Immune System Dysfunction in PD: What Centralized Medicine has missed

The common misconception is that most of the current treatments to PD are not leading to good  long-term outcomes. Use of L-dopa medication such as levodopa in PD beyond very short-term use poses several concerns. Neurotoxicity is one of the key issues, as preclinical studies indicate that  levodopa can induce oxidative stress and mitochondrial dysfunction. Motor complications such as  dyskinesia, wearing-off, and on-off phenomena are prevalent, with studies showing that 71.4% of  patients on long-term therapy develop these issues, significantly impacting quality of life.

Additionally, cognitive functions can be adversely affected due to the dopamine overdose  hypothesis, where exogenous dopamine can impair cognitive functions based on baseline dopamine  levels in different brain regions. Furthermore, regular L-dopa administration can elevate  homocysteine levels, contributing to oxidative stress and mitochondrial dysfunction, exacerbating  neurodegeneration. If the body makes it, don’t take it. Simply by supplementing dopamine the body  undergoes a reduced endogenous synthesis of the very little dopamine it was able to make. This can  sometimes drop endogenous production almost to nothing forcing a reliance on medication and  guarantee of long-term consequences related to this treatment. [study, study, study, study, study].  Many Parkinson’s patients who take an excess of L-dopa experience ‘Tachyphylaxis’ which describes  an acute, sudden decrease in response to a drug after its administration, i.e. a rapid and short-term  onset of drug tolerance.

When L-dopa no longer works to alleviate Parkinson’s symptoms, the next line of treatment for Parkinson’s Disease is to implement deep brain stimulation (DBS). These electrodes are implanted within the brain into the substantia nigra to electrically stimulate the brain due to the lack of  sunlight through the eye and skin that the patient is lacking, and it works temporarily. But because  the charge is not produced endogenously due to the poor photoelectric properties of degraded  neuromelanin within this area of the brain, PD symptoms usually remain. We know the therapies that help, and we know why, but the education required to elucidate the reactivation of endogenous  photoelectrical communication within the human brain is not taught in medical schools leaving  centralized neuro specialists with L-Dopa supplementation as an easy moneymaking temporary fix being reused for decades. The onset of PD is occurring faster than ever before in human history  given the speed at which endogenous melatonin suppression, dopamine destruction and melanin degradation occurs in an environment dominated by manmade electric, magnetic and  electromagnetic fields. That means it’s really easy to develop a serious brain disease in a 5G  environment with 25 wireless technological devices in the average home in 2024. When a person  lives around nnEMF their free electrons are being oxidized and stolen. This leaves the body’s biological surfaces (eyes, skin, gut and lungs) unable to capture sunlight as effectively.

This means  oxidative environmental effects need to be removed, with the most powerful in this modern world being artificial visible and non-visible light and then adding back in electrons to the biologic system via the myriads of ways of collecting electrons from the natural environment and then reintroducing  powerful sunlight.

Thus, reducing the destructive fields must occur first for any hope of regenerating  the dopamine neurons in the substantia nigra to restore motor function and all the other symptoms  of PD. This process respects that the body is in somewhat of a state of informational disorder and  reorganizing needs to take place before large amounts of powerful full spectrum native energy is  added and effectively accepted by the body. You can see that the solution is not just a pill or a single  practice but a rational process involving some education, discipline and guidance from experts along  the way if necessary.

When sunlight enters the eye, it is photoelectrically tunneled like a fibre optic transfer through to  the suprachiasmatic nucleus (SCN) within the hypothalamus and onto the habenula nucleus, where the energy and information are distributed throughout the brain and body, regulating biochemistry.  The tract between the retina and habenula nucleus has no synapses, indicating light conduction into  the brain with photoreceptive tissue at the habenula nucleus. This tract is filled with  semiconductors, water networks, photoreceptive pigments, and Mueller cells. The first synaptic stop  for this photoelectrical signal after the SCN is the pituitary. When this signal is disrupted or received  from an artificial unbalanced light source, this pathway and all subsequent secretions from the  hypothalamus, pituitary, and prefrontal center are affected.

