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NIH Study Finds Two Pesticides Associated with Parkinson's Disease

Posted By Administration, Monday, February 14, 2011
Updated: Friday, April 18, 2014


New research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson's disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users.

The study was a collaborative effort conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, and the Parkinson's Institute and Clinical Center in Sunnyvale, Calif.

"Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. "Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson's disease.

The authors studied 110 people with Parkinson’s disease and 358 matched controls from the Farming and Movement Evaluation (FAME) Study ( to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. FAME is a case-control study that is part of the larger Agricultural Health Study (, a study of farming and health in approximately 90,000 licensed pesticide applicators and their spouses. The investigators diagnosed Parkinson's disease by agreement of movement disorder specialists and assessed the lifelong use of pesticides using detailed interviews.

There are no home garden or residential uses for either paraquat or rotenone currently registered. Paraquat use has long been restricted to certified applicators, largely due to concerns based on studies of animal models of Parkinson's disease. Use of rotenone as a pesticide to kill invasive fish species is currently the only allowable use of this pesticide.

"These findings help us to understand the biologic changes underlying Parkinson’s disease. This may have important implications for the treatment and ultimately the prevention of Parkinson's disease," said Caroline Tanner, M.D., Ph.D., clinical research director of the Parkinson’s Institute and Clinical Center, and lead author of the article.

The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit Subscribe to one or more of the NIEHS news lists ( to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs,

Reference: Tanner CM, Kamel F, Ross GW, Hoppin JA, Goldman SM, Korell M, Marras C, Bhudhikanok GS, Kasten M, Chade AR, Comyns K, Richards MB, Meng C, Priestly B, Fernandez HH, Cambi F, Umbach DM, Blair A, Sandler DP, Langston JW. 2011. Rotenone, paraquat and Parkinson’s disease. Environ Health Perspect; doi:10.1289/ehp.1002839 [Online 26 January 2011].

Source: National Institutes of Health (NIH). February 11, 2011. NIH study finds two pesticides associated with Parkinson's Disease.

Tags:  NIH  parkinson's disease  toxins 

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Staying Ahead of the Curve on Parkinson's Disease

Posted By Administration, Monday, August 9, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO 4090198486_ef681509fb_o   

More recently, doctors are being urged to treat dementia more aggressively in Parkinson's patients, as it would optimize quality of life for the patients and their caregivers. It is established that one third of patients with Parkinson’s disease experience dementia. Cognitive impairments are the hallmark features, including decreased attention span, executive functioning and memory deficits. Obtaining a legitimate diagnosis of dementia can be quite tricky in that symptoms may widely fluctuate and therefore the diagnostic instruments that physicians use to diagnose Parkinson’s dementia may not always give reliable results.  Research is conflicting at this point as to which is the best medical agent to use in this population. 


Optimize Diet 

There are multiple safe nutritionally oriented treatments that patients may engage in to help prevent early onset dementia as it is related to Parkinson’s disease.  First and foremost, optimization of diet is critical. There is much research to suggest that a diet that is high on the glycemic index scale can exacerbate dementia.  Insulin resistance, associated with a diet that is chronically high on the glycemic index, has been associated with Alzheimer’s disease. The connection has been labeled type 3 diabetes by some. (See my published article under the References section of my website on this topic).

Low Glycemic Index, No Pesticides, No MSG 3013741860_ab25d8ce03_z  

Eating organic, MSG and pesticide free foods that can exacerbate both Parkinson’s as well as dementia is important.  Remember that MSG can trigger glutamate receptors in Parkinson’s and non-Parkinson’s patients alike.  Following a Mediterranean style diet that is high in unheated extra virgin olive oil, fish and poultry, nuts, vegetables, low glycemic index fruits, whole grains that are gluten free and unprocessed foods is key.   

Just Do It


3218300813_2a10d6453c_bAdding a daily exercise component is imperative. Exercise can trigger dopamine levels to rise, help with coordination, drive down cortisol, improve insulin resistance, and help with mental acuity. These are all essential when hoping to help prevent dementia and improve Parkinson’s symptoms. Exercise should include weight bearing exercise as well as core bodywork.



