Parkinson's is a disorder of cellular health, not just low dopamine

When it comes to Parkinson's disease, if we are only talking about “low dopamine levels”, then we are missing a very important part of the conversation. Dopamine levels are reduced because of the death and destruction of the cells that normally make dopamine in the body. In Parkinson's disease, this mostly occurs in the substantia nigra, a part of the brain with lots of dopamine-producing cells (called dopaminergic neurons).   

A more important question is: why are these cells, which should ordinarily be producing dopamine in the first place, sick and dysfunctional? And what can we do to improve their cellular health? 

The main drugs still used today to treat Parkinson’s are L-Dopa and Carbidopa. L-Dopa is made in the brain and kidneys, and is a precursor to dopamine. In other words, it’s used by the body to create dopamine. However, we can also take it synthetically in the form of a drug. By taking L-Dopa medication, L-Dopa levels are increased to help synthesise more dopamine.  

Yet L-Dopa medication has potent side effects. L-Dopa medication causes an increase in dopamine production around the body, not just the brain (remember, dopamine is used by cells around the entire body). This increase in L-Dopa causes your blood vessels to dilate (contributing to common side effects of light-headedness, headache and dizziness), your kidneys to produce more sodium so you urinate more (leading to increased dehydration and dry mouth symptoms), and your gut motility to slow down so that you lose your appetite and get nauseous.   

Because of these common side effects, L-Dopa is often prescribed with Carbidopa. Carbidopa inhibits L-Dopa breakdown, so that more of the L-Dopa can reach the brain, and less is synthesised into dopamine in the gut or periphery. Unfortunately, it’s suggested that < 1% of L-Dopa reaches the brain unchanged.   

L-Dopa and dopamine supplementation is a band-aid solution. Our cells are capable of producing dopamine, however in Parkinson's disease, they are sick and dysfunctional. By shifting the conversation away from just talking about "low dopamine", and beginning to talk about "cellular health", we move closer towards finding a cure, and begin to talk about health, not just disease.   

The mechanisms of Parkinson's disease is likely due to a combination of factors. Current scientific hypotheses include: 1) mitochondrial dysfunction; 2) potassium (K+) channelopathy; 3) alpha-synuclein aggregation causing neuroinflammation; 4) impaired cellular autophagy; 5) gut dysbiosis; 6) nigral iron accumulation; and 7) excessive oxidative stress.  Therapies such as laser therapy work with the body’s natural healing processes to improve the functioning of cells. Specifically, laser therapy can improve mitochondrial function, stimulate ion channels, promote a healthier gut microbiome, reduce neuroinflammation and trigger antioxidating cascade effects. And that’s just the tip of the iceberg! 

This is why light therapy is so promising as a treatment modality for Parkinson’s: it can help reduce the stress and inflammation of our cells and optimise their ability to heal and function by working with the body's natural processes. The net result is better cellular health, in the body and in the brain. 

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