Imagine waking up one morning and discovering that you are having tremors and may find that it takes longer to walk across the room to get dressed. It would be very unnerving to say the least, especially if it continued to get worse. Is it just old age? Well, maybe, but it could be the first signs of a very common illness known as Parkinson’s disease.
What is Parkinson’s Disease?
Parkinson’s disease is a progressive neurological disorder that affects the nerves responsible for muscle tension and movement. Parkinson’s disease (PD) is characterized by tremor, muscle rigidity, slow movements, and postural abnormalities. It is the result of the death of cells in one of the movement centers of the brain.
Parkinson’s disease, identified as a disease for over 200 years, currently affects approximately one million men and women in the United States, with as many as 60,000 new cases appearing every year. It most often afflicts people in their late 50’s or early 60’s. About 15% of the American population between the ages of 65-74 will get PD to some degree, and the figures rise to about 30% of those between 75-84. It progressively advances in patients, deteriorating their ability to control the speed, consistency, and smoothness of their bodily motions.
It’s a bit concerning to know that after 200 years of examination and investigation, researchers, scientists and clinicians have identified neither the cause nor the cure for Parkinson’s disease. And with the baby-boom generation now in their retirement years, the need for definitive answers has never been more critical.
The mechanics of how this illness works have been the subject of much research for many years. It is not fully understood, but there are some things that we do know. There is an area of the brain called the “substantia nigra” (black substance) that is one of the primary movement control centers of the brain. Parkinson’s disease appears to cause nerve cells (neurons) in the substantia nigra to degenerate and eventually die. Normally, these specialized cells release a chemical called dopamine that transmits neurological signals between the substantia nigra and the “corpus striatum,” another part of the brain associated with muscular movement. Under normal conditions, this process enables the muscles to operate in a smooth, controlled fashion. When these cells begin to die, less dopamine is produced, and muscular movement deteriorates. The dying cells also develop a unique substance called “Lewy bodies,” which can be used to help identify PD. The loss of dopamine producing cells is a natural result of aging in everyone, but PD patients may lose over 50% of the neurons in the substantia nigra.
What Causes Parkinson’s Disease?
Despite a huge amount of research over the years, scientists are still not sure about the exact cause of Parkinson’s disease. The leading theories speculate that there is most likely both an environmental and a genetic link to PD, but the specifics are as of yet unknown. Some believe PD may be caused by exposure to a genetic or environmental factor early in life that worsens over time until symptoms begin to appear. Makes ya’ think twice about what we may be exposing our children to, doesn’t it?
Statistics show a slight (5%) increase in the risk of contracting PD if you have a first-degree relative, such as parent, child, or sibling, who has the disease. In light of that fact, much of the research has focused on families who have more than one member with the illness. These families are rare, so studies such as these are precious to researchers. This line of research has revealed a bit more about the genetic puzzle. They have discovered that many PD patients have an abnormality in a certain protein (alpha-synuclein) that accumulates in their dying brain cells. Another clue points to a breakdown of systems that dispose of unwanted proteins in the bodies of PD patients. These two factors are common in most all PD sufferers.
There are also some clues about the connection of environmental factors with PD. Studies over the years have shown that statistically there is a slightly higher of incidence of PD in people who have had unusual exposure to herbicides and pesticides. People who live in a rural area, drink well water, or are involved in farming also have a slightly higher risk for PD. That is all we know. No specific substance or substances have been implicated.
Another clue was uncovered recently when it was discovered that a chemical called MPTP, a byproduct of the manufacture of some illegal narcotic drugs, causes PD like symptoms in people who ingest it. The symptoms appear almost immediately, within hours, and are permanent. Studies indicate MPTP works through free radical damage, and this has stimulated some research into possible treatments for PD that focus on using antioxidants to fight free radicals.
There are some medications that can trigger PD symptoms as well, if they are taken at higher than normal dosages for extended periods of time. The main culprits are two drugs given for psychiatric disorders, haloperidol (Haldol) and chlorpromazine (Thorazine). Other medications include metoclopramide (Reglan), prescribed for nausea, and valproate (Depakene), an epilepsy drug.
Gender and Hormones
Other risk factors for PD include gender (more men get PD than women), and reduced estrogen levels. Studies have shown that menopausal women are at a greater risk than non-menopausal women.
