Depression is one of the most debilitating neuropsychiatric disorders, with significant impact on socio-occupational and well-being of individual. The exact pathophysiology of depression is still enigmatic though various theories have been put forwarded.
Depression can be defined as “feelings of severe despondency and dejection.” It has many symptoms though and has been traditionally thought of as an issue with neurotransmitters; but new evidence shows that depression is more likely a result of inflammation and mitochondrial damage caused by oxidative stress than an overall deficiency of say, serotonin.
Let me start by defining what the mitochondria are. The definition you will find on a search is that a mitochondrion is “an organelle found in large numbers in most cells, in which the biochemical processes of respiration and energy production occur”. Basically, they are the batteries of the cell and they create the energy we need to function.
Next, I need to define what oxidative stress is. Again, the search definition is that “oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage”. What that means is that the body produces these by-products of its normal functioning called free radicals, and these free radicals need to be quickly bound to an anti-oxidant, otherwise they create what can be likened to “rust” inside us.
Finally, inflammation. Most of us recognise that inflammation is pain, redness, swelling, heat and possibly loss of function.
So why how is the research linking these as root causes of depression?
A growing body of evidence suggests that inflammation, mitochondrial dysfunction and oxidant-antioxidant imbalance do indeed play a significant role in the development and progression of depression. It is theorised that elevated levels of reactive oxygen and nitrogen species – a result of oxidant-antioxidant imbalance – may lead to increased damage of biomolecules, including DNA. This was confirmed last year when depressed patients in a research study conducted by a team and other scientists had elevated numbers of a biomolecular marker called 8-oxoguanine. This is a specific marker of oxidative DNA damage and was found to be elevated in the patients’ lymphocytes, urine and serum.
Furthermore, it was shown that the patients’ cells repaired peroxide-induced DNA damage less efficiently than controls’ cells and that some single nucleotide polymorphisms (SNP) of the genes involved in oxidative DNA damage repair may modulate the risk of depression. A similar mechanism may result in mitochondrial dysfunction, which is observed in depression.
These biochemical changes may have their roots in central, systemic and/or peripheral sites, including in the gut, as well as in developmental processes, such as prenatal stressors and breastfeeding consequences.
Consequently, conceptualizations of depression’s causes have dramatically moved from simple psychological and central biochemical models, such as lowered brain serotonin, to a conceptualization that incorporates whole body processes over a lifespan developmental timescale.
Recent findings have sparked renewed appreciation for the role of mitochondria in many intracellular processes coupled to synaptic plasticity and cellular resilience. New insights in the development of depression are revolving around the impairment of neuroplasticity, the brains ability to grow new synapses and repair itself. Mitochondria play a pivotal role in ATP (energy) production, keeping oxidative stress in balance and to executing the complex processes of neurotransmission and plasticity. Thus it makes sense that understanding the various concepts of mitochondrial dysfunction in pathogenesis of depression helps to generate novel and more targeted therapeutic approaches for depression treatment. Impairment in the mitochondrial functions lead to the generation of various insults that exaggerate the progression of depression. So, it is useful to study mitochondrial dysfunction in relation to mood disorders, synaptic plasticity, neurogenesis and enhancing the functions of mitochondria show positive effects in the treatment of depressed patients.
So, what can you do about inflammation, oxidative stress and your mitochondria? Well the good news is that there is plenty you can do without even visiting a specialist!
The first thing to address is your diet. The food you choose to eat can either promote inflammation or quell it. Inflammatory foods can easily be identified as they are foods made in factories, or food that your grandparents wouldn’t recognise. Highly processed, high in the wrong types of salts and preservatives, all of these promote inflammation. Anti inflammatory foods are real foods, organic and unprocessed. Colourful plants and healthy fats from avocados and nuts (not the seed oils though as they can promote inflammation as they are high in Omega 6’s).
Anti oxidant foods are similar to the anti inflammatory foods. A general rule of thumb when it comes to eating fruit and vegetables that are packed full of anti oxidants is that you aim to eat 10 portions, only 2 portions can be fruit and also try to eat a rainbow every day, so eat reds, oranges, greens, blue and yellow, getting the full spectrum of goodness from the plants.
Check your lifestyle; remove toxins from your home, skin products and food. Get 8 hours of good sleep every night, exercise, even if its moderate, choose healthy foods and support your liver and thyroid. These should all help bring you back into balance and ease the fire in your brain.