The Controversy Surrounding GDNF
The existence of GDNF has been known for well over twenty years. Only in 2006, at the World Parkinson’s Congress held in Washington DC, was it first announced that GDNF is produced in the brain, by the glial cells, and that GDNF repairs the damaged brain cells.
If everybody in the Parkinson’s world knew about GDNF in 2006, why do only a few people, outside of the scientific world, know anything about it yet?
If the medical profession does know about GDNF then they should have jumped onto the bandwagon, in 2006, and made every effort to tell their patients about it!
That has not happened, at least not in my neck of the woods. Does this mean that this vital information is not being disseminated amongst all the players in the medical world?
If so, why would that be?
At that World Congress, we were told that fast walking is the best way to go about producing GDNF in the brain. Patients should all be shown that they are capable of walking, at least most of them can. Whatever walking they do manage to do would be better than nothing.
Getting better, even by a little bit is better than continuing to get worse.
As far as I know, scientists knew about the existence of GDNF, long before 1993, when the first clinical test was performed in England. If they knew about it so long ago, why did we all not know about it?
- I assume that it must have been found first inside the brain of a human being.
- The purpose of GDNF must have been known, otherwise, why would Amgen have made an artificial version of it?
- When the 1993 trials were started, they must have known that GDNF repairs the damaged brain cells, and they were conducting these trials to see how effective it is!
- I must therefore assume that because GDNF - a natural cure, which is produced in the brain - does not generate income for anybody; it was more important to do trials using artificial GDNF, rather than getting some pd patients to do some walking and then measure how much they managed to improve over a period of time, as they did before the 2006 World Parkinson’s Congress.
- That would have cost next to nothing, compared to what that first artificial GDNF trial must have cost.
- Are we all so powerless that we are unable to take action against this silence on what fast walking can do for us?Artificial GDNF has been produced in the USA by a company named Amgen. This GDNF was first used in the trial mentioned above in 1993, carried out by Dr Steven Gill, at the Frenchay hospital in Bristol, England. This was the published result of that trial:Results: “After one year, there were no serious clinical side effects, a 39% improvement in the off-medication motor sub-score of the Unified Parkinson's Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living sub-score. Medication-induced dyskinesias were reduced by 64% and were not observed off medication during chronic GDNF delivery. PET scans showed a significant 28% increase of dopamine storage after 18 months, suggesting:Methods: A brain autopsy was performed on one of the Bristol, United Kingdom phase I GDNF trial participants, who had died of an unrelated heart attack.Results: The autopsy analysis revealed re-growth of nerve fibers in the putamen area of the brain. Professor Love, who examined the brain stated that ***********************
- “This was the first neuropathological evidence that infusion of GDNF in humans causes sprouting of dopamine fibers, in association with a reduction in the severity of Parkinson’s Disease."
- “A direct effect of GDNF on dopamine function.”
Why won't they let Parkinson's sufferers take a life-changing drug?
By NIKKI MURFITT
When Tom Isaacs was 27 he was diagnosed with Parkinson's disease. The condition gradually destroys the brain's ability to control the muscles - there is no cure.
Determined to give himself the best possible prognosis, Tom embarked on a very personal journey to meet leading scientists in the hope of finding new treatments that would help him.
Three years ago it seemed he'd found the answer: a new drug GDNF (glial derived neurotrophic growth factor). A group of Parkinson's patients had been treated with GDNF at Bristol's Frenchay Hospital in 1993 and their transformation had been remarkable: sufferers who'd been trapped in a living hell were suddenly able to walk, talk and smile again.
Parkinson's is caused by a shortage of dopamine, a chemical messenger involved in movement, mood and behaviour. Why this happens is still not known.
GDNF seems to work by stimulating dopamine production and preventing degeneration of the brain cells. The drug is delivered via a catheter permanently implanted in the brain. The catheter is connected to a Jaffa cake-sized pump sewn into the abdomen.
When GDNF was given to the Bristol patients the results were astonishing. 'Men who had been unable to get up out of a chair unaided were walking normally across a room. Their hand co-ordination was unbelievable, in exercises they could move their hand easily from left to right, something that had previously been impossible under the onslaught of Parkinson's,' says Tom.
So impressive were the results that the study was rolled out to North America and by September 2004, 50 patients were receiving the drug. The Parkinson's Disease Society in the UK planned to hand over** £1.2 million to fund further trials in Bristol.
