- Tweet thisThe grim truth is that those diagnosed with Parkinson’s will get worse. And for every patient, a community is affected, as the impact of the disease ripples to loved ones and caregivers. This is a global problem, but one that we can solve.Parkinson’s disease is a slow violation of your life; an inexplicable, unstoppable, defining yet indefinite disintegration of everything you have built in your life. The suffering comes from the awareness of the violation and the lack of power to intervene. It comes from the burden of “should have done more in the past” and what I can’t do now and in the future. It is knowing when the violation is over there will be nothing left of me. A life in ruins.
Yet I can admire a ruined building and what a life leaves behind. That is my aim now: to live a life in the present to the best of my ability and ensure through the process of living something of me remains.
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Is Parkinson’s a deadly disease? Is it lethal? Will it kill me? The Parkinson’s community has conflicting interests in how they answer this question. First, they want to comfort those who have been diagnosed, to help them adjust and lead as much of a normal life as possible. On the other hand, they want to convey the seriousness of the disease. It is more than just an inconvenience.
But ultimately, the answer is a matter of semantics. Many diseases considered deadly have similar mortality and longevity statistics. Including Alzheimer’s disease. Most diseases considered deadly do not stop the heart directly. You die of something else. But in any case, the sufferer probably wouldn’t have died as soon as they did were it not for the disease in question. That’s a deadly disease.
We don’t feel it benefits the Parkinson’s community, sufferers and soldiers, to gloss over the disease’s lethality. Because for years the mantra by the various Medical authorities is that you die with Parkinson’s, not from Parkinson’s. Why the mantra? People who think they have a deadly disease might be less satisfied with drugs designed only to reduce symptoms, rather than slow or stop massive death of brain cells. Patients might get uppity, start demanding more. They might ask their doctor about experimental treatments using existing substances that have been shown to work on animals.
Doctors and their medical organizations, including some Parkinson’s organizations, would like sufferers to be satisfied with their current drugs, and need more and more of them.PD is not considered a “fatal” disease, but mortality in patients with PD selected from the community is generally higher than that of the general population, regardless of levodopa or other therapy. Death is typically caused by secondary complications of the disease; pneumonia is the most common, followed by cardiovascular events (including stroke) and cancer.
Life expectancy in PD mirrors its association with increased mortality. Estimates for life expectancy (LE) and age at time of death (AAD) were calculated based on literature review and comparison with the general United Kingdom population. LE and AAD were shown to be reduced for all ages of onset and was greatest in young-onset PD. For the younger cases with onset of PD between 25 and 39 years of age, LE and AAD were 38 years and 71 years, respectively—each about 10 years shorter than for the general population.
In the Sydney trial, mean disease duration from diagnosis until time of death was 9.1 years.This meta-analysis indicated that among patients with PD, the all-cause mortality increased by 2.22-fold compared with the general population.There are many questions that are awkward to ask and just as difficult to answer. While some people see life in platitudes, others find hope in being pragmatic and proactive. Every patient deserves the best answer and to know the arguments out there.
So what is the answer to the question, “Will I die of Parkinson’s Disease?” If you give the stock answer that you read at almost every PD and medical site, no one dies of Parkinson’s Disease; they die of other causes. They die with Parkinson’s Disease but not from it.
The problem that many people might have with this response is that if it weren’t for the Parkinson’s disease, most of these deaths would not have occurred. We know that eventually we’re all going to cede life to entropy but both the quality and quantity of life might have been improved and prolonged had it not been for the presence of PD.
Perhaps the problem with the common medical answer is a semantic issue which does not take the “people” factor into consideration.“If you [have cancer and] don’t want to die of cancer, live long enough to die of something else first.” Several people told me what a liberating “mind pop” that was. Similarly, with PD, you might choose to live long enough – or slow your decline long enough – for the next amazing breakthrough to come along. Who knows?? There are no guarantees, but then there are no guarantees something good won’t happen. Until you’re dead, be fully alive!
