on the autonomic nervous system, CFS is often correlated with autonomic impairment, causing a reduced functional work capacity through a decline in oxidative metabolism.
6) Differences in onset.
Where depression traditionally has a slower onset, CFS is more rapid and often sets in after a cold, flu or other type of viral infection.
Now that we have an established the foundation of similarities and differences between CFS and depression, it should be clear that the two conditions are not "one in the same."
[History of CFS]
Fukuda, Straus, Hickie, Sharpe, Dobbins & Komaroff. (1994). The chronic fatigue syndrome: a comprehensive approach to its definition and study, Annals of Internal Medicine, 121(12): 953-959.
Kelley, Bluthe, Dantzer, Zhou, Shen, Johnson & Broussard. (2003). Cytokine-induced sickness behavior. Brain, Behavior, and Immunity, 17: s112-s118.
Kurup & Kurup. (2003). Isoprenoid pathway dysfunction in chronic fatigue syndrome. Acta Neuropsychiatrica, 15(5): 266-273.
Suhadolnik, Reichenbach, Gabriel & Gaughan. (2004). Clinical and biochemical characteristics differentiating chronic fatigue syndrome from major depression and healthy control populations: relation to dysfunction in the RNase L Pathway. Journal of Chronic Fatigue Syndrome, 12(1): 5-31.
* Neurotransmitters are only in certain areas of the brain in small quantities and are thus measured through metabolites in the blood, urine and cerebrospinal fluid.