Category: Spring, 2017 Issue

What is the Gut-Brain Axis?

We have long known that constipation is a common non-motor feature of Parkinson disease (PD) (1). One study of 7000 men over a period of 24 years showed that those with initial constipation (less than one bowel movement per day) had a three-fold risk of PD after an average of 10 years (2).  Thus, unexplained and persistent constipation in adults is associated with an increased risk of PD: 1/3 will have constipation a year prior to PD diagnosis, and 2/3 will have constipation after diagnosis (3,4).  Ultimately, greater than 80% of PD patients will have GI dysfunction of some type early in disease.  Investigators have tried to explain this for many years.  In the 1970s, one idea was the “slow transit hypothesis,” the idea that slowing down of the gut allowed the absorption of toxins which might trigger PD (5).  Though this fell out of mainstream discussion, and may have seemed an oversimplification, the idea is not so far from current thought.

To understand what we now call the gut-brain axis, it helps first to know that your gut, or your digestive tract, contains a lot of bacteria, tens of trillions of them. Largely because of the population in the gut, there are more bacteria than human cells in our bodies.   One way they get away with this is that they tend to be much smaller than our cells.  Bacteria tend to be about 0.1-5 micrometers in size (millionths of a meter).  Human cells range from about 10 to 100 micrometers, so our cells tend to be many times bigger than bacteria.  And, as long as they stay in specific locations, bacteria work with, not against us; but when they go to the wrong place, illness occurs: think diarrhea, nausea, vomiting, etc.  Under ideal circumstances, among several jobs, many gut bacteria help us to digest food and collect certain nutrients we otherwise would not be able to extract or produce.  In exchange for this, they are given food, shelter, and a chance to move along to some other environment – a great reason why we should all wash our hands when leaving a restroom.  Half of the dry weight of our stool is bacteria, and if it winds up travelling the fecal-oral route, e.g., hand to doorknob to someone else’s hand to mouth, the consequences can be bad.  A few minutes spent in a busy public restroom will alert you that hand washing is not a universal practice.

A healthy gut requires a healthy population of bacteria.  To understand this a little better, let’s define a few terms.  A single bacterial cell is a microbe.  The terms microbiome and microbiota are used a lot when discussing this topic, and for our purposes, they are the collection of bacteria in the gut.  There is a group of over a thousand different species of microbes in the gut.  Their library of unique genes is over 100 times larger than the number of genes in a person’s DNA library.  That is a considerable genetic power. The balance among types of organisms present in the gut is important as well.  When there is too much or too little of one type or another, this is imbalance, which we call dysbiosis.  Dysbiosis has been linked to inflammation, metabolic disease, certain cancers, and neurologic disease.

Dysbiosis can cause disease because one of the roles of a healthy microbiome is to regulate gut and bodily inflammation.  They do this by the release of tiny chemical messengers.  In PD, delayed gastric emptying and slow transit of stool may increase the over-production of some types of bacteria, which not only upsets the local balance, but creates the symptoms of gas, colic, and inflammation (6,7).  This makes it even easier to get their messengers into the bloodstream.  Further, as if pretending to be nerve cells, bacteria can produce neurotransmitters and neuromodulators such as GABA, serotonin, dopamine, or short-chain fatty acids (8).  This may allow bacteria to communicate with our nervous system (9).

It also goes the other way.  The drugs PD patients take may influence the microbiome (10).  One study evaluated 197 PD patients and 130 controls without PD.  They were able to identify the types and numbers of microbes taken from stool of each person.  Investigators took into account 39 potential confounders such as medications, diet, GI symptoms, and demographics.  The gut microbiome was different in PD, and multiple families of bacteria were much more robust.  In the PD patients there were also different balances corresponding to different drugs, such as COMTs and anticholinergics.  In the study, the effect of L-dopa could not be separated out as 90% of PD patients were taking the drug.