The Centers for Disease Control (CDC) keeps track of mortality data in the United States, and certainly isn’t shy about allocating blame for deaths of Parkinson’s sufferers on the disease itself.Parkinson’s disease is the 14th leading cause of death in the United States, according to the Centers for Disease Control and Prevention’s annual analysis of mortality data. The CDC also released data this week showing there was a 4.6% increase in deaths attributable to Parkinson’s disease in 2010 (the most recent year for which they have data).
And ultimately, arguing over longevity or mortality misses the point. Why talk about longevity when there is disease? The most important thing is quality of life. This is reason we are working as hard as we are.[Parkinson’s] doesn’t kill you, but you might get to the stage where you wish it had.
- Tweet thisParkinson’s is so much more than just a movement disorder. It can also lead to depression and anxiety, and a host of distressing day-to-day problems like bladder and bowel dysfunction,” says Oliver Bandmann, a researcher at the Sheffield Institute for Translational Neuroscience (SITraN).It is our hope that this new educational tool will help the public understand that Parkinson’s is so much more than a movement disorder and that the challenges people with Parkinson’s face every day are often not even the ones you may notice.Nonmotor symptoms can be primary complaints and, for some patients and family members, can cause greater disability than motor symptoms. For instance, depression and cognitive problems contribute to a decline in quality of life regardless of the degree of motor impairment.Many symptoms of PD are unrelated to movement. Nonmotor (“invisible symptoms”) of PD are common, and may affect everyday life more than the more obvious movement difficulties. These symptoms may include impaired sense of smell, sleep disorders, cognitive symptoms, constipation, bladder symptoms, sweating, sexual dysfunction, fatigue, pain (particularly in a limb), tingling, lightheadedness, anxiety and depression.In early PD, including the phase before dopaminergic treatment is initiated, non-motor symptoms are more important for reduced health-related quality of life than motor symptoms. Fatigue, depression, sensory complaints and gait disturbances emerge as the most relevant symptoms and should be given corresponding attention in the management of patients with early PD.In fact, in some patients these non-motor features can be more troublesome than the motor symptoms and may predate the motor features by years. It therefore becomes important to identify and treat the non-motor features in order to maintain optimal quality of life. The possible non-motor features include difficulties with sleep, mood, cognition, autonomic nervous system problems, and abnormal sensations, among others.It is now appreciated that neurodegeneration in PD is more widespread than was initially suspected, and involves nerve cells in the cerebral hemisphere, olfactory system, upper and lower brain stem, spinal cord, and peripheral autonomic nervous system that use serotonin, acetylcholine, and norepinephrine as a neurotransmitter. Degeneration of these “non-dopaminergic” neurons is associated with a variety of non-motor clinical features including sleep disturbances; sensory dysfunction; mood disorders; psychosis; cognitive impairment; and dementia that do not adequately respond to dopaminergic therapies. Indeed, in the levodopa era, these non-dopaminergic features are the major source of disability for advanced PD patients.There is a lack of awareness among physicians of the considerable disability caused by non-motor symptoms (NMS) in PD.
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Believe it or not, many newly diagnosed Parkinson’s patients are lied to by their doctors. They are told that there are drugs that can stop their disease. These patients are shocked to learn that Parkinson’s is progressive (i.e. degenerative). Many still think that the drugs they take stop or slow the progression of the disease.
