The rising amount of research displaying clear links between high levels of inflammation in the body and depression is revealing how the serotonin model, which purports that low mood is caused by a deficiency in serotonin and therefore supports the use of anti-depressants, is becoming defunct. A recent study published in JAMA Psychiatry, found a 30% increase in inflammation in multiple brain regions in those suffering from depression.

Around 350 million people around the world have been affected by depression, suffering symptoms that are nothing short of debilitating. Many respond positively to treatment such as cognitive behavioural therapy and anti-depressants, however, many do not, which has led to scientists exploring new frontiers of mental health and other possible causes.

Research in the field of Psychoimmunoneurology, which studies the interaction between the immune and nervous system, is finding how an overactive immune system causing persistent elevated levels of inflammation in the body can alter mood and lead to depression. At the University of Cambridge, Dr Golam Khandaker and his colleagues, reviewed data from 20 clinical trials in which patients suffering from depression positively responded to anti-cytokine drugs, which are commonly used to treat conditions such as rheumatoid arthritis and psoriasis. 

Dr Khandaker, who led the study, says: “The current approach of a ‘one-size-fits-all’ medicine to treat depression is problematic. All currently available antidepressants target a particular type of neurotransmitter, but a third of patients do not respond to these drugs. We are now entering the era of ‘personalised medicine’ where we can tailor treatments to individual patients. This approach is starting to show success in treating cancers, and it’s possible that in future we would use anti-inflammatory drugs in psychiatry for certain patients with depression.”

When we are exposed to an infection, in normal circumstances, immune cells will identify the foreign pathogen and mount an inflammatory response to eradicate the infection. This causes levels of pro-inflammatory cytokines, cell-signalling proteins, to rise. However, some suffer from errant immune responses where immune cells are no longer able to distinguish between foreign pathogens and the body’s own tissue cells. This leads to an autoimmune response where the immune system begins to attack the body’s own cells, which can consequently lead to chronic low-grade systemic inflammation.

New types of anti-inflammatory drugs called anti-cytokine monoclonal antibodies are now being researched for use in mainstream psychiatry. However, we must ask ourselves, why is our immune system acting in this way in the first place? What is driving our cells to behave in this way and cause these symptoms? Can we use nutrition and a functional medicine approach to try to understand the underlying drivers causing this inflammatory state? 

The gut-brain link is currently a hot topic in the medical world due to fascinating research being published on the strong correlation between our gut flora and our health. It is well known that our gut houses about 60% of our immune system and more than 80% of antibody-producing cells are located in the mucosa of the gastrointestinal tract. Studies have shown how our gut microbiome is profoundly impacted by the food that we eat, which in turn has a direct effect on the well-being of the immune cells in the gut.  Our T-regulatory cells, found in the mucosa of our digestive tract, are critical for immune tolerance in the intestines through active control of innate and adaptive immune responses. In other words, these cells help to prevent the immune system from hyperactivity, which can lead to chronic inflammation.

Refined flours, high levels of sugars, trans fats, rancid fats as well as pesticides and preservatives, have all been shown to have a negative influence on our gut microbiome leading to dysbiosis. As a consequence, an inflammatory response is mounted, which at a persistent level can lead to tissue damage and systemic inflammation. So how can we reduce inflammation and prevent mental health disorders, such as depression, using personalised nutrition? There are key nutrients that have been shown to have anti-inflammatory benefits on the body, such asomega 3 fatty acids, B12 and Vitamin D, which have been well researched for their positive impacts on symptoms of depression. Studies have shown how fish oil is able to suppress neuroinflammation, reduce oxidative stress, and protect neurons from injury. Vitamin B12 deficiency is common, which may be due to use the increase of antacids, proton pump inhibitors, as well as gut dysbiosis, all of which prevent proper absorption and assimilation of this important nutrient. This nutrient is essential for making our red blood cells and nerve cell membranes, also regulating our DNA expression that plays a vital role in synthesising neurotransmitters and maintaining the function of our immune system. Studies have shown how deficiency can cause symptoms of depression, as well as in extreme cases, psychosis. Lastly, research has shown how vitamin D modulates immune responses to infection, including reducing pro-inflammatory cytokines like TNF-α and IL-1 that are associated with depression.

There are many other factors that have been shown to be influential in symptoms of depression such as obesity, lack of exercise, chronic sleep deprivation, hypothyroidism and stress. This shows how there is much more to depression than the simplistic ‘chemical imbalance’ model that supports the theory that depression is caused by a deficiency of serotonin, which is still being followed by western medicine. It is clear that in order to move forward, there must be a radical change in perspective. The research is there. It is now time that mainstream psychiatry started listening to what it is saying.

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