Let’s park here for a while because I believe this is very important information — information your doctor may not know or completely understand.
MedicalNewsToday.com wrote in 2013 the following headline: Fungus May Cause Symptoms Of Parkinson’s Disease. The direct links between candida and PD have indeed already been identified in the scientific literature: Chronic polysystemic candidiasis as a possible contributor to onset of idiopathic Parkinson’s disease.
PD is usually recognized by the symptom of tremors. What is the cause of these tremors? Those knowledgeable in this area will tell you that tremors are caused by tremorgens. Tremorgens, by definition, are a “group of toxins produced by fungi, e.g. Penicillium spp,. which causes serious muscle tremor”. Stay with me here. Penicillium is a mold, and the mycotoxin (poison) it produces is called “penicillin.”
The following excellent information about the link between Parkinsons’s Disease and fungus is from Doug Kaufmann at Know the Cause:
“…I do believe that larger or prolonged doses of Penicillium-derived antibiotics could definitely cause Parkinson’s and a host of other neurological diseases. I’m not talking about the “symptoms” of PD, as they do, however, and I make my assertion on solid scientific grounds. You see, our scientists first learned that Penicillium caused nerve toxicity, as seen in PD, in 1945!
I don’t believe that the damage done by antibiotics is instantaneous. If it were, we’d have proven 50 years ago that antibiotics caused PD. By reducing our immune-enhancing ‘good guy’ gut bacteria, you might imagine how antibiotics could favorably impact neurotoxic diseases even decades later.
If that weren’t enough evidence to implicate long-term antibiotic use in PD, consider this. In 2011, the British Journal of Clinical Pharmacology published an article on the neurotoxic effects associated with antibiotic use.
Their conclusion begs more questions than I have time to ponder in this article, but you will likely understand as you read this: ‘Neurotoxicity is common among many groups of antibiotics in at-risk patients and can range from ototoxicity, neuropathy and neuromuscular blockade to confusion, non-specific encephalopathy, seizures, and status epilepticus. Populations at risk of neurotoxicity associated with various groups of antibiotics include those with extremes of age, critical illness, renal dysfunction and prior neurological disease.’
Really? Does that say that many groups of antibiotics can commonly cause epilepsy, confusion, neuropathy, seizures and block normal synaptic nerve transmission in muscles? And all pregnant women get antibiotics … why? Rarely are we told that antibiotics themselves may contribute to the ‘populations at risk’ causing critical illness, renal dysfunction and prior neurological disease.” About the only things antibiotics can’t do is add to your chronological age!
Antibiotics are neurotoxic poisons…Antibiotics are not the only fungus that I believe play an integral role in PD and other neurological diseases. Brewer’s yeast is a fungus and the poison it makes is called ‘alcohol.’ Because booze, like antibiotics, is a neurotoxic poison, I’m certain that it, too, plays a significant role in PD.”
Candida and the Brain – Candida Albicans is the most common type of yeast infection found in the mouth, intestinal tract and if the immune system is not working properly, a candida infection can also migrate to other areas of the body, such as the blood and membranes around the heart or brain.
It turned out that the fact that candida can indeed damage the brain has been known since at least 1970: Cerebral candidiasis: case report of brain abscess secondary to Candida albicans, and review of literature:
More current research sheds light on how candida gets into the brain: Traversal of Candida albicans across Human Blood-Brain Barrier In Vitro:
Candida has also been be found to cause cognitive dysfunctions common to PD: Yeast infection linked to mental illness: Candida infections also more common among those with memory loss
It seems one of the major mechanisms is via spores breaking through the intestinal walls and getting into the rest of the body, including the to brain.
Candida and the Vagus Nerve – “By disrupting gut health, candidiasis also affects the vagus nerve – a major nerve that connects the digestive system and major organs including the heart and lungs, to the limbic system in the brain [the portion of the brain that deals with three key functions: emotions, memories and arousal (or stimulation], as it’s part of the parasympathetic nervous system.”
Remember: FUPO – Fungus Until Proven Otherwise!
What is known is that certain risk factors can make someone more susceptible to developing Parkinson’s disease, which can include:
- Being a man, especially during older age. Research suggests that men in their 50s and 60s are most likely to develop Parkinson’s.