Another reason dysbiosis may be a risk factor for disease is that our gut bacteria protect us by breaking down xenobiotics (herbicides, flame retardants, insect repellents we encounter in the environment).  Living in agricultural settings is a known risk factor for PD and this may explain why.  In the lab we know that xenobiotics can cause the death of dopamine-producing cells and motor abnormalities in animal models of PD.  Therefore, dysbiosis might expose humans to toxins which would otherwise have been broken down.  The toxins may trigger disease.  The evidence that this may be happening is supported by the observation that the pathologic hallmark of PD, the Lewy body, may be seen in neurons of the gut years prior to the development of motor symptoms of PD, and may be seen in the gut of lab animals given xenobiotics.   These observations helped lead to the hypothesis that PD starts in the gut (11).

The most common protein in Lewy bodies is called alpha-synuclein (aSyn). This little protein is found at the point of communication between neurons called the synapse.  The job of aSyn is to stabilize little bags of dopamine (vesicles), and to help control synaptic plasticity (the formation of new neural pathways in the brain involved with learning).  This protein, like all others, has a very specific three-dimensional shape which it must maintain in order to work.  This is similar to a key, which must be shaped a certain way to fit into a lock and turn the tumblers.  If the key is bent, it will not work.  If aSyn is misfolded, it does not work, dopamine is not released, and new pathways are not made.  It may be that exposure to certain toxins triggers the misfolding of aSyn, or there may be other factors such as gene mutations.  Whatever the cause, misfolded aSyn may behave very much like a prion, where one bad protein warps others of the same class (think one bad apple spoils the whole bunch).

Testing this idea, researchers exposed lab mice to the pesticide rotenone, which has long been associated with risk of PD in humans (12).  The mice developed misfolded aSyn in the gut.  Abnormal aSyn in the gut activates immune cells in the brain known as microglia (13).  These microglia are then primed to destroy neurons containing abnormal aSyn.  This is one of the ways PD patients lose neurons.  If present long enough, misfolded aSyn will also travel up the long vagus nerve to the brainstem, where it will spread upwards in the same way the protein spreads in humans with PD.  Of note, mice and men with a severed vagus nerve have a lower risk of PD.

In order to test the effects of microbes and molecules on animals, researchers relied on the first gene abnormality identified in PD, the PARK1 gene (14).  The PARK1 gene causes the overproduction of aSyn.  When the gene is present in mice, they manifest a form of parkinsonism very early in life.  However, if the mice are treated with antibiotics to kill the microbiome, motor symptoms of disease become minimal, and there is reduced activation of microglia (15).   This led the investigators to raise PARK1 mice in a sterile environment with no microbiome.  These mice too, had minimal motor issues. When colonized with a microbiome (transplanted feces) from humans without PD, the mice were unchanged.  When given the microbiome from PD patients, the mice developed impaired motor function.  This supports the “two-hit” hypothesis, that PD is likely caused by genes and environment.  In other words, if someone is predisposed to develop PD because of genes, they may not do so until exposed to some trigger such as a toxin.   Researchers were also able to normalize the affected mice by adding normal chemical messages such as short chain fatty acids that a normal microbiome would produce.

Thus, the gut-brain axis raises several interesting questions:

  • Would a simple stool test reveal risk to PD and other diseases?
  • Would understanding the microbiome help physicians in selecting the appropriate drugs for people with PD, or lead to the formation of new treatments?
  • Would changing the microbiome improve disease for people with PD?

If you know, tell me.  Otherwise, stay tuned.  This is a big topic in PD.

 

Stylistic and copy editing of this article, as well as helpful insights, by Sarah Savard, RN, and Liz Stamey, RN.

 

