Dr. Mercola: Depression And Inflammation, Positive Links Define Psychoneuroimmunology

From the past couple of years or even more, depression is the only condition that has been truly studied, brought out in open and supported on a vast scale. Its links with inflammation have been long sought after and results have been unfortunately positive on the mental health.

The study of the connection between mental health and inflammation is known as psychoneuroimmunology.

In 2012, a study quoted, “Elevated biomarkers of inflammation, including inflammatory cytokines and acute-phase proteins, have been found in depressed patients, and administration of inflammatory stimuli has been associated with the development of depressive symptoms. Data also have demonstrated that inflammatory cytokines can interact with multiple pathways known to be involved in the development of depression, including monoamine metabolism, neuroendocrine function, synaptic plasticity, and neurocircuits relevant to mood regulation. Psychosocial stress, diet, obesity, a leaky gut and an imbalance between regulatory and pro-inflammatory T cells also contribute to inflammation and may serve as a focus for preventative strategies relevant to both the development of depression and its recurrence.”

In this model of psychoneuroimmunology, it has been believed that depression is a body’s response to inflammation. It protects the body from an inflammatory response, involving hormones and chemicals which work as neurotransmitters. These chemicals are a result of chronic inflammation which cause depression to build up and hence the symptoms as thinking changes, perception alterations, mood changes, etc. one characteristic change is avoidance of people.

Depression metabolites for example, cytokines, C-reactive proteins, interleukin-1,6 and Tumor necrosis factor-alpha predict and correlate the inflammation to the condition.

Monocytes express genes that are linked with pro-inflammation in turn secreting cytokines on provocation. This happens especially during melancholic depression, depression from bipolar disorder and postpartum. Vagus nerve transmits all the information from the body to the brain and is an important vehicle in transmitting depression.

 What happens is more of science and follows the exact psychoneuroimmumology model. The brain cells called microglia are sensitized during depression. It further activates release of an enzyme called as indoleamine 2,3-dioxygenase, IDO. IDO shifts tryptophan father from synthesizing melatonin and serotonin and directing it to synthesize instead, NMDA agonist quinolinic acid, which in turn triggers anxiety and nervousness.

BBC reports on depression as, “The focus is on an errant immune system causing inflammation in the body and altering mood, Professor Ed Bullmore, Ph.D., head of psychiatry at the University of Cambridge and an employee of GlaxoSmithKline says, ‘Depression and inflammation often go hand in hand. If you have flu, the immune system reacts to that, you become inflamed and very often people find that their mood changes too. Their behavior changes, they may become less sociable, sleepier and more withdrawn.  They may begin to have some of the negative ways of thinking that are characteristic of depression and all of that follows an infection. Inflammation is part of the immune system's response to danger. If it is too high, it causes damage. And for some reason, about one-third of depressed patients have consistently high levels of inflammation.”

The depression linked to chronic diseases can be cured when proper treatment of the disease is done. Eating nuts, optimal exposure in sun, eating healthy fruits and vegetables including berries have all been linked to better moods and fight depression. Having a ketogenic diet is the new age alternative to fight depression and one must surely give it a pick.

References:

Mercola.com

Neuropsychopharmacology 2012 Jan;37(1):137-62

 

Brain, Behavior and Immunity 2013 Jul;31:1-8

 

Neurodegener Dis Manag. Dec 1, 2012; 2(6): 609–622

 

Psychosom Med. 2009 Feb;71(2):171-86

 

Translational Psychiatry (2014) 4, e344

 

Neuropsychiatr Dis Treat. 2011; 7: 431–439

BBC August 24, 2016

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