- Genetic susceptibility: Studies have now identified several gene mutations that can put someone at a greater risk. Parkinson’s has also been found to run in families, and having a sibling or parent increases someone’s risk.
- Damage to the area of the brain called the “substantia nigra,” which produces brain cells that are responsible for making dopamine.
- Toxicity and exposure to chemicals, including pesticides present on produce from non-organic farming. Living in a rural area and drinking well-water that might contain chemicals is another environmental risk factor.
- Poor diet, nutrient deficiencies, food allergies and an unhealthy lifestyle.
- Hormonal imbalances and other medical conditions that affect cognitive health and increase inflammation.
- Fungal issues especially if one has consumed large or prolonged doses of Penicillium-derived antibiotics during their lifetime.
What Are the Symptoms of Parkinson’s Disease?
These are the common primary symptoms:
The most well known symptom of PD is tremors. They may begin on one side of the body at a time, and usually first appear in the hands or even only in one finger. The classic PD tremor is called the “pill-rolling tremor,” because it is a back and forth movement that resembles the rolling of a pill between the thumb and forefinger, usually occurring about three times per second. Tremors in the legs are also common.
This is the clinical name for ‘’slow movement.” PD patients may find that they slow down or sometimes even freeze-up (akinesia) during familiar movements such as walking, eating, or combing their hair.
This occurs in many patients as a reaction to changes in balance and posture. The gait (festination) is often adopted to avoid falling.
As the movement function of the brain deteriorates, people with PD tend to lose their ability to move smoothly. Movement becomes stiff and jerky.
Patients often lose most of their facial expressions and may also experience decreased eye blinking.
Many folks will begin to lose the inflections in their voice and speak in a monotone.
Secondary symptoms include:
- Rapid, unclear speech
- Difficulty sleeping, such as insomnia, restlessness, and nightmares
- Emotional changes such as irritability, fear, and paranoia.
- Changes in handwriting, such as letters becoming smaller from left to right (micrographia)
- Difficulty swallowing, often found in the latter stages of the illness.
- Dementia: A small percentage of PD patients develop this complication that affects memory and reasoning skills. It often starts out as slowed thought processes, and difficulty concentrating.
What Treatments Are Available for Parkinson’s Disease?
At this time there is no cure for PD, but there are a slew of mainstream options that include numerable medications and surgeries. Let’s talk about a few of these options.
- Levodopa – The standard of treatment for PD since the 1960’s has been Levodopa, a natural substance found in plants and animals. It is a precursor to dopamine, and is converted into dopamine by neurons in the brain. The discovery of Levodopa was a breakthrough for scientists because they thought that supplementing PD patients with dopamine would help, but because of its structure, dopamine was not absorbable by the brain. There is a tissue known as the blood-brain barrier which screens out many substances to protect the brain. While dopamine cannot cross that barrier, Levodopa is of a different structure, and it can pass through the blood-brain barrier. In more recent times, a drug called carbidopa has been added to the Levodopa to make it more efficient. It helps Levodopa to convert more dopamine in the brain, where it is most needed for PD patients, rather than in other parts of the body. Carbidopa also reduces some of the side effects of this therapy. This has been and is today the preferred medication for the treatment of PD. The main drawback to this course of treatment is that it only treats the symptoms, and is not able to stop the disease from progressing. Therefore, after the disease reaches a certain stage, these drugs stop being as effective. Some of the side effects can be significant as well, such as hallucinations and hypotension (low blood pressure) when standing, causing many patients to have dizzy spells.
- Low protein diet – In the last few years, some very interesting research has been done which focuses on the importance of a low protein diet in treating PD, especially in conjunction with Levodopa therapy. One doctor recommends limiting the amount of protein patients consume during breakfast and lunch to no more than 7 grams. Dinner should be the heavy protein meal of the day. Studies using this plan have shown very encouraging results, with many patients experiencing marked improvement in their symptoms especially during the main waking hours.
- Caffeine-based chemical compounds – A study by researchers at the University of Saskatchewan in 2016 found a potential way to halt the progression of Parkinson’s. These researchers formulated caffeine-based chemical compounds — which also contained nicotine, metformin and aminoindan — that prevented the misfolding of alpha-synuclein, a protein necessary for dopamine regulation.