REFERENCES

  1. https://mainepdnews.org/2016/06/12/constipation-in-pd/
  2. Abbott.  Neurology 2001; 57: 456–62
  3. Pfeiffer RF.  Gastrointestinal dysfunction in Parkinson’s disease. Parkinsonism Relat Disord 2011; 17: 10-15.
  4. Mulak A, Bonaz B.  Brain-gut-microbiota axis in Parkinson’s disease. World Journal of Gastroenterology.  2015;21(37): 10609-10620.
  5. Singharam.  Lancet 1995; 346: 861–64.
  6. Hasegawa, et al.  Intestinal dysbiosis and lowered serum lipopolysaccharide-binding protein in Parkinson’s disease.   PLoS ONE 2015;10, e0142164.
  7. Keshavarzian, et al.  Colonic bacterial composition in  Parkinson’s disease.  Mov. Disord. 2015; 30: 1351–1360.
  8. Lyte M.  Microbial endocrinology: Host-microbiota neuroendocrine interactions influencing brain and behavior.  Gut Microbes 2014; 5:381-389.
  9. Mayer , et al.  Gut/brain axis and the microbiota.  J Clin Invest 2015; 125: 926-938.
  10. Hill-Burns et al.  Parkinson’s Disease and Parkinson’s Disease Medications have Distinct Signatures of the Gut Microbiome.  Movement Disorders. 2017:00: (00)epub online Feb, 2017.
  11. Braak H.  Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiology of Aging, 2003 24: 197.
  12. Pan-Montojo, et al.  Progression of Parkinson’s disease pathology is reproduced by intragastric administration of rotenone in mice.  PloS One  2010;5:e8762.
  13. Erny, et al.  Host microbiota constantly control maturation and function of microglia in theNS. Nat. Neurosci. 2015; 18: 965–977.
  14. Polymeropoulus, et al.  Mutation in the α-Synuclein Gene Identified in Families with Parkinson’s Disease.  Science 1997: 276 (5321);2045-2047.
  15. Sampson et al.  Gut Microbiota Regulate Motor  Deficits and Neuroinflammation in a Model of Parkinson’s Disease.  Cell 167, 1469–1480, December 1, 2016.

 

Boxing is a Big Hit

In the Summer 2016 issue of MPDN we included an article titled Balance in Parkinson Disease (1) which noted that among various interventions, boxing training may be useful in PD.  The article summarized a boxing trial published in the journal NeuroRehabilitation (2) which described patients working with certified trainers at the University of Indiana who focused the participants on a circuit of stretching, punching bags, resistance exercises, and aerobic exercise training.   Before and after completion at many weeks, those involved demonstrated significant improvements in gait velocity, endurance, balance, mobility, and quality of life.  The investigators were building upon an earlier boxing intervention trial published in the journal Physical Therapy (3).  Boxing and exercise at large are part of an ongoing effort over the last few decades to identify physical approaches that will not only improve mobility and dexterity, but decrease fall risk, and possibly slow down disease.  More on various exercise approaches may be found in the Fall 2016 article by Dr. Kleinman (4).

Building in this direction, in 2016 Cate Parker, MS, RN, CEP, Director of Mid Coast Center for Community Health & Wellness, formed a team of specialists and began a series of ongoing exercise programs at the Landing YMCA in Brunswick (5).  There are three classes: a general exercise class for people with PD, a class for graduates of the LSVT program, and Rock Steady Boxing (RSB).  I can say anecdotally that feedback from those taking RSB has been very positive.

Cate Parker is happy these programs are taking off, and would stress that physical activity has many potential benefits in PD, including improved strength, mobility, flexibility and balance.  “To obtain the greatest benefits, patients must commit to daily exercise for life, just like medicine.  Many of our support group participants commented on how difficult it was to exercise on their own or how they were challenged to maintain any improvements they achieved during the LSVT program.  The group asked for help.  As a result we investigated the best exercise options and decided to collaborate with the YMCA to develop a multi-option approach.  Exercise is only helpful if you ‘do it,’ so we decided to provide different options for different people. Our programs include LSVT, dance, yoga and boxing.  Almost any exercise is good medicine for someone with Parkinson’s disease.”

Boxing coaches from right to left are Zach Hartman, Kristy Rose Follmar, and Jennifer Anderson.

RSB trainers Zachary Hartman, EP, and Jennifer Anderson, PT, MPT, flew to Indianapolis to learn the technique and become certified instructors.  In a written response to questions about the programs, they note that “Parkinson’s specific programs at the YMCA Brunswick Landing offer a range of activities for those of all ability levels.  The staff emphasizes safety of each of the participants, while pushing each individual to their intensity threshold in order to help them reach their full potential.  After the Rock Steady Boxing class, participating athletes have reported immediate improvements in symptoms such as bradykinesia, posture, and fine motor skills. One boxer reported that he was able to type for the first time in a few years.  Other boxers have been able to learn to transfer off the floor independently.  A few participants have been quick to report that the high intensity exercise has improved their ability to sleep at night.  Participants not only report improvements in physical strength, balance, and range of motion; but they also appreciate improvements in mental and emotional health. The exercise programs allow for great comradery, and they truly feel like they are members of a team working together in order to improve quality of life. The group members are quick to encourage one another.  Staff members have heard them commenting to each other on the improvements they can see from one week to the next.  Individuals may have good or bad days but as a whole the group is always improving and having fun while doing it.  These exercise groups are intentionally not focused on what the athletes cannot do, but instead on what they can do.  That positive atmosphere is therapeutic in itself.”  Boxing classes for PD take place from 1:30 to 3:30pm, Tuesdays and Thursdays (6).