But suddenly, at the end of 2004, and without warning, this lifeline was snatched away. Amgen, the American drug company which holds the patent for manufacturing GDNF, claimed the drug was dangerous as it could cause brain damage and refused to continue prescribing it.
The below link is to an online book by Anders Bjorkland which discusses some truly interesting aspects of the Bristol study:
Case Inspires Parkinson’s Crusade
Parkinson’s patients in the US, who are suing a drugs company for withdrawing a pioneering treatment, say a man treated in Bristol has given them fresh hope.
Amgen halted medical trials of glial cell line-derived neurotrophic (Repair) factor (GDNF) because of side effects. But an autopsy on the brain of Henry Webb, who volunteered to undergo tests at Frenchay Hospital, showed signs that his nerve fibers were re-growing.
The company said it had no plans to restart the trials.
Mr Webb, from Blackwood in South Wales, died from a heart attack last December. He was one of six patients with advanced Parkinson's Disease involved in the GDNF trials at Frenchay.
He told BBC News in 2003 the drug had given him back his life.
"Mr. Webb's case is important because it shows that GDNF is a safe and effective treatment."
Kristen Suthers, daughter of one of the US patients fighting to get the medical trials restarted, said: "We believe high doses of GDNF causes lesions. But we've seen the study from Mr. Webb, and that it is not the case, if you give patients a lower dosage of GDNF.
A spokeswoman for Amgen told the BBC: "It is a case of interest, but you have to remember, it was phase one of the study."In the phase two study, those on placebos did well, sometimes better, than those on the drug."
Question: Why would this second study come up showing a totally different result, when the first study, held ten years previously, showed a highly successful result? This looks so very suspicious to me!
This is an interesting bit from Oxford Journal:
Restorative treatments for brain disorders are rare. In neuroscience research, it is not uncommon to suggest that experimental treatment strategies may have great clinical potential. The rescue or regeneration of a few cultured neurones may be sufficient to entice such optimism. However, the path to a new clinical therapy is typically painstakingly long and difficult to navigate. In our minds, we would like it always to be a straight path starting with tests in cell models in rodents providing us with mechanisms of action and leading to trials in non‐human primates. Then open‐label tests can be performed in small patient groups and eventually large controlled clinical trials are conducted. In reality, however, the path may be tortuous, filled with detours that set the field back, as well as shortcuts and parallel tracks that yield different strategies which develop at their own speed. The development of glial cell line‐derived neurotrophic factor (GDNF) as a treatment for tgciq’s disease over the past nine years provides an example of such an interesting journey. Moreover, it illustrates one role of non‐human primates in preclinical development of a novel therapy.
In this issue, Grondin and co‐workers (Grondin et al., 2002) present evidence for structural and functional benefits of infusions of GDNF in rhesus monkeys previously rendered parkinsonian by unilateral intracarotid injection of 1-methyl-4phenyl-1,2,3,6- tetrahydropyridne (MPTP).
Using mini‐pumps, they infused 5–15 µg/day GDNF either into the lateral ventricle or the dopamine‐depleted dorsal putamen. Starting during the first month, there was a gradual and marked reduction in parkinsonian symptoms, including bradykinesia and rigidity, without any signs of adverse effects. Post‐mortem examination revealed partial restoration of dopamine and its metabolites in the corpus striatum, as well as evidence for an increased number of nigrostriatal dopaminergic fibres and cell bodies in the substantia nigra. Interestingly, there were no significant differences between the intraventricular‐ and intraputamenal‐ infusion groups, so the data for both groups were pooled. This is the first demonstration that GDNF infused directly into the brain parenchyma of non‐human primates is effective in restoring dopaminergic function. The treatment was not initiated until over 3 months after the MPTP lesion, when most of the dopaminergic cells had probably died due to the toxin. Therefore the authors argue that GDNF most likely worked through a neuroregenerative mechanism as opposed to one of acute neuroprotection (Grondin et al., 2002).
Read more on:
This is interesting! It tells why the drug company making GDNF stopped the trial – or the reasons given by them — and the Michael J. Fox Foundation’s role in halting the trial:
Trial of New PD Treatment Halted: Some Patients and Advocates Protest
By Robin Elliott
On Friday, February 12, Amgen Inc. announced that, after much internal hand wringing, it was denying a request by participants in trials of a molecule known as GDNF, an experimental Parkinson's treatment, to continue receiving the treatment following termination of the trials.