- Deep brain stimulation – I’d like to mention one surgical option just to let you know what’s available out there. I am not recommending this. In my mind the possible side effects are too risky. But it is one of the more recent innovations. It is called deep brain stimulation. An electronic transmitter, much like a pacemaker, is implanted into the chest. Then tiny electrodes are surgically inserted deep within the brain into a section that controls many major motor functions called the “subthalamic nucleus.” Use of these devices has shown improvement in the symptoms of some patients. And now for the rest of the story…Some of the possible side effects are brain hemorrhaging, stroke-like issues, infection, subsequent surgeries to replace parts if they wear out, possible increase of thinking and memory issues, and surgical replacement of the battery every few years. I’m just not sure it’s worth it; however, it’s a personal decision that should be made between patient and practitioner.
Natural Approaches for Parkinson’s Disease
As said above, currently there is no cure for Parkinson’s Disease, but there are some alternative treatments that may help slow the progression of Parkinson’s Disease.
One of the more popular therapies is Coenzyme Q10. Researchers have discovered that this substance can help to slow the progression of PD symptoms, especially in the early stages of the disease. CoQ10 is produced by mitochondria, the energy producing structures within our cells. Its purpose is to transport electrons during cellular respiration, which is how cells get energy from oxygen. Most PD patients have insufficient levels of CoQ10 in their bodies. This is a natural supplement with no known side effects.
Tyrosine, phenylalanine, vitamin B6, zinc, DHEA.
Vitamins C and E, polyphenols, bioflavanoids, proanthocyandins,tocotrienols, curcumin, glutathione. A major spotlight in treating Parkinson’s disease is the reduction of oxidative stress. Intravenous infusion of chelators eliminates from the brain iron and other toxins that contribute to the formation of free radicals. Antioxidants also act as chelators, and best results are had when a combination is used. Alternatives include vitamins C and E, polyphenols found in green and black teas, bioflavanoids that provide the red, pink, and purple colors in flowers, fruits, and vegetables, proanthocyandins from grape seed extract, tocotrienols from palm oil, and curcumin.Of particular significance is the role of glutathione which is a metabolite of the essential amino acid methionine. Glutathione is stored in the cells of all living organisms. Glutathione is not readily obtainable from food sources, but is available in supplements and can be introduced directly via an IV infusion. Adequate levels of glutathione in the body depend on cysteine, glycine, and glutamic acid. Of these, only cysteine ever seems to be in short supply. Cysteine is derived from methionine, an essential amino acid that transports methyl groups and sulfur into the body to form proteins. To ensure adequate glutathione, one may consume foods rich in sulfur, such as egg yolks, red peppers, and onions. Another way to raise glutathione levels is to supplement the body’s cysteine with N-acetylcysteine or L-cysteine. It is important to note that eating vegetables that naturally contain nicotine, such as bell peppers and tomatoes, may reduce your risk of developing Parkinson’s disease, according to a study that came out in 2013.
CoQ10, phosphatidylserine, L-carnitine, creatine.
NSAIDs, polyphenols, holy basil, thunder God vine, Nexrutine®.
Healthy Plant-Based Diet
“There are so many cellular factors involved with Parkinson’s that we have to enlist every possible means of support to fight it,” notes Eric Braverman, MD, director of New York City-based PATH Medical and an expert on brain-related illnesses. “Nutrition cannot be underestimated, and there’s a whole dopamine diet available to Parkinson’s patients. Even when physicians didn’t know what dopamine was, they treated Parkinson’s symptoms with a diet rich in fava beans (a natural source of levodopa), and it helped.
Suggestions for diet include:
- Keep proteins levels moderate to low.
- Eliminate grains.
- Drink organic green tea.
- Consume foods rich in Omega-3.
- Consume healthy fats such as wild-caught fish, avocado, coconut, pastured butter, and sprouted nuts or seeds like walnuts and flax.
- Consume large amounts of raw and organic fruits and vegetables.
- Consume high fiber foods.
- Stay hydrated with purified water.
- Use cold-pressed oils for cooking and salad dressings.
- Eliminate artificial sweeteners including refined sugar.
