Mood Series: Associated Pathways & Biochemical Markers
Tue Aug 28 2018 16:38:02 GMT+0000 (Coordinated Universal Time)
Associated Pathways & Biochemical Markers.
In my last post we talked about the link between environment, lifestyle and mood symptoms. We saw that our environment and lifestyle can directly effect how the pathways in our bodies work.
No matter what supplements we take, if the environmental cause, trigger or contributor is not addressed, then it is unlikely the issue will be resolved.
If you missed it, you can read that post here (insert link).
Studies show that the development, progression and treatment of depression is strongly influenced by lifestyle factors including sleep, diet and exercise (Lopresti, A et al. 2013, p.1).
Depression and these three lifestyle factors have been assessed in their relationship with the following pathways:
- Neurotransmitter Imbalance
- HPA (Hypothalamic-Pituitary-Adrenal) Axis Disturbance
- Oxidative and Nitrosative stress
- Mitochondrial Disturbance
(Lopresti, A et al. 2013, p.1).
Below is a brief educational summary of these pathways.
In learning about these areas, and the linkage between our external and internal worlds, you will have a better understanding of what influences your mood and general wellbeing. If you have any questions about the content below, please contact myself or your local qualified health practitioner.
The making and transport of neurotransmitters may be compromised. This includes dopamine, serotonin, glutamate and noradrenalin in the central nervous system, which are essential neurotransmitters for mood. An imbalance in this area has been linked to depression (Lopresti, A et al. 2013, p.2).
In major depression, disturbance of the HPA (Hypothalamic-Pituitary-Adrenal) axis is often present. This can present as either increased or decreased cortisol levels depending on the type of depression (melancholic or atypical) (Lopresti, A et al. 2013, p.2).
Elevated oxidative stress along with decreased antioxidant levels are seen in major depression. This is shown through deficiencies of coenzyme Q10, Vitamin E and Vitamin C in the plasma. The antioxidant enzyme glutathione peroxidase is also shown to have reduced activity.
Antioxidant deficiencies such as these lead to loss of protection against ‘Reactive Oxygen Species’ (ROS), which can result in damage to DNA, proteins and fatty acids (Lopresti, A et al. 2013, p.2).
Brain-derived neurotrophic factor (BDNF) is an abundant neurotrophin in the central nervous system involved in the proliferation, survival and and growth of neurons. BDNF levels can be assessed and supported in cases of major depression (Lopresti, A et al. 2013, p.2).
Mitochondria are intracellular organelles mainly known as the ‘energy makers of the cell’, responsible for the making of adenosine triphosphate (ATP), commonly know as ‘energy’. Increased rates of depression have been seen in mitochondrial disorders (Lopresti, A et al. 2013, p.2).
Three recent meta-analysis have confirmed that increased inflammation is associated with major depression. This can be assessed through looking at levels of C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-1 (IL-1) (Lopresti, A et al. 2013, p.2).
In clinical practice, we are able to use testing, nutritional medicine and diet to target and support the functioning of these pathways. In my next post, we will be looking at how diet and nutrition correlate with these pathways, plus, the role of sleep in regulating mood.
The information provided on Nutrition Mind Collective is for educational and informational purposes only. The information provided on this site is not, nor is it intended to be, a substitute for professional advice or care. Please seek the advice of a qualified health care professional in the event something you have read here raises questions or concerns regarding your health.
Lopresti, A, Hood, S, Drummond, P 2013, ‘A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep…’, Journal of Affective Disorders, vol. 148, no. 1, pp. 1 – 16, viewed 28th August 2017,