The adrenal hormone DHEA has been shown to boost dopamine levels. There is also a significant amount of research pointing to DHEA helping with improvement in memory in dementia patients. DHEA is ever present in brain tissue and helps to offset the negative effects of cortisol.  It is, however, a precursor to many of the other hormones and needs to be used judiciously and under medical supervision. 

Follow an Anti-Inflammatory Program

Low grade chronic inflammation may be a precursor to neurodegenerative disease. An excellent anti-inflammatory program, including diet and supplements may help to quiet the inflammation down. 

Polyphenols, excellent antioxidants found in green tea, have recently been studied to see if they modify the course of Parkinson’s.  The Chinese study enrolled 410 untreated people with Parkinson’s disease and were randomized to receive 0.4g, 0.8g, or 1.2 g of green tea polyphenols daily. As a reference, 2 cups of green tea contain approximately 300mg of polyphenols.  At 6 months a significant improvement was noted in each dosage category based on the Unified Parkinson's Disease Rating Scale. At 12 months, however, unexplainably, the scores did not differ from placebo. Improvements were more profound for those with a greater severity of disease.  There were no notable side effects except for insomnia for those not accustomed to green tea intake. 

The reduction of oxidative stress on neurologic tissue in Parkinson’s as well as dementia patients is important.  Utilization of polyphenols, vitamin C, tocotrienols, bioflavanoids, proanthocyandins from grape seed extract, coenzymeQ10, and curcumin may have a beneficial effect.   

Tags:  parkinson's disease 

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Glutathione and Parkinson's Disease

Posted By Administration, Wednesday, June 16, 2010
Updated: Friday, April 18, 2014


by Zina Kroner, DO

Glutathione has been used to help alleviate some of the symptoms of Parkinson's disease.  Glutathione is a small peptide made up of three amino acids – glutamic acid, cysteine and glycine.  The active group of this peptide is the sulfhydryl or thiol (SH) group, a bond formed between the amine (NH2) group of cysteine and carboxyl group (COOH) of glutamic acid.  

In the human body, glutathione occurs in two forms:

1. the majority of glutathione is present in the reduced form (GSH) 

2. and a small percentage of it is present in the oxidized form (GSSG or glutathione disulphide).  

The reduced form of glutathione is the active form, and it donates its electrons to highly reactive molecules like free radicals, peroxides and superoxides to stabilize them.  The process is called neutralizing the free radicals.  During this process, glutathione is oxidized and the harmful free radicals are reduced and neutralized.  

The free radicals, peroxides and superoxides are unstable and highly reactive molecules formed as part of normal metabolic processes.  These can literally snatch electrons from the surrounding molecules (like DNA, cell membrane and other cell organelles) to stabilize themselves, making the other molecules unstable, that repeats the process, setting off a chain reaction producing more unstable molecules, which can easily result in the collapse of the cell membrane and the membranes of other cell organelles.  

Glutathione is synthesized internally in the liver and does not need to be supplied in the diet.  A balanced diet has all the necessary precursors for the internal synthesis of glutathione. The ability of glutathione to neutralize these harmful free radicals makes it a major powerful intracellular antioxidant.  For glutathione to be active, it needs to be kept in the reduced form in the blood.  The oxidized glutathione is immediately recycled back to its reduced form by an enzyme called glutathione reductase, and glutathione is again ready to donate electrons to free radicals.  The reduced and oxidized forms of glutathione together are called a redox couple.  

Glutathione preserves the integrity and fluidity of the cell membrane.  It is available in the cells in relatively high concentrations in the reduced form.  Depletion of glutathione levels in the cells leads to excessive formation of reactive oxygen species which puts more stress on the cells.  This is called oxidative stress.  This increased oxidative stress causes the cell organelles to burn out gradually and lead to eventual cell death.  Increased oxidative stress plays a major role in increasing the risk for a variety of cancers, inflammatory and degenerative diseases.  

Glutathione and Parkinson’s disease

Glutathione has been extensively studied for its role as an antioxidant in Parkinson’s disease, an adult-onset progressive neurodegenerative disorder.  In Parkinson’s disease, there is a selective degeneration of dopaminergic neurons in the substantia nigra of midbrain.  Substantia nigra is the part of the brain responsible for physical movement (like walking, moving hands and legs, etc).  Hence, degeneration of dopaminergic neurons in substantia nigra causes physical symptoms like tremors, bradykinesia (slow movements), muscle stiffness and loss of automatic movements in Parkinson’s disease. 