California-based Amgen, the world's largest biotechnology company, had abruptly concluded its own double-blind trial almost six months earlier, saying that the treatment had not been shown to be effective and citing safety concerns in two areas. In one of these, several subjects were found to have developed antibodies that could potentially attack the body's own GDNF, a naturally occurring product that is essential for the production of dopamine, the chemical messenger that is deficient in Parkinson's.
The other safety concern came out of a separate trial involving monkeys. It turned out that a few of the animals were found to have evidence of lesions in the area of the brain known as the cerebellum.
Several leading scientists and advocacy groups take issue with Amgen's decision
Several of the scientists who had served as investigators in the Amgen trials, including Drs. Michael Hutchinson of New York University, Don Gash and Greg Gerhardt of the University of Kentucky, Richard Penn of the University of Chicago and Steven Gill at the University of Bristol, England, have challenged Amgen's interpretation of both the efficacy and the safety data. As to efficacy, some have argued that the wrong statistical test was used, and that an alternative test would have showed GDNF to be effective. (Amgen, supported by several investigators including Drs. Jay Nutt of the Parkinson Center of Oregon and Anthony Lang of the University of Toronto, has held to its original opinion that the trials failed to show efficacy.)
As to the safety issues, some of the doctors have argued that Amgen has overreacted on both counts. The antibody issue, they say, is frequently seen in such studies and does not necessarily have any adverse effects on the health of the patient. (Indeed, they note that when the antibody findings first surfaced in the spring of 2004, Amgen seemed unconcerned by the data and would have continued with preparations for a larger-scale Phase III trial of GDNF, had the second wave of monkey data not come along.)
As for the monkey data, some of these doctors point to evidence that suggests that the cerebellar damage was caused, not by the toxicity of the intervention, but by its precipitate withdrawal (six months into the trial). They also point out that the dose used for the monkeys was many times the doses used in the human trials.
Michael J. Fox Foundation stages "Scientific Summit" on GDNF
At a meeting in Chicago in early August 2004, where the efficacy data on GDNF were announced, Debi Brooks, President and CEO of the Michael J. Fox Foundation for Parkinson's Research, offered to host a scientific summit on the subject. The summit, which was held in November, drew some 30 scientists from North American and European centres for Parkinson's research and concluded with a broad consensus that while GDNF remained a promising potential treatment, more animal studies should be done to assess the health concerns before any new human trials should be undertaken.
What this discussion did not address was what should be done about the 48 people in the U.S. and the United Kingdom who have participated in one of the Amgen-sponsored trials, several of whom have indicated that they wish to continue receiving the treatment. Most observers believe that the "risk-benefit" calculus for these people is different from what it would be for a new patient because all of them have already undergone the surgery necessary to participate in the trial, and several of them have been on GDNF for as long as three years. Representatives of this group have set up a website - www.GDNF4Parkinsons.org - which has be-come a rallying-point for the Parkinson's community.
Not surprisingly, Amgen's February announcement was especially galling to this group - many of whom had written personal letters to Amgen pleading for reinstatement of GDNF. They were backed by several of the community's advocacy groups, including the Parkinson's Disease Foundation, the Parkinson's Action Network and the Parkinson Pipeline Project.
To understand how GDNF got to this point, we need to look at the scientific history of the molecule.
GDNF - The trials and tribulations of a promising Parkinson's treatment
Glial-cell line-derived neurotrophic factor, or GDNF, is one of the most powerful naturally-occurring human factors known to nourish and foster the growth of dopamine-generating neurons. Soon after GDNF was identified in 1993, Dr. Gash and colleagues at the University of Rochester and later at the University of Kentucky showed that the injection of GDNF protein into both rat and monkey models of parkinsonism showed therapeutic promise.
Dr. Gash's work was soon followed by the first gene therapy trial of GDNF, conducted in a rat model by Dr. Martha C. Bohn and her colleagues at the University of Rochester. This seminal study, which was published in the journal Science in 1997, showed that continuous delivery of GDNF at low levels using a so-called "viral vector" was able to protect dopaminergic neurons from neurotoxin-induced cell death.
Drs. Jeffrey H. Kordower and Marina E. Emborg, along with their colleagues at Rush University Medical Center in Chicago and the University of Lausanne in Switzerland, picked up the ball by conducting the first study of GDNF gene therapy in a monkey model. Their studies showed improved motor performance in the animals which received the GDNF gene (compared with animals that received no treatment). In the treated animals, parkinsonian symptoms were reduced, and, after the animals were sacrificed, the numbers of healthy dopamine neurons were found to be significantly enhanced. A summary of the findings was published in Science in 2000.
