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Some researchers think depression is analogous to inflammation: both conditions evolved to protect us from environmental dangers, but may become serious health problems in their own right. Other researchers think the relationship is closer: inflammation may be the direct cause of depression for a substantial portion of all depressed patients.
The molecular mechanism for depression is not yet established. Your doctor may have told you that you have a deficiency of seratonin or other neurotransmitters, but that theory is no longer supported by available data, according to a recent review article in Journal of Clinical Psychiatry. This article (Reference 2) summarizes the results of a conference on antidepressant development and clinical trial design. The financial disclosures show extensive funding by the pharmaceutical industry. And the conclusion states: “it is critical that we avoid the mistakes of the past that sought to find a simple biochemical explanation of major depression (e.g. relative depletion of monoamines norepinephrine and seratonin).”
One of the problems in understanding the molecular mechanism of depression is the wide range of symptoms that qualify a patient for diagnosis of major depressive disorder. According to Ref. 2, two patients can both fully satisfy the diagnostic criteria without a single symptom in common. For example, one patient may have:
1. Depressed mood
2. Weight gain
3. Hypersomnia (too much sleep)
4. Fatigue or loss of energy
5. Recurrent thoughts of death
The second patient may have:
1. Diminished interest or pleasure
2. Weight loss
3. Insomnia (too little sleep)
4. Psychomotor retardation
5. Feelings of worthlessness or guilt
6. Diminished ability to think or concentrate
Reference 3 explains why depression may be the result of an inflammatory process in the brain for a subset of patients diagnosed with major depressive disorder. The evidence includes the following:
1. Inflammatory disorders and drugs that increase inflammation are associated with depression,
2. The anti-inflammatory drugs celecoxib (Celebrex) and etanercept (Enbrel) have both been shown to decrease depression in clinical trials,
3. Molecular mechanisms linking inflammation and depression have been demonstrated.
See Part 2 for more details.
References:
1. Andrews PW et al, “Depression's evolutionary roots”, Scientific American Mind 2010 Jan/Feb: 57-61.
2. Gelenberg AJ et al, “The history and current state of antidepressant clinical trial design: A call to action for proof-of-concept Studies”, J Clin Psychiatry 2008 Oct; 69(10): 1513- 28.
3. McNally L et al, “Inflammation, glutamate, and glia in depression: A literature review”, CNS Spectr 2008 Jun; 13(6): 501- 10.
Linda Fugate is a scientist and writer in Austin, Texas. She has a Ph.D. in Physics and an M.S. in Macromolecular Science and Engineering. Her background includes academic and industrial research in materials science. She currently writes song lyrics and health articles.
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