A Functional Approach to Parkinson’s: Main Triggers & Drivers

So let’s start at the beginning and think some things through. First, there is a genetic component. People aren’t just unlucky, but they have the cards they were dealt and most likely haven’t been taught to try and avoid triggers, facilitators, and aggravators.

The first thing is to try and avoid the known triggers if at all possible. It can be very hard to detect and find these triggers given that several can happen decades before a person will present with motor symptoms (hand shaking, trouble initiating movement, etc) and some are even thought to happen early in life of people that develop Parkinson’s. 

Some examples of triggers can be:

• GI perturbations like increases in lactobacillus, akkermansia, bifidobacterium and decreases in prevotella, blautia, and faecalibacterium (commonly called SIBO)
• Infections such as M. Paratuberculosis, Norovirus, Hep B and C
• Pollution like diesel exhaust fumes and carbon monoxide
• Pesticides, specifically Rotenone and Paraquat
• Mycotoxins
• Heavy Metals like iron, copper, manganese
• Traumatic Brain Injury

Now, lots of people have these triggers but clues that something has shifted for the worse would be long-term gut dysfunction, chronic inflammation in certain tissues, and misfolding of alpha-synuclein.

• GI Tract 

Two areas of the body that will first start to misfold these proteins would be in the olfactory part of the brain (leaky nose)  and the GI tract (leaky gut). Most of the time the actual first symptoms are constipation and not only trouble smelling, but identifying smells like anise, peppermint, and coffee. The proteins from the gut make their way up the vagus nerve to a part of the brainstem called the medulla with the big fancy name of the ‘dorsal motor nucleus of the vagus’ or DMV for short. It isn’t until later in the disease process that these proteins make it to the midbrain and selectively kill the neurons that make dopamine. 

• Infections

Mycobacterium avium ss paratuberculosis has been shown to have a link to Parkinson’s. The most common way people get exposure is from drinking water. It is thought that due to the same genetics that misfold the proteins in Parkinson’s are connected to the genes of how the cells can fight certain types of pathogens called intracellular, and this includes the mycobacterium, and this quality control system gets exhausted. 

Also, viruses for most people are something that comes and goes but for people with the wrong genes and susceptibility (their allostatic load is too much) these viruses can stay latent in cells that are called post-mitotic that usually hang out for a long time. These would include the nervous system because hopefully those cells hang around for a long time. Norovirus is commonly called a ‘stomach flu’ and is usually something that a person will get earlier in life. This length of time between infection and development of motor systems that is a common feature in Parkinson’s is what can make it hard for a clinician to correlate. 

• Mycotoxins

Some mold toxins are specifically linked to destroying these cells as well. One type of mold toxin called Ochratoxin A is made by Aspergillus and Penicillium that not only causes high amounts of oxidative damage destroying cells in the brainstem and basal ganglia, but will inhibit an enzyme called tyrosine hydroxylase which is required to make dopamine. It is very common for people with mold exposure to have a ‘leaky nose’ and ‘leaky lungs’ since mold spores are really good at making spears and chemicals to stab and burn through barriers and create a biofilm to protect them from being removed.

• Pesticides

There are a few ways that pesticides can be an issue – inhibiting mitochondria, making oxidative stress, and stimulating inflammation to name a few. People with a certain gene SNCA-A53T that affects neurons that make and use dopamine have a real tough time even at low levels of these pesticides.

• Head injuries

A head injury is never a good time. These can be a large contributing factor due to how the support cells and neurons themselves change after such a large trauma. Not only that, but the brainstem is at a pivotal point where the weight of the cortex (large part of the brain) meets the brainstem is called the mesencephalon, or midbrain. As a person’s brain is shaken around in their skull, the tension in these tissues is usually high. Take the ability to accommodate or follow a finger going to their nose after a head injury. This is a cranial nerve 3 process which lies in the midbrain. This ability to accomodate is one of the first ‘sideline’ tests that is performed in athletes after a concussion to start determining when they can return to play.

 

The things that will facilitate or keep this process going after a trigger would be a list that looks like:

• Systemic Inflammation
• Mitochondrial Dysfunction
• Gut Barrier Dysfunction
• Excitotoxicity (neurons burn themselves out)

After all, it can take a while before enough of the neurons themselves break down or lose connectivity for a person to really start noticing symptoms. 

Since cells and organs (the brain in particular) were meant to heal, how come this process is still being aggravated?

The first process that is usually losing steam is called autophagy or ‘self-eating’ which is the usual way the cells handle these misfolded proteins. They use chemical scissors and some of the most affected scissors that can’t cut the proteins up are called lysosomes.

The second process is chronic inflammation in certain parts of the brain and the immune cells that wreak the havoc are called microglial cells. Back to the traumatic brain injuries, once these immune cells are turned ‘on’ sometimes they never turn ‘off’ and even small amounts of inflammation can start the cascade all over again. Once these cells get going, they cause excitation that makes the neurons burn out even faster.

The gut barrier is very foundational to getting nutrients to our body and cells, but is also the bottom of the funnel in terms of detoxification. So not only is it an initial fuel for the Parkinson’s fire, but it can keep the body from getting fire extinguishers to put out the fire on the brain. Since the alpha-synuclein travels from the gut to the brain via the vagus nerve through a retrograde process, there is potential to increase the rate of protein traveling through the vagus nerve with vagal activation. 

Lastly, the underlying issues going on have a tendency to make neurons keep firing, and firing, and firing. Imagine if you just kept pushing weights over your head without resting – everyone will eventually get hurt regardless of strength if they don’t rest. The same is true for the nervous system and unfortunately when the immune system gets excited in the brain this will excite the neurons themselves and the big words are the ‘neuro excitotoxicity.’

Since there is so much to consider due the high number of variables, it is important to piece together the whole picture before ‘killing a virus’ or ‘detoxing mold’ or ‘stimulating the basal ganglia’ so that way the underlying problems are being corrected and the neurons themselves can handle the increased activation of brain-based exercises, as well as maintain the connections that were made instead of regressing again once the stimulation stops.