Progressive degeneration of dopaminergic neurons in substantia nigra is caused by:

1. Excessive formation of reactive oxygen species (ROS)

2. Increased oxidative stress accumulation of abnormal proteins in the cells

3. Drastic depletion of glutathione (GSH) levels 

Dopaminergic neurons are more prone to oxidation due to a combination of factors like the metabolism of dopamines, auto-oxidation, increase in iron levels, decrease in glutathione levels and excessive formation of ROS. Oxidative stress needs to be reduced to slow down the progression of symptoms of Parkinson’s disease. Research suggests that oxidative stress can be effectively reduced by increasing the glutathione levels or slowing its degradation in the substantia nigra.

In the body, glutathione is synthesized from 3 amino acids – glutamic acid, cysteine and glycine.  The availability of cysteine is the deciding factor (or rate limiting factor) in the synthesis of glutathione.   

Dr. Perlmutter’s Research

Dr. David Perlmutter, a board certified neurologist from Naples, Florida, started using intravenous glutathione in 1998 for his Parkinson's patients after he did extensive research on Parkinson’s disease and effects of supplemental glutathione on improving the symptoms of Parkinson’s disease.  He is the pioneer in using intravenous glutathione in the treatment of Parkinson’s disease.  His research opened new doors in the treatment of Parkinson’s disease and other neurodegenerative diseases.  Dr. Perlmutter has successfully used intravenous glutathione in patients with significant improvement in the symptoms.  Although glutathione treatment cannot prevent the occurrence of symptoms, it significantly slows down the occurrence of symptoms with improvement in the existing symptoms.

Glutathione supplements do not directly raise the dopamine levels in the brain, instead they improve the efficiency of dopamine in the brain and also increase the sensitivity to dopamine and serotonin.

Glutathione Treatment

Glutathione supplements are available in oral, intramuscular, and intravenous forms.

Oral – Glutathione is available in capsule form and also precursors of glutathione are available in powder form to be used as oral supplements.  However, recent research suggests that glutathione is digested in the gastrointestinal tract and broken down to its constituents even before it enters the blood.  So, oral glutathione supplements are not effective.  I prefer to give the natural precursors to glutathione to my patients.  

Intramuscular – Glutathione injections are also given intramuscularly.  These are mildly effective according to anectodal data.

Intravenous – Glutathione injections given intravenously are the best and most effective form of supplementation. Not only does it reach the brain and potentially improves Parkinson’s symptoms, it also reaches the liver and helps in a variety of functions like neutralization of free radicals via detox pathways.  Standard dosage for glutathione supplements is 1400 milligrams mixed with saline, given intravenously for ten minutes three times a week.  

Contraindications and Safety:

Glutathione is in the GRAS (generally regarded as safe) category, according to the FDA.  However, if you are taking other prescription medicines, glutathione supplements may reduce the efficacy of these medicines.  This is because glutathione plays a role in the detoxification function in the liver, removing foreign substances from the body.  Prescription medicines may therefore be removed from the system, thus reducing their efficacy



1.Hauser, RA, Lyons, KE, McClain, T, et al. Randomized, Double-Blind, Pilot Evaluation of Intravenous Glutathione in Parkinson’s Disease. Movement Disorders. 2009;24(7): 979–983.

2.Sechi, G, Deledda, MG, Bua, G, et al. Reduced intravenous glutathione in the treatment of early Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996;20(7):1159-70. 

3.Perlmutter, D. “New Advances in Parkinson’s Disease.” From Last updated 2004, currently unavailable. Chapter found at

4. Bharath S, Hsu M, Kaur D, Rajagopalan S, Andersen JK, Glutathione, iron and Parkinson's disease. Biochem Pharmacol. 2002 Sep;64(5-6):1037-48.

5. Martin HL, Teismann P. Glutathione--a review on its role and significance in Parkinson's disease. FASEB J. 2009 Oct;23(10):3263-72. Epub 2009 Jun 19.

6. Chinta SJ, Andersen JK. Redox imbalance in Parkinson's disease. Biochim Biophys Acta. 2008 Nov;1780(11):1362-7. Epub 2008 Mar 4.

Tags:  glutathione  parkinson's disease 

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