This is the first in a series of lies that Parkinson’s sufferers are told. But very simply, there are no prescription drugs that can slow, stop or reverse the progressive degeneration of brain cells associated with Parkinson’s disease. There are only treatments for Parkinson’s symptoms, not for the disease itself.There are treatments available to lessen the effects of Parkinson’s symptoms for some window of time, but this is all they can do — offer symptomatic relief. What we don’t have is a disease-modifying treatment, something that would actually halt or slow the progression of the disease. Nevertheless, significant research is being performed in the pursuit of such treatments — this is the top priority of The Michael J. Fox Foundation and many of its research partners.The medications currently available for Parkinson’s are directed at controlling symptoms. They can be very effective. Unfortunately, despite decades of intensive research, no drugs have been proven to slow the progression of Parkinson’s disease.What are the treatments for Parkinson’s disease? There is no cure for PD, and no treatment prevents the disease from progressing.There is no treatment proven to slow the progression of Parkinson’s disease (PD); thus medical therapy is directed at treating the symptoms.No treatment can arrest or slow neurodegeneration in Parkinson’s disease. The aim is to relieve symptoms and avoid the complications of therapy.How is Parkinson’s disease treated? At this time no treatment has been proven to slow or stop the progression of Parkinson’s disease. Instead, therapy is directed at treating the symptoms that are most bothersome to an individual.The real challenge now is not just to find treatments for the symptoms, but to find treatments for the underlying disease. And this is much more complicated because we have to understand what that underlying disease process really is. All the treatments we have right now deal with symptoms. They are basically bandaids for the disease. They don’t address the underlying disease which just keeps getting worse anyway. So we need to understand that underlying problem before we can do something about it.The current gold standard in treatment is the drug levodopa, or L-dopa, which neurons can convert into dopamine to replenish the brain’s dwindling supply. Although the drug is remarkable at stopping Parkinson’s symptoms, it isn’t a permanent cure.
“It wears off,” Smeyne says. “Eventually it doesn’t work anymore, and the cells even regulate against it. Also, some people think — and we’re among them — that giving L-dopa actually causes the disease to progress faster.”Although compounds such as Levodopa (L-DOPA) improve the striatal dopamine content, their long-term usage is associated with progressive decrease in drug response, motor fluctuations, dyskinesias and drug-induced toxicity. In addition, these drugs fail to prevent the progression of the degenerative process. This has shifted the focus onto alternative therapeutic approaches involving natural products that could provide independent therapy or offer neuroprotective support to the existing drugs.Dopaminergic therapies such as levodopa have provided benefit for millions of patients with Parkinson’s disease (PD) and revolutionized the treatment of this disorder. However patients continue to experience disability despite the best of modern treatment. Dopaminergic and surgical therapies are associated with potentially serious side effects. Non-motor and non-dopaminergic features such as freezing, falling, and dementia are not adequately controlled with available medications and represent the major source of disability for advanced patients. And, the disease continues to relentlessly progress. Major therapeutic unmet needs include a dopaminergic therapy that is not associated with serious side effects, a therapy that addresses the non-motor and non-dopaminergic features of the disease, and a disease-modifying therapy that slows or stops disease progression.“For the first two to five years of treatment, levodopa produces a sustained response, but as the disease progresses, the duration of benefit from each dose becomes shorter—the wearing-off effect,” says Mark Abramowicz, MD, editor-in-chief of The Medical Letter on Drugs and Therapeutics, a non-profit newsletter that critically appraises drugs. “Still later, some patients develop sudden, unpredictable fluctuations between mobility and immobility—the ‘on-off’ effect. As the disease progresses, patients often develop levodopa-resistant motor problems including difficulties with balance, gait, speech and swallowing. Non-motor symptoms, including cognitive and psychiatric difficulties, become more prominent.”Major therapeutic unmet needs include a dopaminergic therapy that is not associated with serious side effects, a therapy that addresses the non-motor and non-dopaminergic features of the disease, and a disease-modifying therapy that slows or stops disease progression.The Parkinson’s Disease (PD) market is dominated by symptomatic treatments targeting functional impairment in PD. Levodopa has remained the gold standard treatment for almost 40 years and has significantly improved patient quality of life.
There is currently there is a huge unmet need for disease-modifying treatments that slow progression or have neuroprotective properties.