To learn more about boxing in Brunswick, see the online articles and videos that have been produced lately (7,8,9,10).

footnote:  None of the participants were punched in the making of this article.

REFERENCES (URLs accessed 3/25/17)

  1. https://mainepdnews.org/2016/06/07/balance-in-parkinson-disease/
  2. Combs et al., Community-based group exercise for persons with Parkinson disease: a randomized controlled trial. NeuroRehabilitation. 2013;32(1):117-24.
  3. Combs, et al, Boxing Training for Patients WithParkinson Disease: A Case Series Physical Therapy. 2011;91(1):132-142.
  4. https://mainepdnews.org/2016/09/24/exercise-and-parkinsons-disease/
  5. http://www.midcoasthealth.com/wellness/parkinsons-disease/
  6. https://docs.google.com/viewerng/viewer?url=http://bathymca.org/wordpress/wp-content/uploads/2014/12/Class-schedule-Spring-2017-2.pdf&hl=en_US
  7. http://www.timesrecord.com/news/2016-12-21/Front_Page/Hitting_back_at_Parkinsons.html
  8. http://bangordailynews.com/2017/03/24/next/parkinsons-patients-are-fighting-back-against-the-disease-literally/?goal=0_715eed3192-69816d43f8-82460469 BDN article with video
  9. https://youtu.be/XR5spbBbwao Maine Public video
  10. http://www.sunjournal.com/news/lewiston-auburn/2017/01/14/new-way-battle-parkinsons-boxing/2050682#.WHvsfypcXcU.email  (by subscription)

200th Anniversary of An Essay on the Shaking Palsy

In 1817 James Parkinson, a member of the Royal College of Surgeons in London, published his famous paper, An Essay on the Shaking Palsy (1).  In this document he described “shaking palsy (paralysis agitans).”*  This term was used in reference to a partial description given by the Greek physician Galen in the second century A.D.**  Parkinson’s general description for recognizable cases was that of “involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported: with a propensity to bend the trunk forwards, and to pass from a walking to running pace…”  This is, of course, a state of advanced disease with tremors, rigidity, subjective weakness, flexion of posture, and festination of gait.   However, he was a student of history, a physician, scientist, and paleontologist.  He knew the value of taking a detailed account of the natural history of disease, and meant not just to describe obvious or striking examples, but also to give physicians and science at large a formal understanding of the genesis of paralysis agitans.  He took care to make others understand the indolent and secretive inception of this condition, which he explained is difficult to establish.

“So slight and nearly imperceptible are the first inroads of this malady, and so cextremely slow its progress, that it rarely happens, that the patient can form any recollection of the precise period of its commencement.”

He described history taken from his own patients, and in two cases, histories taken from sufferers he met on the street.  The patients discussed as case examples included a 50 year-old gardener, a 62 year-old prior attendant at a magistrate’s office who, after eight years had become disabled and was the “inmate of a poor house,” a 65 year-old ex-convict of a Spanish prison, a 55 year-old man whose onset had been during an acute inflammation five years earlier, and a 72 year-old man who’d lived a life of temperance.  He finally described a man he had simply observed walking in a public street.  With these histories and observations, Parkinson carefully described the relentless forward march of disease in a detailed fashion reflective of his classical education.  However, there was also embedded in his lengthy paper the soul of the patient, and the agony of his era, when no western medicines were known to be of benefit.  Parkinson gave voice to his patient “harassed by this tormenting round,” when trying to simply eat with utensils.  He described a sense of loss and the intensity of effort devoted to living with this disease.

“The submission of the limbs to the directions of the will can hardly ever be obtained in the performance of the most ordinary offices of life…Walking becomes a task which cannot be performed without considerable attention.  The legs are not raised to that height, or with that promptitude which the will directs, so that the utmost care is necessary to prevent frequent falls.”

