If your therapy for Parkinson’s Disease is making you sicker, a new treatment provides hope
By Dr. Brian Lum, DC
Parkinson’s disease is a devastating illness and the rate of people dying from this condition continues to skyrocket. We now know the reason why and what you can do about it.
Almost all of those with Parkinson’s are taking a medication that has recently been shown to increase symptoms and cause the disease to progress leading to premature death.1,2
WHAT’S HAPPENING IN PARKINSON’S DISEASE?
The nervous system works like electricity; there must be sufficient signaling in order for the body to function properly. If there is damage to enough nerves, also called neurons, then signaling and function will be disrupted causing symptoms and/or disease. This is the primary disease process seen in Parkinson’s.
Parkinson’s disease is characterized by permanent damage of dopamine neurons in part of the brain called the substantia nigra. These nerves, responsible for fine motor control, and damage to this part of the brain can lead to tremor and other movement abnormalities.
WHAT’S THE CURRENT TREATMENT?
Eighty-nine percent of all Parkinson’s patients take Sinemet, which is a combination of two medications: Carbiodopa and Levodopa (L-dopa).
THE PROBLEMS WITH CURRENT THERAPY
1. Carbidopa makes the disease worse
Carbidopa has been proven to bind irreversibly to vitamin B6 (pyridoxal 5’-phosphate) and permanently deactivate and deplete the entire vitamin B6 reserve pool.2,3
Why is this a Big Deal?
*Click here to see the full list of Carbidopa induced side effects
2. Continued Brain Damage/Nerve Death
A neurotoxin is any substance that can cause damage to the nervous system. The body’s best defense against these harmful substances is glutathione. Glutathione is made within the body and allows us to neutralize dangerous compounds within the system so we can safely get rid of them.
Neurotoxins are responsible for continued destruction of nervous tissue and thus continued disease progression in Parkinson’s.5 In the current treatment model there is no strategy to prevent further damage to the brain by neurotoxins. Therefore, the root cause of the disease is never addressed.
L-dopa administration causes sulfur amino acids to be depleted. The body uses sulfur amino acids to make glutathione. As sulfur amino acids are depleted, so is the level of glutathione and also the body’s ability to neutralize toxins and their consequential damaging effects. Therefore, chronic L-dopa without replenishing the depleted sulfur amino acids actually accelerates brain damage due to neurotoxins.
L-dopa→depletes sulfur amino acids→decreased glutathione production = increased susceptibility to nerve damage by neurotoxins
3. Causes Imbalances in the Body
A relative nutritional deficiency (RND) occurs when the body’s requirement for a specific nutrient is higher than what can be met through normal or even optimal diet. Numerous relative nutritional deficiencies (RND) exist in Parkinson’s disease.
- L-dopa depletes:6
- L-tyrosine: inadequate tyrosine levels will cause dopamine levels to fluctuate, which may result in increased symptoms such as movement abnormalities. Tyrosine also important in thyroid hormones.
- Sulfur-amino acids: leads to increased susceptibility to nerve damage by neurotoxins
- Serotonin: causes severe depletion and may contribute to the development of depression
- Tryptophan: precursor to serotonin
- Carbidopa depletes:
- Vitamin B6: DEPLETION- contributes to increasing death rate and disease progression.
- Serotonin, dopamine, epinephrine, norepinephrine.7
A BETTER WAY: THE SOLUTION
A group of medical doctors developed a cutting-edge treatment protocol using 17 years of clinical research. This nutritional approach replaces carbidopa while effectively addressing the nutritional deficiencies associated with Parkinson’s disease and L-dopa. This has proven to be the first real advancement in L-dopa and Parkinson’s disease treatment in 50 years.
PHYSICIAN ADMINISTRATION: L-DOPA + AMINO ACIDS
L-dopa Restores Brain Function: Parkinson’s disease patients do not have enough dopamine in their brains. This causes the symptoms of Parkinson’s disease. The only way for the brain to make enough dopamine is by taking L-dopa. In all Parkinson’s disease patients, a relative nutritional deficiency exists since high enough levels of the nutrient L-dopa cannot be obtained from even an optimal diet. Treatment with L-dopa is necessary as soon as possible to maintain or restore optimal brain function.
Balance to Restore Health: As previously discussed, L-dopa is the best therapy for Parkinson’s; but administered without other neurotransmitter precursors can cause numerous side effects and multiple nutritional collapses in the body. Therefore, in addition to L-dopa, other amino acid precursors and nutrients must be administered skillfully to balance the system.
Eliminate Need for Carbidopa: By properly administering serotonin precursors, we can eliminate nausea associated with L-dopa ingestion and serotonin depletion. Serotonin precursors are a superior and infinitely safer therapy than carbidopa.
Protection from Toxic Damage: Properly administering sulfur amino acids will prevent glutathione depletion by the disease process and L-dopa ingestion. This approach enables the body’s defense against damaging neurotoxins.
WHAT ARE THE EXPECTED OUTCOMES OF TREATMENT?
For Parkinson’s disease patients who are early in the course of the disease, expectations should be complete restoration of function, with few or no symptoms, with slowed progression of the disease. For patients who have had the diagnosis for many years; time, the disease, and drugs may have taken their toll. While complete restoration of normal function may not be possible, the expectation should be to achieve the highest level of function possible without experiencing unmanageable L-dopa side effects.
WHAT MAY HAPPEN IF I DELAY TREATMENT? IS IT NECESSARY?
Without this treatment approach, Parkinson’s patients experience significant nutritional deficiencies that cause the disease to get worse. L-dopa can be the most effective therapy for Parkinson’s disease, but is only successful long-term with this approach. Delaying this type of treatment may prevent you from achieving complete symptom relief, as this is the only way to fix the real problem. Each day without these relative nutritional deficiencies being treated is another day that Parkinson’s Disease progresses and permanent damage takes place.
1.) National Parkinson Foundation. The National Parkinson Foundation’s Help- line Speaks: Lessons from the 2011 Sinemet Shortage. Miami, FL: National Parkinson Foundation; 2012. Available from: http://www.parkinson.org/ Files/PDFs/NPF-Content-Documents/White-Papers/NPF466-_2011- Sinemet-Shortage_WhitePaper-_Full-art.
2.) Hinz, M., Stein, A., & Cole, T. (2014). The Parkinson’s disease death rate: carbidopa and vitamin B6. Clinical pharmacology: advances and applications, 6, 161.
3.) DaidoneF,MontioliR,PaiardiniA,etal.Identificationbyvirtualscreen- ing and in vitro testing of human DOPA decarboxylase inhibitors. PLoS One. 2012;7(2):e3161
4.) Hinz, M., Stein, A., & Cole, T. (2014). Parkinson’s disease: carbidopa, nausea, and dyskinesia. Clinical pharmacology: advances and applications, 6, 189.
5.) Zeevalk G, Manzino L, Sonsalla PK, Bernard LP. Characterization of intracellular elevation of glutathione (GSH) with glutathione monoethyl ester and GSH in brain and neuronal cultures: Relevance to Parkinson’s disease. Exp Neurol. 2007;203:512–520.
6.) Hinz, M., Stein, A., & Uncini, T. (2011). Amino acid management of Parkinson’s disease: a case study. International journal of general medicine, 4, 165.
7.) Hinz, M., Stein, A., & Uncini, T. (2012). Relative nutritional deficiencies associated with centrally acting monoamines. Int J Gen Med, 5, 413-430.