Glutathione is the body’s main and most powerful antioxidant. Glutathione is produced by the cells in the body and helps to neutralize a wide array of free radicals that threaten our day-to-day health. Depletion of a person’s glutathione stores allows excessive free radical damage to occur, which can result in a large number of detrimental shifts in our health, eventually resulting in disease. Recognizing and addressing this fact is one of the hallmarks of addressing chronic illness, and nowhere is this more important than with Parkinson’s disease.
Glutathione Collapse
As we discussed in our post on The Critical Importance of Glutathione Levels with Neurotransmitter Optimization the leading cause of Parkinson’s disease is damage to the dopaminergic neurons in the brain. This damage is caused by free radicals; this occurs because of severely depleted glutathione levels. In Parkinson’s disease, there are three primary causes of glutathione collapse: (1) Depletion due to the disease itself (which starts prior to the onset of symptoms), (2) L-dopa induced depletion and (3) carbidopa induced depletion. It is thought that the two largest contributors are glutathione collapse due to the disease itself, as well as the use of carbidopa.
Glutathione levels can become severely depleted over time in people with Parkinson’s disease. This is thought to happen due to a large amount of neurotoxic exposure, which effectively uses up a person’s glutathione stores. Once those stores have been depleted, the neurotoxins damage the dopaminergic neurons in the brain, eventually resulting in the symptoms of Parkinson’s disease. The longer glutathione levels remain depleted, the further the disease can progress.
Carbidopa is often administered to those with Parkinson’s disease, even though it is now known that carbidopa itself is likely a main cause of the progression of Parkinson’s disease. Carbidopa works by irreversibly binding to vitamin B6 as well as the active site of B6-dependent enzymes in the body. The manufacture of glutathione in the body is dependent upon B6 and B6-dependent enzymes. By irreversibly binding to B6 and B6-dependent enzymes, carbidopa essentially blocks the production of glutathione and facilitates further glutathione depletion which causes further irreversible neurotoxic damage. This can lead to disease progression and an increase in symptoms.
Restoring Glutathione Status
The only way to effectively manage the symptoms associated with Parkinson’s disease and slow or halt the progression of the disease is to properly address the body’s glutathione collapse. This can be done through the proper use of glutathione precursors (L-cysteine, L-glutamic acid, glycine, L-methionine, N-acetyl cysteine (NAC) and/or S-adenosyl-methionine (SAMe)) as well as the administration of properly balanced amino acid therapy, whereby the body’s serotonin and dopamine levels are restored to optimal levels.
Restoring glutathione status and optimizing neurotransmitter function allows a person with Parkinson’s disease relief from symptoms without the need for carbidopa and provides them the only way currently known to possibly halt the progression of this degenerative condition.