Parkinson discussed multiple motor and later non-motor issues characteristic of the disease which are commonly reported today.  He reviewed key signs of disease at length and proposed a mechanism for paralysis agitans which correctly identified the brainstem as a focus of spread.

“A diseased state of the medulla spinalis, in that part which is contained in the canal, formed by the superior cervical vertebrae, and extending, as the disease proceeds, to the medulla oblongata.”

This work called attention to a disease which had not been described or categorized in western medicine and opened the door to 200 years of progress in the understanding, treatment, and hopefully prevention and cure.  In the days of James Parkinson there were no medications in Europe known to improve symptoms.  His patients were doomed to a progressive disability and no social safety net.  Those without family able to care for them presumably died in the poor house, the prison, or on the street.   Even in the United States, as late as the pre-levodopa era of the 1960s, some hospitals contained Parkinson’s wards in which patients who had lost the ability to walk passed their days in bed, and once completely deconditioned, often succumbed to aspiration pneumonia or deadly blood clots caused by immobility.  The dawn of levodopa treatments ended those wards.  Life expectancy of most PD patients became that of the general population, a huge victory which cannot be understated.  Though the disease still has the potential to be devastating, we now live in a time in which we understand much of the genetic and molecular mechanisms of this incredibly complicated syndrome affecting so many systems of the human mind and body.  Medications have advanced and deep brain stimulation is in common use.  Ongoing trials of vaccines, monoclonal antibodies, stem cells, and other interventions give a great deal of hope.  I thank James Parkinson and appreciate his discipline and deeply scientific approach, as well as his profound empathy for those who suffer under the disease of his namesake.

 

FOOTNOTES

* It was not Parkinson, but the French physician Charcot who would in 1850 apply Parkinson’s name as eponym.

**Ancient Ayurvedic texts refer to the syndrome of PD as Kampavata, though it appears this was unknown in western literature at the time of An Essay on the Shaking Palsy.

 

REFERENCE

  1. Sherwood, Neely, and Jones (London, 1817).

http://neuro.psychiatryonline.org/doi/abs/10.1176/jnp.14.2.223?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed

 

 

 

 

Portland Area Atypical Parkinson’s Support Group

by Janet Edmunson

Occasionally, someone originally diagnosed with Parkinson’s may later have the diagnosis changed to one of the atypical Parkinsonian disorders.  These include progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA) and Lewy Body Dementia (LBD).  While each of these have some movement and non-movement symptoms similar to Parkinson’s disease (PD), they also have other distinctive symptoms that are difficult to manage and deal with for the person affected and the caregiver.  In addition, PSP, CBD and MSA progress much more quickly than PD and LBD. 

Since their needs are unique, Barby Johnson and I started an atypical Parkinson’s support group here in Maine over 10 years ago.  Barby’s husband died of PSP and mine of CBD. 

Our group meets four times a year in Falmouth on Sundays from 1 p.m. to 3 p.m.  During the meeting we usually go around the room and allow every family to discuss what’s been happening since the last meeting and bring up any issues and concerns they are facing.  The group has a positive attitude and addresses issues in a supportive, uplifting way. 

If you are dealing with one of these diseases, we’d love to have you join us.  You can email or call us to get information on the dates of our upcoming meetings as well as directions to our meeting location in the MaineHealth Learning Center at 5 Bucknam Road in Falmouth. 

–Janet Edmunson (207) 799-4963 or janet@janetedmunson.com

–Barby Johnson (207) 633-0881

Camp Lejeune

In January the Public Health website of the U.S. Veterans Affairs (1) reported that “From the 1950s through the 1980s, people living or working at the U.S. Marine Corps Base Camp Lejeune, North Carolina, were potentially exposed to drinking water contaminated with industrial solvents, benzene, and other chemicals.”  The VA has established a presumptive service connection for disability claims of Veterans, Reservists, and National Guard members exposed to contaminants in the water supply at Camp Lejeune from August 1, 1953 through December 31, 1987, if they later developed PD or one of seven malignancies.  The new rule will be in effect March 14, 2017, and is funded by an allocation from the final days of the Obama administration.

