More and more evidence is linking inflammation to depression. Inflammation is associated with many different illnesses including heart disease, diabetes, and now brain disorders such as depression, schizophrenia, and Alzheimer’s disease. People with chronic diseases that have high levels of inflammation associated with them are prone to depression. Evidence is stacking up that the inflammation is the cause of the depression.
- Depressed patients tend to have higher levels of inflammatory markers that are associated with depression. You can inject people with inflammatory messengers and produce depression likewise. Think about the use of interferons in multiple sclerosis and the depression that it causes as a result of the inflammatory messengers produced.
- In children exposed to adversity/stress, inflammatory markers such as CRP and Interleukin-6 increase and this was associated with increased levels of depression in the children. Of course not all became depressed, but the elevation of these inflammatory markers was associated with increased risk of depression over the next 6 months ( “Clustering of Depression and Inflammation in Adolescents Previously Exposed to Childhood Adversity” by Gregory E. Miller and Steve W. Cole (doi: 10.1016/j.biopsych.2012.02.034). Biological Psychiatry, Volume 72, Issue 1 (July 1, 2012))
- Data from the Avon Longitudinal Study of Parents and Children gives support to the hypothesis that the inflammatory response predisposes to depression. The results showed that children at age 9 with the highest levels of the cytokine Interleukin-6 (IL-6) were 50% more likely to be depressed by the age of 18! Thus inflammation is a risk factor for depression. The Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort as a resource for studying psychopathology in childhood and adolescence: a summary of findings for depression and psychosis
- There is evidence that treatment of the inflammatory cytokine TNF (tumor necrosis factor) with infliximab was associated with less depression in those who had elevated levels of TNF at the beginning of the study. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers Thus treatment for depression in some individuals by lowering inflammatory markers may work in specific individuals with elevated levels of the inflammatory markers at the outset of treatment, however, it may not be appropriate for those without inflammatory marker elevation.
- Are Anti-inflammatory Therapies Viable Treatments for Psychiatric Disorders? Where the Rubber Meets the Road –>
- The article listed above is an excellent summary of concepts in the role of inflammation in psychiatric disorders. Key concepts that are brought out include: We cannot indiscriminately use treatments for inflammation in psychiatric disorders unless inflammation exists in that particular patient. (2) Specific circuits in the brain are targets of inflammation such as the basal ganglia and cortical circuits (dorsal anterior cingulate, amygdala, and insula) which mediate anxiety, arousal and alarm. These pathways inhibit motivation and activate arousal to allow the body to shunt energy to fight infection and heal wounds while increasing vigilance against attack. This is a self-preservation measure. (3) Not all anti-inflammatory agents are equal. Some anti-inflammatories have off-target effects in which they modify a disorder indirectly. For example, minocycline, an antibiotic, is effective in some schizophrenia patients by inhibiting microglia activation , which is inflammatory. However, the minocycline also alters the gut biome, which also effects and mediates behavior. (4) The bottom line is that there will probably be need for direct anti-inflammatory agents, such as monoclonal antibodies that target TNF and IL-1 without affecting peripheral targets. (4) The only measure of actual inflammation are the peripheral markers that include CRP, IL-6, and TNF, which are elevated in inflammatory conditions. How they relate to central inflammatory markers is unknown.
- Association of serum interleukin 6 and C-reactive protein in childhood with depression and psychosis in young adult life: a population-based longitudinal study
- Biological Psychiatry Press Releases
- CRP, IL-6 and depression: a systematic review and meta-analysis of longitudinal studies
- Childhood adversity and inflammatory processes in youth: a prospective study
- Child maltreatment, inflammation, and internalizing symptoms: Investigating the roles of C-reactive protein, gene variation, and neuroendocrine regulation
http://www.sobp.org/files/public/BPS%20Press%20Release_Miller%20and%20Cole_FINAL.pdf <<< Childhood Adversity Increases Risk for Depression and Chronic Inflammation