Individuals with Parkinson's Disease (PD) have higher incidences of melanoma and hypothyroidism due to disrupted native full spectrum light signals. When the necessary light signal is altered before  reaching the hypothalamus, pituitary, or habenula nucleus, it affects the pituitary’s regulation of the  thyroid, leading to hypothyroid conditions. The thyroid hormone T3 powers neuron and motor  functions, explaining why PD symptoms worsen and cognitive changes occur. The degradation of  melanin in the substantia nigra due to artificial EMF or lack of full spectrum sunlight results in its  migration, leading to melanoma when exposed to artificial blue light and non-native EMF. The loss of  neuromelanin in PD sufferers causes reduced melanin in the skin, a feature of early PD.

Solar light, rather than drugs or hormone therapies, is crucial in regulating the human adaptive  immune system. In cases of Parkinson’s Disease (PD), the immune system becomes dysfunctional,  leading to the accumulation of misfolded proteins in the brain. Restoring the brain’s circadian  rhythm through the suprachiasmatic nucleus (SCN) within the hypothalamus can enhance  mitochondrial function, reduce perivascular spaces, and improve glymphatic flow. This process helps  clear alpha-synuclein, beta-amyloid, tau proteins, and other misfolded proteins, thereby restoring  coherence within the brain’s water networks, including cerebrospinal fluid (CSF), blood, lymph,  interstitial fluid, and cytoplasmic fluid. Such restoration improves dopamine and melatonin levels,  leading to the recovery of the substantia nigra and motor cortex to a functional neuromuscular  state.

To support this, it is essential to ensure that dopamine, neuromelanin, noradrenaline, melatonin,  serotonin, thyroid hormone, and nicotinamide adenine dinucleotide (NAD) are restored and well  regulated. This requires the eyes and skin to receive balanced ultraviolet sunlight, including a full  spectrum of light rays, with 51% red and infrared light. This light excites the benzene rings within the aromatic amino acids tyrosine and tryptophan, facilitating the restoration of brain function.  Additionally, consuming key nutrients found in the marine food chain, such as the omega-3 fatty acid  docosahexaenoic acid (DHA) and trace minerals like magnesium, potassium, calcium, iron, zinc,  copper, manganese, selenium, iodine, and sodium chloride, is crucial. These steps can revitalize the  brain’s complex systems, often referred to as the "quantum computer" of the body.

Accumulating neuromelanin in the substantia nigra through disciplined exposure to full-spectrum  sunlight and proper nutrition can restore dopamine-producing neurons, leading to improved  executive cognition and neuromuscular function. This approach may offer significant benefits over  traditional medical solutions. Before opting for drugs, supplements, diet plans, or exercise regimes,  consider prioritizing light hygiene. Furthermore, while treatments like L-Dopa supplementation or  deep brain stimulation (DBS)/pallidotomy may repair the substantia nigra, they do not address the  skin, pituitary, SCN, or retina, meaning that PD may not be fully reversed without a comprehensive  approach.

Examples of poor immune function, such as Lyme disease, Bartonella, and viral particles in the  blood, indicate environmental defects rather than internal issues. Functional medicine and  alternative doctors often mislead patients into unnecessary treatments, unaware of how solar light programs the adaptive immune system. Prioritize changing your light hygiene before resorting to  drugs or supplements. Light controls the immune response depending on the time of day, affecting  test results based on natural settings or timing. When infections arise, it suggests an environment  filled with non-native electromagnetic fields (nnEMF) and blue light, causing toxic pathogens to  escape and harm mitochondria.

The energy and information emitted during healing, known as biophotons, were identified by Dr.  Fritz Albert Popp and later detailed by Dutch biophysicist Roeland van Wijk. These ultra-weak  ultraviolet light photons, when leaked excessively, signal unwellness, revealing struggling organs  through photomultiplier readings. Chronic energy and information loss lead to severe diseases, first  affecting the neocortex. For adults, this very commonly manifests as Parkinson’s, Alzheimer’s, and  ALS, while in children or those in utero, it appears as Autism, ADD, and ADHD. Diseases like major  depressive disorder, PD, and ADHD are characterized by low dopamine levels in the brain, whereas  schizophrenia involves erratic, often elevated dopamine levels, showcasing the varied expressions  and behaviors stemming from dysfunctional dopamine levels.