This is part of an ongoing story.  Contamination was tragically not detected for decades.  Since the base opened in 1942, up to 30 supply wells were used on the 236 square mile base.  Water from the supply wells was mixed at treatment plants before being used by residents of the base.  Reportedly, tests of sampled Camp Lejeune water from 1980-1985 detected toxic solvents.  Contamination points were identified as a landfill on the base used for chemical dumping, leaks from underground storage tanks, and “waste disposal practices” (2).  The main contaminant in the system was trichloroethylene (TCE) with a maximum detected level of 1,400 µg/L, followed by tetrachloroethylene (PCE) at 100 µg/L, benzene, and breakdown products of TCE: trans-1,2-dichloroethylene (DCE) and vinyl chloride.  U.S. maximum contaminant levels (MCL) for TCE, PCE, and benzene are 5 µg/L. TCE, vinyl chloride and benzene are all classified as a human carcinogens (3,4,5).  PCE is a “likely” or “probable” human carcinogen.  TCE exposure has been identified by multiple authors as a risk factor for PD (6).

The Environmental Protection Agency (EPA) placed the site on the Superfund program’s National Priorities List (NPL) in 1989 because of contaminated groundwater, sediment, soil and surface water.  Next, the EPA, the North Carolina Department of Environment and Natural Resources (NCDENR), and the US Navy investigated the site and “took steps” to clean the base.  For some time since, the wells have been closed.  The problem is not over, and is not small.  Multiple sources cite a Department of Veterans Affairs estimate that up to 900,000 service members might have been exposed to the contaminated water.  It is not clear what number of family members or civilian workers were exposed.  And, diseases such as those reported may be many years in the making before one is even aware they are sick.  However, following discovery of clusters of cancers and other illnesses among those who lived, served, and worked on the base, increasing calls came for investigation.  Grassroots efforts to acknowledge the problem began, multiple legal actions were taken, and political attention was given.  In spite of these efforts, the issue was not as widely known until 2008 when Congress ordered the VA to notify exposed veterans of the problem.  There were, of course, calls to treat those with conditions related to these exposures.

In 2012 the Camp Lejeune Health Care Bill, signed into law by President Obama, covered 15 conditions related to contaminated water exposure, most of them cancers.  The law states “VA provides cost-free health care for certain conditions to Veterans who served at least 30 days of active duty at Camp Lejeune between January 1, 1957 and December 31, 1987.”  Eligible veterans were allowed to enroll in VA health care and receive medical services for covered health conditions at no cost.  Families of vets who lived on the base were included.

This 2017 decision taking effect 3/14/17 is an amendment to the 2012 law and has come after intense scrutiny by several government agencies.

Data collected on those who lived or worked at Camp Lejeune by the Agency for Toxic Substances and Disease Registry (ATSDR) (7) noted that civilian workers would likely have had the highest exposure to toxins in the the water.  A study compared 4,647 Camp Lejeune workers with a similar number from the same time period at Camp Pendleton in California.  These full time civilian employees started working at either base between April 1973 and December 1985.  Researchers carefully screened workers and asked about water consumption and bathing (some showered on the base).  In order to give enough time to detect the slow development of some diseases, they evaluated the health these large cohorts from 1979-2008, noting among multiple other serious health issues, higher rates of PD among the Camp Lejeune civilian workers with higher cumulative exposures to the contaminants.

Federal Register (8) published an online article in January stating this final rule establishes a presumption that Parkinson’s disease, which had originally not been included in the Camp Lejeune Act, is a condition for which there is “strong evidence of a causal relationship and evidence that the condition may be caused by exposure to the contaminants.”  Parkinson’s disease was included as a presumptive cause of disability due to a recommendation made by the Institute of Medicine (IOM), part of the National Academies of Science, in a 2015 report (9).

In Maine there are over 127,000 veterans (10).  At the time of writing this article, I have been unable to determine by online sources or by inquiry to the Department of Veterans Affairs the number of Mainers who served, lived, or worked at Camp Lejeune.

