Depression and the role of inflammation

Depression and the role of inflammation

Depression affects more than 168 million people worldwide. Depression is also one of the key factors for impaired quality of life in patients affected by chronic diseases [1]. New research suggests that depression and inflammation are biologically linked ― a finding that may have important implications for patients whose condition fails to respond to treatment with antidepressants [1]. In a large examination of genetic, environmental, lifestyle, and medical drivers of inflammation in major depressive disorder (MDD), levels of the key inflammation marker C-reactive protein (CRP) were higher in patients with depression than in those with no mental disorder [2]. It seems that the activation of depression and inflammation is also connected to other stress responses.

Inflammation and depression:

Inflammation is an immune response to infection or other stresses on the body. High inflammation levels are associated with autoimmune disorders and can be risk factors for cardiovascular illness or other ailments [1].

Pariante, professor of biological psychiatry at the Institute of Psychiatry, Psychology, and Neuroscience, Kings College London says that the immune factors that are circulating can cross the blood-brain barrier and perpetuate depressive symptoms by changing the function of the brain areas responsible for the interpretation of emotions.

This results in a negative feedback loop in which inflammation makes the body believe it is under threat, produces a more robust immune response, and perpetuates or exacerbates depressive symptoms [1]. Inflammation also dampens the effectiveness of antidepressants by reducing the brain's production of mood-determining chemicals such as serotonin.

The neurological after-effects experienced by some patients after covid-19 may also shed some light on the connection between inflammation and depression [3]. Scientists are still uncovering how the new coronavirus impacts the brain and the central nervous system, but they believe the infection could inhibit blood and oxygen flow to the brain and in some cases, trigger brain swelling.

Diet and lifestyle:

Research on the effect of inflammation on depression sheds light on dietary and lifestyle habits that need to be reviewed.

Overweight and more specifically the presence of visceral fat- the fat wrapped around our organs, leads to triggering inflammatory pathways in the body and signaling molecules that disrupt the body’s normal cause of hormonal actions. Visceral fat itself also becomes inflamed [4].

Your dietitian can help you to incorporate the following lifestyle interventions to combat inflammation and indirectly depression and mood:

  • Weight loss if overweight.
  • Moderate exercise.
  • Lower intake of refined carbohydrates, sugar and sugary drinks, and fruit juice.
  • Avoid highly processed foods.
  • Avoid vegetable oils.
  • Increase intake of anti-inflammatory omega 3 fatty acids.
  • Consider anti-inflammatory supplements such as turmeric, ginger, krill oil, vitamin D3, pre, and probiotics.
  • Intake of high-quality protein and healthy fats.

References:

  1. Chieh-Hsin L., Fabrizio F. The Role of Inflammation in Depression and Fatigue. Front Immunol. 2019;10:169.
  2. Pitharouli M.C., Hagenaars S.P., Glanvilee K.P., Coleman J.R.I., Hotopf M., Lewis C.M., Pariante C.M. Elevated C-Reactive Protein in Patients With Depression, Independent of Genetic, Health, and Psychosocial Factors: Results From the UK Biobank. American journal of psychiatry. 2021. Available from: https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2020.20060947
  3. Mazza MG, De Lorenzo R, Conte C, Poletti S, Vai B, Bollettini I, Melloni EMT, Furlan R, Ciceri F, Rovere-Querini P; COVID-19 BioB Outpatient Clinic Study group, Benedetti F. Anxiety, and depression in COVID-19 survivors: Role of inflammatory and clinical predictors. Brain behave Immun.2020;89,514-600.
  4. Item F., Konrad D. Visceral fat and metabolic inflammation: “The portal theory revisited” pt.2, Obesity reviews.2012;13:30 -39.

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