Instead of being a discrete disease entity, depression is a symptom, like nausea, tremors, sweating, or a cough. The evidence points to an inflammatory cytokine model of depression, whereby inflammatory intercellular signaling molecules like interleukin-1 (IL-1), IL-6, interferon (IFN) gamma, and tumor necrosis factor (TNF)-alpha, produced by the innate immune system, penetrate the blood brain barrier and create mood disorders including anxiety, panic attacks, and depression—which are symptomatic of systemic inflammatory processes (Dantzer, 2008).
In fact, elevations in inflammatory cytokines are observed in subjects with major depressive disorder, and a concomitant “resolution of a depressive episode is associated with normalization of levels of circulating inflammatory cytokines” (Hannestad, DellaGioia, & Bloch, 2011). Likewise, administration of the cytokines, such as IFN-gamma, which is given as a treatment for hepatitis C, induces a predictable major depressive episode in one fourth of patients (Udina et al., 2012).
The inflammatory model of depression is further buttressed by studies demonstrating that the pro-inflammatory cytokines IL-6 and TNF-alpha are significantly higher in depressed patients compared to controls (Dowlati et al., 2010). Further, inflammation, as indicated by elevations in serum high sensitivity C-reactive protein (hsCRP), is an independent risk factor for de novo major depressive disorder in women, which researchers posit, “supports an aetiological role for inflammatory activity in the pathophysiology of depression” (Pasco et al., 2010, p. 372).
Another line of evidence is that the intravenous injection of Salmonella abortus equi endotoxin is accompanied by increased circulating levels of cytokines such as IL-6 and TNF-alpha, the levels of which are significantly correlated with transient escalations in anxiety and depression (Reichenberg et al., 2001.
Beck et al. (2013) submits this and several other lines of evidence in his ground-breaking paper where he discusses that, “Depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity… It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder”. Rather than a Prozac or Zoloft deficiency, Beck (2013) provides scientific proof that depression is induced by systemic inflammation related to factors such as vitamin D deficiency, psychosocial stressors, smoking, obesity, nutrient-poor diets, a sedentary lifestyle, leaky gut, atopy, dental caries, and impaired sleep (Beck et al., 2013).
Cytokine induced sickness behavior—a more accurate description of clinical depression—
Much more at; GreenMedInfo; Depression is not a Prozac Deficiency…and Other Fallacies of