Many people with Parkinson’s disease either do not respond well to conventional treatments or do not achieve significant improvements with the standard protocol of medications, such as carbidopa/levodopa. Several natural products may offer some relief.

There are many integrative and complementary approaches that can be used by those with Parkinson’s disease. Here, I’d like to highlight two additional compounds that can play a unique role in possibly halting the progression of the disorder while reducing symptoms.

Taurine

Taurine is an organic compound that plays a number of important roles in human health. In regards to dysfunctions related to Parkinson’s disease, taurine can help improve mitochondrial function in several important ways:

  • Taurine has been shown to protect against glutamate excitotoxicity. Glutamate toxicity can cause neurons to die, which could exacerbate numerous neurodegenerative disorders, including Parkinson’s disease and dementia.
  • Taurine can also provide significant antioxidant protection, preventing oxidative damage to neurons and muscle cells.
  • Taurine has been shown to protect against toxicity related to heavy metals and other toxins. Damage related to heavy metal toxicity is one possible mechanism related to the initiation and propagation of the neurotoxicity thought to cause Parkinson’s Disease.
  • Taurine is also one of the few known substances that can stimulate the repair of damaged synapses between neurons, which can improve motor function, memory and memory retention.

Taurine can be synthesized in the body from the amino acid cysteine, but this is dependent on dietary intake and the correct functioning of specific enzymes within the body. Taurine is only found in fish and meat, with the average diet containing between 8-270 mg of taurine daily, with an average daily consumption of 58 mg/day.

Therapeutic doses of taurine generally start at 1000 mg three times/day and can increase up to 4-10 grams 3x/day.

Palmitoylethanolamide (PEA)

Palmitoylethanolamide (normally abbreviated as PEA) is an endocannabinoid-like compound with analgesic and anti-inflammatory properties. It too has several interesting functions that may beneficial for those suffering with neurodegenerative disorders like Parkinson’s disease:

  • PEA has been shown to bind with select neuronal receptors which can inhibit the expression of proinflammatory genes and pain-related signals in both the central and peripheral nervous systems.
  • In a mouse model of Parkinson’s disease, sustained administration of PEA over one week has been shown to protect dopaminergic neurons and improve motor performance.

Standard dosing for PEA usually begin with 300-600 mg 1-2x/day. After 3 weeks, the dose can be increased up to 600 mg 2-3x/day.

Based on available research, taurine and PEA offer those with Parkinson’s disease additional ways to possibly improve overall physical and mental functioning while providing an opportunity to halt the progression of neurodegeneration.

References

  1. Leon R, Wu H, Jin Y, Wei J, Buddhala C, Prentice H, Wu JY (2008). “Protective function of taurine in glutamate-induced apoptosis in cultured neurons”. Journal of Neuroscience Research 87: 1185–1194.
  2. Gürer, H; Ozgünes, H; Saygin, E; Ercal, N (2001). “Antioxidant effect of taurine against lead-induced oxidative stress”. Archives of Environmental Contamination and Toxicology 41 (4): 397–402.
  3. Sinha, M; Manna, P; Sil, PC (2008). “Taurine protects the antioxidant defense system in the erythrocytes of cadmium treated mice”. BMB Reports 41 (9): 657–63.
  4. Zhang M, Izumi I, Kagamimori S, Sokejima S, Yamagami T, Liu Z, Qi B (2004). “Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men”. Amino Acids 26 (2): 203–7.
  5. Jong CJ, Azuma J, Schaffer S. Mechanism underlying the antioxidant activity of taurine: prevention of mitochondrial oxidant production. Amino Acids. 2012 Jun;42(6):2223-32.
  6. Shalbaraj MC, et al. Plos One 2012;7(8):e42935.
  7. Suarez LM, et al. Amino Acids 2016;48(5)1199-208.
  8. Del Olm N, et al. Eur J Neurosci 2004;19(7):1875-86.
  9. Brosnan J, Brosnan M (2006). “The sulfur-containing amino acids: an overview”. J Nutr136 (6 Suppl): 1636S–40S.
  10. Huxtable RJ (1992). “Physiological actions of taurine”. Physiol Rev72 (1): 101–163.
  11. Shao A, Hathcock JN (2008). “Risk assessment for the amino acids taurine, L-glutamine and L-arginine”Regulatory Toxicology and Pharmacology : RTP50 (3): 376–99.
  12. Esposito E et al. PLoS One. 2012;7(8):e41880.
  13. Iannotti FA et al. Prog Lipid Res. 2016;62:107-128.
  14. Lo Verme J et al. Mol Pharmacol. 2005;67(1):15-19.