 

REFERENCES

1. http://www.publichealth.va.gov/exposures/camp-lejeune/
2. Bove, et al., Mortality study of civilian employees exposed to contaminated drinking water at USMC Base Camp Lejeune: a retrospective cohort study. 2014;13:68.
3. Environmental Protection Agency (EPA): Final health assessment for TCE. 2011.
4. Guha, et al., Carcinogenicity of trichloroethylene, tetrachloroethylene, some other chlorinated solvents, and their metabolites. Lancet Oncol 2012, 13:1192–1193.
5. Chiu, et al., Human health effects of trichloroethylene: key findings and scientific issues. Environ Health Perspect 2013, 121:303–311.
6. Locke, et al., Solvents and Parkinson disease: a systematic review of toxicological and epidemiological evidence.Toxicol Appl Pharmacol. 2013 Feb 1;266(3):345-55.
7. https://www.atsdr.cdc.gov/sites/lejeune/qa_healthstudyactivities.html
8. https://www.federalregister.gov/documents/2017/01/13/2017-00499/diseases-associated-with-exposure-to-contaminants-in-the-water-supply-at-camp-lejeune
9. https://www.nap.edu/catalog/18991/review-of-va-clinical-guidance-for-the-health-conditions-identified-by-the-camp-lejeune-legislation
10. http://www.maine.gov/veterans/about/media-kit/demographics.html

Stride. Walk. Jog. Run.

by Hunter de Garmo

I am an Husband, Son & soon to be Father (April 4th is coming soon!!!) living in Wiscasset, Maine and I will be running a 50K  (31 miles) on the indoor track at the Boothbay Region YMCA in support of the Maine Parkinson Society.  100% of the proceeds will go to this organization which helps not only my Mom Barbara, but hundreds of Mainers with PD pay for exercise classes, medication and exercise therapy through the Maine Parkinson Society (MEPS) Respite Care program.

STRIDE will take place on Tuesday May 2nd, 2017 and I will be running my ultra distance of 50K from 8am – 4pm while throughout the day participants can make a $10 donation and walk, jog or run ANY distance the choose.  People from all over the State of Maine will be coming back to support and experience this event while enjoying the Food, Music, Vendors & Activities in the Coastal Club Room from 9am – 12 Noon.

The Journey.

Running has been my passion ever since 2009 after over a decade of battling drug & alcohol addiction. Somehow I survived and now I ‘Run For Recovery’ and use the gift of the endurance athlete to inspire ALL to be of service to themselves, their family & their community.  During training for my first marathon I helped to create a 5k Power Run & Walkathon in Stowe, Vermont when I was on the board for the American Parkinson’s Disease Association.  This event is now in it’s 8th year and has GROWN raising over $25,000 for Vermont families statewide. My running journey has lead me to run two 50 Mile Ultramarathons, a 50K for STRIDE and 3 Marathons fundraising for Team Fox & The Micheal J. Fox Foundation.  I was featured in 2013 on their Blog ‘Fox Focus’ as being one of a handful of runners EVER to run an Ultramarathon for the organization.

My long term mission for STRIDE is to give everyone that is involved with Parkinson’s Disease a chance to connect with individuals, businesses and community programs to inspire a healthy lifestyle.   With the growing population of Mainers being diagnosed each year – events like this are going to be pivotal in educating entire generations and inspiring caregivers to reach out and understand there are opportunities and people who care.

Please spend some time on my Instagram @runlivethrive and learn more about my story on the Facebook Event Page and let me know if your organization would be interested in supporting my mission for 2017.

One of my greatest inspirations, Ultra Runner – Dean Karnazes, once said… “Run when you can, walk if you have to, crawl if you must; just never give up.” …this echoes true in both my adventure as an Ultra Endurance Athlete and my Mom’s grace while living with Parkinson’s Disease.

WATCH the BRCTV Channel 7 Documentary on STRIDE 2016 >>> https://vimeo.com/165595939

LEARN more about Hunter de Garmo & STRIDE 2017 >>> Facebook Event Page : https://www.facebook.com/events/181875098965201

Instagram : @runlivethrive

MAKE a Donation to Parkinson’s Disease Research, Awareness & Support in Maine >>> www.maineparkinsonsociety.org

Sponsorship Donations can be made out to ‘Maine Parkinson Society’ and mailed to : Maine Parkinson Society ATTN: Morgan Knox 359 Perry Road Bangor, Maine 04401