The investigation in humans
While the animal studies were continuing, scientists began to examine how GDNF might work in humans. Based on the preliminary results of Dr. Gash's studies in rat and monkey models, Amgen initiated a human, randomized, double-blind trial of GDNF, led by Dr. Nutt. The results, published in a 2003 edition of the journal Neurology, were disappointing; the treatment showed little benefit and several side-effects, confirming that benefit in animals does not necessarily translate to benefit in humans.
Some two years later, a British team conducted a follow-up study that greatly raised world interest in the promise of GDNF. In this study, led by Dr. Gill and his colleagues at Frenchay Hospital in Bristol, scientists implanted catheters in the brains and pumps in the abdominal walls of five people with moderate Parkinson's. The pumps continuously fed GDNF into specific areas of the brain via the catheters at a precise rate of infusion. All five patients showed improvements in "off" states comparable to their "on" states within two months of the onset of the trial. Their motor skills continued to show improvement and even gait difficulties were eased. Brain scans documented the patients' progress while the dosage of anti-Parkinson's medications was steadily reduced. The results showed significant improvement in the functioning of the dopaminergic system.
The Amgen "double-blind" trial
Impressive as the new data appeared to be, the Bristol trial did not provide an answer as to whether GDNF works. The reason is that it was of the so-called "open-label" variety, in which every participant received the treatment and some of them - human nature being what it is - may have imagined that they felt better than they really were. To correct for this factor, known as the "placebo effect," scientists try to confirm early data by conducting what is known as a "double-blind" trial, in which some patients are randomly placed on the treatment and the others are given a sugar pill. To test the validity of the British data, Amgen initiated such a trial for GDNF in 2003 with 34 patients.
As reported by Dr. Lang at a meeting of the American Neurological Association in October, 2004, the study did not prove the efficacy of GDNF. The investigators judged the patients' "off" periods to be somewhat improved, but saw no improvement in "on" periods.
The Uncertain Future of GDNF
Dr. Clive N. Svendsen of the University of Wisconsin (co-investigator in the Bristol study), as well as other investigators involved in GDNF research, has suggested that the studies' dissimilar results may have been a consequence of the different dosages used, as well as by the different sizes of the catheters used to infuse the treatment.
Dr. Bohn says she is encouraged by the Bristol results but believes that a delivery system utilizing gene therapy rather than infusion via catheter may ultimately be safer (since it does not require the administration of live virus to the brain) and may offer a better long-term outcome for patients. Dr. Svendsen agrees, and suggests that another potential delivery technique might be the implantation of genetically-engineered stem cells that could in turn release GDNF.
Dr. Svendsen also reports that he and other study participants are meeting with Amgen to analyze the differing results of the studies to date and to seek consensus on whether and when there will be further studies of GDNF. Meanwhile, additional animal studies are being pursued.
The reinstatement issue continues
While discussions continue concerning the long-term future of GDNF, the short-term issue of the patients who were in the trials to date remains unresolved. Some have indicated that they would like to go back on GDNF if the opportunity were to be offered, but several have now had their pumps and catheters removed. Voluntary organizations such as PAN and PDF are continuing to explore options of persuading Amgen to reconsider its position. In the words of a recent open letter from leaders of the Parkinson Pipeline Project, a group of patient advocates: "[Reinstatement] is important not only to today's patients but to our prospects of being able to recruit sufficient numbers of people for future trials…[without people to participate] all of us - companies as well as patients - will be the losers."
Robin Elliott is the Executive Director of the Parkinson's Disease Foundation.
If you are keen on reading medical evidence, both for and against GDNF infusion into the brain, then read more:
This article discusses the mixed results of the trial, concerns over GDNF, and is a good, brief read:
Is all this argument about how to get GDNF into the brain and what dose we should take really worth all the money t is costing?
Are we not forgetting that the brain produces GDNF as a natural product, which has no side effects?
Surely the medical profession should be leading the charge and telling their patients to start doing some FAST WALKING and to slowly reduce their Pd medication until they get to the point - at which I have been for the past 13 years - Pd medication-free and able to live a normal life
I am not cured, but hey, I am healthier than most people of my age!
Perhaps this is just a pipe-dream on my part. I hope not!
Email from John Shea
Name: John Shea
Date: 2015-05-03 01:05
I bought your book and I know what you are talking about!
