Inflammatory changes in the brain parenchyma have also been associated with depression. Increased levels of TNFα in the hippocampus and striatum have been associated with anxious and depressed behavior in EAE studies, with the changes in the striatum occurring before the onset of clinical symptoms (49, 50).
Another pivotal point is that increased inflammation not only occurs in depression but also in multiple other psychiatric diseases including bipolar disorder, anxiety disorders, personality disorders, and schizophrenia.
Such enhanced levels of pro-inflammatory cytokines in the brain may exert direct and indirect neurotoxic effects. The association between increased inflammation and anxiety disorders may be explained by neuroinflammation-induced toxic effects on specific brain regions implicated in each anxiety disorder.
Brain states that produce mental illness also tend to activate inflammation. And inflammation is equally capable of producing depression, anxiety, fatigue, and social withdrawal.
Nutritional supplements – such as l-methylfolate, curcumin and omega-3 fatty acids (especially eicosapentaenoic acid), have indicated antidepressant potential, especially in patients with major depression and increased levels of inflammatory biomarkers.
The new study, published recently in Nature Translational Psychiatry, suggests that depression occurs independently of inflammation for many older adults. Furthermore, depression-inflammation links are due to the greater incidence of inflammatory conditions, which in general are common in older people.
First, higher inflammation hampers response to antidepressants, and effective antidepressant treatment decreases inflammation.
Psychological stress triggers inflammatory activity and affective-cognitive changes that play a critical role in the onset, maintenance, and recurrence of depression.
Depression, anxiety, and OCD apparently stem from mild brain inflammation. However, when brain inflammation becomes extreme, as in autoimmune encephalitis, psychosis and very bizarre behavior can result.
“High levels of phobic anxiety are associated with increased levels of leptin and inflammatory markers.” Leptin is a hormone that helps regulate appetite and therefore caloric intake, but scientists believe that it also plays a part in chronic inflammation.
Depression Pro-inflammatory cytokines, those chemical messengers released in response to physical or psychological stress, can trigger depressive symptoms in some people, leading to lowered mood, fatigue, and lack of normal enjoyment of life.
Chronic stress contributes to inflammation. Use meditation, yoga, biofeedback, guided imagery or some other method to manage stress throughout the day.
The most common reasons for chronic inflammation include: Autoimmune disorders, such as lupus, where your body attacks healthy tissue. Exposure to toxins, like pollution or industrial chemicals. Untreated acute inflammation, such as from an infection or injury.
Experimental evidence that inflammation can contribute to the development of depression even among medically healthy individuals comes from studies in which bacterial endotoxin - which elicits a strong inflammatory response - is administered to healthy individuals.
Serotonin carries out a number of immune functions as a neurotransmitter and as a peripheral hormone. It is critical for the inflammatory response, possibly influencing the development of the systemic inflammatory response syndrome (SIRS).
Anxiety often causes individuals to tighten up their muscles without even realizing it, which makes joints do extra work, and can also lead to excessive inflammation and pain.
An unhealthy lifestyle that includes smoking, a poor diet, alcohol consumption, sedentary behavior, stress, and weight gain can cause this type of persistent inflammation.
Prolonged stress leads to hyper physiological levels of cortisol. This alters the effectiveness of cortisol to regulate both the inflammatory and immune response because it decreases tissue sensitivity to cortisol (Segerstrom, 2006). As the human body heals, inflammation becomes a response to stress.
Cortisol dysfunction results in unmodulated inflammation following reactivation of the stress response, which may contribute to a cycle of inflammation, depression, and pain; pain is a stressor that may reactivate a proinflammatory stress response, now unmodulated due to cortisol dysfunction.
Antidepressants and anti-anxiety drugs have anti-inflammatory properties: Both SSRIs and antianxiety drugs such as benzodiazepines (e.g., Librium, Valium, Ativan) reduce inflammation.
Ibuprofen typically works better for this kind of pain relief, due to the anti-inflammatory effects.
Depression has been found to increase the risk of certain autoimmune diseases, including Grave's disease, celiac disease, and Crohn's disease. Why this happens is not yet fully understood, but the psychological stress of depression may be to blame.