- Tweet thisParkinson’s disease continues to puzzle physicians and biologists alike – even though it is well-established that symptoms like muscle tremors, rigidity, and, during the final stages, immobility can all be traced back to the death of a certain type of brain cell called a dopaminergic neuron. The underlying cause of this cellular death is a complex web of interrelated genetic molecular processes as well as external factors, most of the details of which are well-known. But how the various factors correlate and influence each other continues to elude the scientific community.Researchers no longer view PD as a singular dopamine-centered movement disorder, but something vastly more complicated: A malady with a highly complex etiology, multiple potential disease pathways (involving both dopaminergic and non-dopaminergic circuits), diverse clinical symptoms – from motor (e.g. tremor, rigidity and slowness) to “non-motor” (disabling fatigue, pain, constipation, sudden drops in blood pressure, sleep disorders, depression, anxiety, hallucinations, and dementia – and mixed pathology (involving both alpha-synuclein and tau proteins).
In a sense, in this paradigm every parkie has his/her own version of the disease. This picture makes perfect sense to epidemiologists and geneticists. For example, Parkinson’s Institute’s Caroline Tanner says, “the combination of genetics and environment is central to understanding PD etiology…Take head trauma as a risk for PD… By itself, concussions might be a small risk factor for PD, but when combined with a genetic predisposition – a variant in the alpha-synuclein gene that has a tiny effect in people without head injury – the risk increases 11-fold.”
But what does it mean for therapies? For one thing, it makes clinical trials much more complicated. As Haydeh Payami, Professor of Molecular Genetics at the New York State Department of Health Wadsworth Center put it, “for any given drug there are some responders and some people who do not respond, and the non-responders dilute the effect of a drug.”This may be shocking news to patients, journalists and many researchers but it turns out that neuropathologists have long suspected that something like this was true. Co-author Thomas Beach of the Arizona Parkinson’s Disease Consortium (whose group supplied much of the brain tissue for this study) concedes that, “Neurotrophic factors will only work if you start super early. If you wait until the formal diagnosis has been made, there’s often a lot of destruction, and you can’t really hope to reverse that.” British neuropathologist Chris Hawkes says by the time a patient gets a firm diagnosis of PD, “the pathology is far more advanced than you’d think…. And to put it crudely, the brain is well and truly pickled.”More broadly, a better understanding of the forces contributing to protein conformation and susceptibility to aggregation and transmissibility would be a crucial for unlocking novel diagnostic and therapeutic approaches for neurodegenerative diseases… These findings suggest that fulfilling the promise of therapies targeting these pathways in neurodegenerative disease might be quite complex. Appropriate modulation of inflammatory and immune mechanisms may require combinatorial regulation of multiple factors, with some being activated and others deactivated depending on disease stage and an individual’s genetic profile.While research interests have primarily focused on discovering the cause of PD and detecting candidate targets and neuroprotective agents, it will eventually be necessary to perform clinical trials to establish that a given agent does have an effect on the course of PD. This is essential in order to obtain regulatory approval and to obtain the hundreds of millions of dollars in funding necessary to support this research. This is proving to be an extraordinarily difficult goal to achieve. Early attempts to investigate putative neuroprotective agents using traditional endpoints have been confounded by an inability to differentiate a neuroprotective effect due to slowing of disease progression from a symptomatic effect which simply masks ongoing disease progression. Indeed, even the term neuroprotection is subject to question as it is obvious that one cannot tell with certainty in a living patient that nerve cells have been “protected”.The real challenge now is not just to find treatments for the symptoms, but to find treatments for the underlying disease. And this is much more complicated because we have to understand what that underlying disease process really is. All the treatments we have right now deal with symptoms. They are basically bandaids for the disease. They don’t address the underlying disease which just keeps getting worse anyway. So we need to understand that underlying problem before we can do something about it.Understanding the pathobiology is clearly very difficult; this is not only illustrated by the enormous amount of ongoing work in this regard in PD, but similar efforts in other complex diseases. Even when a pathobiological mechanism is revealed (or even hinted at), the route to therapy is a long one. The preclinical stage, of identifying efficient and specific drugs or small molecules that appropriately target the pathobiological process, takes many years. Even when this is achieved, the clinical and approval stage takes close to a decade. Perhaps as important as understanding these time limitations, is acknowledging that the vast majority of therapies that transition from preclinical to clinical stages fail to make it to market.Translating new findings in the laboratory into therapies for patients is a slow and expensive process. The development of therapies for neurodegenerative diseases is further complicated by the difficulty in determining whether the drug truly retards the slow degenerative process or provides only symptomatic benefit.