- Do not consume alcohol.
Exercises like Tai chi and yoga can help lower stress levels, help with relaxation, and increase energy, balance, and flexibility. According to Washington University School of Medicine, exercise is currently at the forefront in the treatment of Parkinson’s Disease. People with PD retain the ability to participate in many forms of exercise and generally respond to exercise interventions similarly to age-matched subjects without PD. As such, exercise is currently an area receiving substantial research attention as investigators seek interventions that may modify the progression of the disease, perhaps through neuroprotective mechanisms. Many other studies indicate that exercise most likely has many anti-inflammatory, antidepressant and neuroprotective mechanisms that help to improve cognitive health.
Essential Oils for Parkinson’s Disease
The use of essential oils may effectively lessen and calm some Parkinson’s disease symptoms such as depression, sleep issues, skin inflammation and digestive concerns. Helichrysum and frankincense has been shown to reduce inflammation of the brain, and vetiver oil has been found to reduce tremors. Place 4 drops each of frankincense, helichrysum and vetiver oil (12 drops total of essential oils per ounce of carrier) in a carrier oil such as jojoba and apply the blend directly to the skin – the arms or legs or wherever tremors are experienced. Other helpful essential oils include Marjoram, Lavender, Basil, and Clary Sage. Make sure to use high-quality essential oils and not perfumed oils.
Reducing pain, anxiety, insomnia and stiffness has, for centuries, been helped by using acupunture. Currently it seems that it can help slow cell death and attenuate oxidative stress that causes damage to dopaminergic neurons in the substantia nigra. Recent research from the Neurodegenerative Disease Research Group at King’s College in London shows that acupuncture can relieve Parkinson’s disease symptoms by generating a neural response in areas of the brain that are particularly affected by inflammation, such as the putamen and the thalamus.
Heavy Metal Detox
Although the relation between aluminum and neurodegenerative diseases is still controversial, it is related with many brain diseases including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Studies link high concentrations of aluminum and low levels of magnesium in the pathogenesis of CNS degeneration and Parkinson’s disease. Performing several chemical and heavy metal detox programs as well as EDTA chelation can be very useful in removing heavy metals from the body.
Even though much is still unknown about Parkinson’s disease, much can be done to hinder its effects. Most important is getting the proper diagnosis and identification of contributing factors related to each individual. Next is getting proper counseling and education – both conventional and natural. Third is formulating a plan that incorporates lifestyle, diet, and treatment options, with initial and continuing emphasis on natural alternatives that is monitored by experienced health care practitioners. With such a plan, one with Parkinson’s disease can successfully implement a slow-down and management of the disease until new research provides a definitive cure.
If you begin to notice progressive changes in your movement control and moods, it’s important tospeak with a knowledgeable healthcare practitioner about your symptoms. The National Parkinson’s Foundation offers resources for recognizing the disease in its earliest stages and highly recommends to consider testing if such changes as loss of smell, sight, grip, stability, or ability to go to the bathroom and walk normally occur.
Research and References
Kelly Changizi, M.D., assistant professor, neurology and co-director, Center for Neuromodulation, Mount Sinai Parkinson and Movement Disorders Center, New York City; Andrew Feigin, M.D., Parkinson’s disease researcher, the Feinstein Institute for Medical Research, Manhasset, N.Y.; Annals of Neurology, news release, May 9, 2013.
Joe Kakish, Kevin J. H. Allen, Troy A. Harkness, Ed S. Krol, and Jeremy S. Lee. Department of Biochemistry, Drug Discovery and Development Research Group, College of Pharmacy and Nutrition, and Department of Anatomy and Cell Biology, University of Saskatchewan Saskatoon, Canada. ACS Chem. Neurosci.2016, 7, 12, 1671-1680.
Scali, Bruse. Natural Prescriptions for Parkinson’s Disease. Life Extension Magazine. June 2004.
Mayo Clinic. Parkinson’s Disease and Risk Factors.
Hirsch EC, Brandel JP, Galle P, Javoy-Agid F, Agid Y. Iron and aluminum increase in the substantia nigra of patients with Parkinson’s disease: an x-ray microanalysis. J Neurochem. 1991 Feb;56(2):446-51.