Focusing on the PD dopamine deficit, dopamine deficit lowers the signal-to-noise ratio in a person's  ability to sense their environment via the five senses integrating within the thalamus in the brain.  This loss of signal-to-noise ratio prevents the body from coherently harmonizing with external  environmental signals. A good example of this is our auditory sense: low dopamine makes it difficult  to distinguish a person in front of you talking from the background noise, and patterns become  harder to detect. With a PD dopamine deficit, following one conversation or train of thought can be  challenging because all conversations or thoughts sound equally loud, making it hard to pick out a  continuous stream. Instead, the unmedicated PD brain often picks up bits and pieces from several  different streams of conversation or thought. Random firing neurons make up the background noise  in the brain, like all the voices at a party not part of your conversation. The person whose voice you  focus on, ignoring all the others, is the signal amidst the noise. When dopamine within the brain  improves, the signal-to-noise ratio increases; the background noise fades, and your conversation  partner’s voice becomes distinct and easy to follow. Dopamine turns up the volume on the audio  signals at the party compared to the background noise, making it easier to decipher the conversation  and act properly on it. This leaves people with PD open to issues with maintaining attention spans.  The main factor in a low dopamine PD brain is the lack of energy available to the body to fold  proteins correctly. The amount of electromagnetic energy that you emit or absorb into your system  is directly proportional to the structure of proteins in your body. This is a crucial point as it  demonstrates how someone with PD can continue to be unable to organize the energy and  information it receives from nature into a healing, regenerative, and restorative program. This  demonstrates that they may need more time in nature to reorganize their brains to begin to accept  the powerful natural signals once again and optimize dopamine, melatonin, mitochondrial function,  and neurological coordination once again.

Pro Tip: Vitamin C + Endogenous melatonin, dopamine and melanin synthesis via sunlight,  grounding, mitigating nnEMF and HEVL + infrared light + a mitochondrial health focus = regeneration  of dopaminergic neurons = optimal dopamine = PD symptom reversal.

References and Citations: 

1. 

• Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. • Volkow ND, Tomasi D, Wang GJ, et al. 

• Jama. 2011;305(8):808-13. doi:10.1001/jama.2011.186. 

• https://pubmed.ncbi.nlm.nih.gov/21343580/ 

2. 

• Acute Radiofrequency Electromagnetic Radiation Exposure Impairs Neurogenesis and Causes  Neuronal DNA Damage in the Young Rat Brain. 

• Singh KV, Prakash C, Nirala JP, Nanda RK, Rajamani P. 

• Neurotoxicology. 2023;94:46-58. doi:10.1016/j.neuro.2022.11.001. 

• https://pubmed.ncbi.nlm.nih.gov/36336097/ 

3. 

• Occupational Exposure to Chronic Ionizing Radiation Increases Risk of Parkinson's Disease  Incidence in Russian Mayak Workers. 

• Azizova TV, Bannikova MV, Grigoryeva ES, Rybkina VL, Hamada N. 

• International Journal of Epidemiology. 2020;49(2):435-447. doi:10.1093/ije/dyz230. • https://pubmed.ncbi.nlm.nih.gov/31722376/ 

4. 

• Comments on the US National Toxicology Program Technical Reports on Toxicology and  Carcinogenesis Study in Rats Exposed to Whole-Body Radiofrequency Radiation at 900 MHz  and in Mice Exposed to Whole-Body Radiofrequency Radiation at 1,900 MHz. • Hardell L, Carlberg M. 

• International Journal of Oncology. 2019;54(1):111-127. doi:10.3892/ijo.2018.4606. • https://pubmed.ncbi.nlm.nih.gov/30365129/ 

5. 

• Parkinson's Disease and Light: The Bright and the Dark Sides. 

• Maggio R, Vaglini F, Rossi M, et al. 

• Brain Research Bulletin. 2019;150:290-296. doi:10.1016/j.brainresbull.2019.06.013. • https://pubmed.ncbi.nlm.nih.gov/31226407/ 

6. 

• A New Threat to Dopamine Neurons: The Downside of Artificial Light. 

• Fasciani I, Petragnano F, Aloisi G, et al.

• Neuroscience. 2020;432:216-228. doi:10.1016/j.neuroscience.2020.02.047. • https://pubmed.ncbi.nlm.nih.gov/32142863/ 

7. 

• https://www.scientificamerican.com/article/could-mitochondria-be-the-key-to-a-healthy brain/?fbclid=IwAR3lbEbnQjD_OpBHhxKlxLKDYxuKeiVijIktyaZTA-FUxxdmmBzw0ABkFRc 

8.  