- Tweet thisAll the treatments we have right now deal with symptoms. They are basically bandaids for the disease. They don’t address the underlying disease which just keeps getting worse anyway.
- Tweet thisAll the treatments we have right now deal with symptoms. They are basically bandaids for the disease. They don’t address the underlying disease which just keeps getting worse anyway.
- Tweet thisThe real challenge now is not just to find treatments for the symptoms, but to find treatments for the underlying disease. And this is much more complicated because we have to understand what that underlying disease process really is. All the treatments we have right now deal with symptoms. They are basically bandaids for the disease. They don’t address the underlying disease which just keeps getting worse anyway. So we need to understand that underlying problem before we can do something about it.
- Tweet this“Indeed, biomedical research continuously gives us many new insights about Parkinson’s. Each year, thousands of new scientific publications appear on the subject – yet no single individual could possibly hope to keep a detailed track of this flood of information.”
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Family resoponsibilities are a large part of the motivation in our fight against Parkinson’s disease. Our family, friends and community depend on us. Our brave struggle gives them hope, and we become good role models. We will never give up, and neither should they in all of their many challenges and struggles.Eleven years ago, at the age of 36, [Roger] Long was diagnosed with young-onset Parkinson’s disease. Like anyone who’s just been dealt such a sucker punch, the father of two boys couldn’t help but wonder how much time he would have to be the provider his family had come to depend on. Within four years after the diagnosis, with his ability to walk becoming more hindered with each passing month, Long was forced to retire from his job. For several years after that, he had to use a cane and leg brace just to be able to walk.
“I struggled for eight years to get my bearings in the fight against PD,” Long said. “My older son joined the Marines, and it was while he was deployed to Afghanistan in 2010 that I became motivated to find a way to stop the steady decline I was on. I just wanted to be better for my son, so that when he came home from the war I would be able to walk beside him through whatever he faced afterward.
On the other side of the coin, progressing Parkinson’s is burdensome to the family. Even the mental and physical health of a spouse suffers. In fact, chance of death increases for spouses of Parkinson’s patients, the most troubling statistic is the rate of suicide of the spouse.…living with a person with Parkinson disease 5 years after first Parkinson hospitalization was associated with higher risk of all-cause mortality for both husbands (1.15 [1.07-1.23]) and wives (1.11 [1.04-1.17]).
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Family and friends, please realize that your loved one with Parkinson’s may need your encouragement to fight. One of the cruelties of Parkinson’s disease is that the disease itself impairs one’s motivation to fight it!Apathy affects anywhere from 17-60% of patients with Parkinson’s disease regardless of disease progression. It is manifested as a reduced lack of interest and participation in purposeful behaviors, difficulty with initiating, sustaining and completing tasks, and lack of concern for yourself and those around you. Family members and friends may be thinking you are just being “lazy” or “uninterested”, but realize that apathy is caused by both physiological changes resulting from changes in the brain, including depletion of dopamine, and external factors of adjusting to a life with Parkinson’s.
- Tweet thisThere is a vested interest in providing medicines that suppress symptoms, rather than actually addressing root cause.Meeting the needs of the drug companies has taken priority over meeting the needs of patients. Unless this corruption of regulatory intent is reversed, the situation will continue to deteriorate.
“We want a specific protocol, based on all the scientific data, that uses safe, natural substances.”Tweet this
Ah, so you prefer real, FDA approved drugs? You are against self-medicating with safe, over the counter, currently-being-researched substances because nobody has proven their effficacy? They are not on your doctor’s list of acceptable drugs?
Be careful where you put your faith.
Ultimately you will have to choose betweeen cutting edge science and big business. Most patients are fooled into thinking that these are the same; that science and business work together to provide you with the safest, most effective ways to improve your life.