Hellenbrand W, Boeing H, Robra BP, et al. Diet and Parkinson’s disease. II: A possible role for the past intake of specific nutrients. Results from a self-administered food frequency questionnaire in a case-control study. Neurology. 1996 Sep;47(3):644-50.
Logroscino G, Marder K, Cote L, Tang MX, Shea S, Mayeux R. Dietary lipids and antioxidants in Parkinson’s disease: a population- based, case-control study. Ann Neur. 1996 Jan;39(1):89-94.
Olanow CW. Attempts to obtain neuroprotection in Parkinson’s disease. Neurology. 1997 Jul;49(Suppl 1):S26-S33.
Schapira AH, Olanow CW. Neuroprotection in Parkinson’s disease. JAMA. 2004 Jan 21;291(3): 358-64.
Teismann P, Tieu K, Choi DK, et al. Cyclooxygenase-2 is instrumental in Parkinson’s disease neurodegeneration. Proc Natl Acad Sci USA. 2003 Apr 29;100(9):5473-8.
Growdon JH, Melamed E, Logue M, Hefti F, Wurtman RJ. Effects of oral L-tyrosine administration on CSF tyrosine and homovanillic acid levels in patients with Parkinson’s disease. Life Sci. 1982 Mar 8;30(10):827-32.
Sandyk R, Pardeshi R. Pyridoxine improves drug-induced parkinsonism and psychosis in a schizophrenic patient. Int J Neurosci. 1990 Jun;52(3-4):225-32.
Li H, Klein G, Sun P, Buchan AM. Dehydroepiandrosterone (DHEA) reduces neuronal injury in a rat model of global cerebral ischemia. Brain Res. 2001 Jan 12;888(2):263-266.
Fahn S. An open trial of high-dosage antioxidants in early Parkinson’s disease. Am J Clin Nutr. 1991 Jan;53(Suppl 1):S380-S382.
Levites Y, Amit T, Youdim MB, Mandel S. Involvement of protein kinase C activation and cell survival/cell cyle genes in green tea polyphenol (-)-epigallocatechin 3-gallate neuroprotective action. J Biol Chem. 2002 Aug 23;277(34):30574-80.
Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci. 2001 Nov 1;21(21):8370-77.
Braverman ER. The Healing Nutrients Within Third Edition. North Bergen. Basic Health Pub. 2003;118-130.
Schulz JB, Henshaw DR, Mathews RT, Beal MF. Coenzyme Q10 and nicotinamide and a free radical spin trap protect against MPTP neurotoxicity. Exp Neurol. 1995 Apr;132(2):279-83.
Calcium, magnesium and aluminum concentrations in Parkinson’s disease. Neurotoxicology. 1992 Fall;13(3):593-600.
Beal MF. Mitochondria, oxidative damage, and inflammation in Parkinson’s disease. Ann N Y Acad Sci. 2003 Jun;991:120-31.
Dzenko KA, Weltzien RB, Pachter JS. Suppression of A beta-induced monocyte neurotoxicity by antiinflammatory com- pounds. J Neuroimmunol. 1997 Dec;80(1- 2):6-12.
Li RW, David Lin G, Myers SP, Leach DN. Anti-inflammatory activity of Chinese medic- inal vine plants. J Ethnopharmacol. 2003 Mar;85(1):61-7.
Mori H, Fuchigami M, Inoue N, Koda A, Nishioka I. Principle of the bark of phel- lodendron amurense to suppress the cellular immune response. Plant Med. 1994 Oct;60(5):445-9.
Sandyk R. L-tryptophan in Neuropsychiatric disorders: a review. Int J Neurosci. 1992 Nov- Dec;67(1-4):127-44.
Parkinson disease and exercise. Compr Physiol. 2013 Apr;3(2):833-48. doi: 10.1002/cphy.c100047.
Current development of acupuncture research in Parkinson’s disease. Int Rev Neurobiol. 2013;111:141-58. doi: 10.1016/B978-0-12-411545-3.00007-9.
Elif Inan-Eroglu and Aylin Ayaz. Is aluminum exposure a risk factor for neurological disorders? J Res Med Sci. 2018; 23: 51. Published online 2018 Jun 6. doi: [10.4103/jrms.JRMS_921_17] PMCID:PMC6040147.