• https://www.annualreviews.org/doi/10.1146/annurev-cellbio-021820-101354 9 

• https://www.parkinson.org/about-us/news/incidence-2022 

10.

• Overview of Sleep and Circadian Rhythm Disorders in Parkinson Disease 

• https://pubmed.ncbi.nlm.nih.gov/31733692/ 

• https://pubmed.ncbi.nlm.nih.gov/35000606/ 

11.

• Association between circadian rhythms and neurodegenerative diseases. – “circadian  rhythm disruptions are more severe in people with age-related neurodegenerative diseases” • https://pubmed.ncbi.nlm.nih.gov/30784558/ 

12. 

• Low Vitamin D in people with PD 

• https://pubmed.ncbi.nlm.nih.gov/35741675/ 

• “Low VD serum levels have been found in patients affected by Alzheimer Disease,  Parkinson” https://pubmed.ncbi.nlm.nih.gov/31142227/ 

• “Interestingly, a significant association has been demonstrated between PD and low levels of  vitamin D in the serum” https://pubmed.ncbi.nlm.nih.gov/22930493/ 

• https://pubmed.ncbi.nlm.nih.gov/24847960/ 

13. 

• Primary and Secondary Features of Parkinson's Disease Improve With Strategic Exposure to  Bright Light: A Case Series Study. 

• https://pubmed.ncbi.nlm.nih.gov/17612949 

• https://pubmed.ncbi.nlm.nih.gov/34052783 

14.

• The Association Between Vitamin D Status, Vitamin D Supplementation, Sunlight Exposure,  and Parkinson's Disease: A Systematic Review and Meta-Analysis 

• https://pubmed.ncbi.nlm.nih.gov/30672512/ 

• “Insufficiency and deficiency of 25-hydroxyvitamin D and reduced exposure to sunlight were  significantly associated with an increased risk of Parkinson's disease. However, vitamin D  supplements resulted in no significant benefits in improving motor function for patients with  Parkinson's disease.” 

15. 

• https://pubmed.ncbi.nlm.nih.gov/26223801 

• Extremely Low Frequency Magnetic Field (ELF-MF) Exposure Sensitizes SH-SY5Y Cells to the  Pro-Parkinson's Disease Toxin MPP(.). 

• Benassi B, Filomeni G, Montagna C, et al. 

• Molecular Neurobiology. 2016;53(6):4247-4260. doi:10.1007/s12035-015-9354-4. 16. 

• https://pubmed.ncbi.nlm.nih.gov/22428905 and  

https://pubmed.ncbi.nlm.nih.gov/24707049 and  

https://pubmed.ncbi.nlm.nih.gov/12091446 

17. 

• Is Levodopa Toxic?. 

• Müller T, Hefter H, Hueber R, et al. 

• Journal of Neurology. 2004;251 Suppl 6:VI/44-6. doi:10.1007/s00415-004-1610-x. 

18. 

• L-Dopa: A Scapegoat for Accelerated Neurodegeneration in Parkinson's Disease?. 

• Lipski J, Nistico R, Berretta N, et al. 

• Progress in Neurobiology. 2011;94(4):389-407.  

doi:10.1016/j.pneurobio.2011.06.005. 

19. 

• Clinical-Pathological Study of Levodopa Complications. 

• Rajput AH, Fenton ME, Birdi S, et al. 

• Movement Disorders : Official Journal of the Movement Disorder Society.  2002;17(2):289-96. doi:10.1002/mds.10031. 

20.

• Dopamine Overdose Hypothesis: Evidence and Clinical Implications. 

• Vaillancourt DE, Schonfeld D, Kwak Y, Bohnen NI, Seidler R.

• Movement Disorders : Official Journal of the Movement Disorder Society.  2013;28(14):1920-9. doi:10.1002/mds.25687. 

21. 

• Levodopa Impairs Probabilistic Reversal Learning in Healthy Young Adults. 

• Vo A, Seergobin KN, Morrow SA, MacDonald PA. 

• Psychopharmacology. 2016;233(14):2753-63. doi:10.1007/s00213-016-4322-x. 22.

• The Vicious Circle Between Homocysteine, Methyl Group-Donating Vitamins and Chronic  Levodopa Intake in Parkinson's Disease. 

• Müller T, Riederer P. 

• Journal of Neural Transmission (Vienna, Austria: 1996). 2024;131(6):631-638.  doi:10.1007/s00702-023-02666-x.