What is the FDA’s record on safety and efficacy?…90 percent of all new drugs approved by the FDA over the past 30 years are little or no more effective for patients than existing drugs.
In fact, these FDA officers propose to approve the drugs without ever knowing if they are therapeutic or not. Their commercialized language presumes the outcome before starting. The job of the FDA, it seems, is to help drug companies open up new markets to increase profits for the FDA’s corporate paymasters.
Advice to readers: Experienced, independent physicians recommend not to take a new drug approved by the FDA until it is out for 7 years, unless you have to, so that evidence can accumulate about its real harms and benefits.Indeed, contemporary enthusiasm for the commercialization and marketing of healthcare seems to offer ever wider opportunities to sell medical treatments. The results of medical research are often distorted or suppressed for commercial gain, and systems that attempt to control clinicians’ behaviour through payment by results drive overdiagnosis and overtreatment. Patients experience well documented harms as more and more often financial imperatives are allowed to trump clinical judgment. Harm is also caused by well meaning doctors trying to save lives.The current review describes the neuroprotective and therapeutic utility of such natural products including herbal extracts, phytochemicals and bioactive ingredients from other natural sources either in isolation or in combination, with potential application in PD, highlighting the relevant patents.
- Tweet this…with PD, you might choose to live long enough – or slow your decline long enough – for the next amazing breakthrough to come along. Who knows?? There are no guarantees, but then there are no guarantees something good won’t happen. Until you’re dead, be fully alive!
- Tweet thisBut the reality is that for the estimated five million Parkinson’s patients worldwide, the status quo is still not good enough. They are living with Parkinson’s movement difficulties and nonmotor symptoms such as mood and sleep disorders as well as cognitive impairment. Medication and therapies alleviate some symptoms, but create their own problems and fail to address all the effects of Parkinson’s.
- Tweet thisAn accurate early diagnostic test for Parkinson’s disease (PD) is a critical unmet need.Of all the challenges, the most urgent is the need for a reliable biomarker for PD that can accelerate the development of treatment.Every parkie is interested in knowing the answer to the question: “how am I doing?” We know we have a progressive disease and we really want some objective feedback on how our condition is different from say a year ago. What symptoms are worse, what’s better, what’s the same? But it’s difficult to get an informative answer. Friends and family tend to be encouraging but vague…“You’re looking great!” And clinicians… well, they aren’t really all that much help, either.
- Tweet thisIt is now appreciated that neurodegeneration in PD is more widespread than was initially suspected, and involves nerve cells in the cerebral hemisphere, olfactory system, upper and lower brain stem, spinal cord, and peripheral autonomic nervous system that use serotonin, acetylcholine, and norepinephrine as a neurotransmitter. Degeneration of these “non-dopaminergic” neurons is associated with a variety of non-motor clinical features including sleep disturbances; sensory dysfunction; mood disorders; psychosis; cognitive impairment; and dementia that do not adequately respond to dopaminergic therapies. Indeed, in the levodopa era, these non-dopaminergic features are the major source of disability for advanced PD patients.The abundance and accumulation of a-synuclein in the vermiform appendix implicate it as a candidate anatomical locus for the initiation of enteric a-synuclein aggregation and permits the generation of testable hypotheses for Parkinson’s disease pathogenesis.AS aggregates were found in the pANS of all 15 LB disease cases (PD, DLB) in stellate and sympathetic ganglia (100%), vagus nerve (86.7%), gastrointestinal tract (86.7%), adrenal gland and/or surrounding fat (53.3%), heart (100%), and genitourinary tract (13.3%)
- Tweet thisI was talking to my oldest son one day about leaving yet another medication behind me, and he became agitated with concern and said, ‘Dad, you’re acting like you’re cured or something.’ That became my motto: ‘Live like you’re cured.’
- Tweet thisA big issue for Parkinson patients is hope: when it disappears, people decline visibly and quickly. Of course, hope isn’t something you can study like a drug; there’s no evidence that it affects progression of the disease.