I am a 67 year old male that was finally diagnosed with Parkinsonâ€™s in 2014 but what is remarkable is that I lost my smell in summer of 1993 and at about the same time I had a bad case of vertigo. The vertigo and loss of smell I now believe is some how related to Parkinsonâ€™s.
I was a long time long distance runner and I religiosity ran 20 to 30 miles a week, year-in and year-out. I started having movement issues in 2008 after I stopped running due to bone and joint pain. I believe if I had never stopped running I may have avoided Parkinsonâ€™s. I have many of the same symptoms as you but no where as severe.
After my diagnosis I was started on Azilect and within a week or two I regained a significant amount of my smell back and much of my movement ability. I believe that my running either stopped or substantially slowed down my Parkinsonâ€™s.
Now after I ride my bike hard for an hour I find my remaining symptoms alleviated. I have also tried your speed walking and I have experienced a noticeable relief although it only lasts for several hours.
Thank you for writing your book.
Email from Atomic64 on the HealthUnlocked Blog
Thank you for your message. I have been reading your website for a couple of weeks now. I am completely convinced by the method you describe. I have been noticing that I can control my walk (this is before I knew I had PD) if I do what i called a "deliberate walk" with swinging arms. I do look as if I am about to conquer a country, especially if I am in boots, but who cares.
Before i knew what i had i thought 'why do i need to think about how i walk'... well, now that i know why it's actually easier. Simpler to think that the brain doesn't get engaged so I am helping with deliberate action as it cannot be automatic. I am walking far better with sticks, i.e. nordic walking as it keeps my posture up and i don't really limp. I am keeping a journal of exercises to see what feels the best. Swimming is great, as is yoga, as is boxing.
The only piece of advice of yours (that i have read on your website) I will have trouble with is reducing stress, in this case at work. I have a job which i cannot walk away from yet as i have kids who will need some support for a few more years. On the other hand, doing research for my PhD on the side gives me the relaxation i need and intellectual stimulus you also mention as required.
THE ONE TRUE CAUSE OF DISEASE
In the early 1800s Isaac Jennings, M.D. quietly started a revolution in health care when he noticed that changes in lifestyle produced EXCELLENT RESULTS.
Dr. Jennings, after practicing as a traditional medical doctor for 20 years without getting any significant results, one day he faced a shortage of drugs during a fever outbreak in the summer of 1815, so people in town came to see him with all kinds of symptoms. But he didn't treat them because there weren't any drugs available.
All he could tell them was to go home, rest, and drink lots of fluids.
And what happened? Surprise, surprise these people got well, WITHOUT ANY MEDICINE!
Based on this, he decided to carry out an experiment: he was going to treat people using only placebos (dummy pills) and some common sense instructions that is, he would advise his patients to correct their lifestyle and diet to a more natural approach.
The results were excellent: his patients recovered in absolute record time compared to patients who had been medicated.
In 1822 he gave up medical pills, plasters, powders and potions and treated patients with pills made from bread and coloured water.
He then practised for a further 20 years the - "do nothing mode of treating disease." - Yale University conferred an honorary degree upon him in recognition of his great success substituting pills with placebos.
NOW WE KNOW THAT OUR BODY IS INHERENTLY HEALTHY AND SELF-HEALING AND ALWAYS STRIVES TO MAINTAIN OR RE-ESTABLISH OPTIMAL HEALTHFUL CONDITIONS.
There is no healing force outside the body. Dr. Isaac Jennings
Dr. Jennings is also the founder of the Natural Hygiene Philosophy. Natural Hygiene is a set of principles that people throughout human history have practiced to achieve and MAINTAIN optimum health. Natural Hygiene principles are based upon meeting the body's inherent, natural needs.
Remember, you can never poison your body into being healthy.
Twenty-five years in which I used prescribed drugs, and 33 years in which I have not used prescribed drugs, should make my belief that drugs are unnecessary and in most cases injurious, worth something to those who care to know the truth.
John H. Tilden, M.D. (1940)
Why Walk? I Hate Walking!
My name is John Pepper. I am a Parkinson’s patient. My Parkinson’s disease started in 1963, when I found that I could not throw a ball properly. However, I was only diagnosed with Parkinson’s in 1992, when I developed a bad walking gait.
Why did it take twenty-nine years before I was diagnosed?
I am neither a doctor nor a gym teacher. Having said that - since diagnosis - I have taken note of every news item I could find, concerning Parkinson's. Many news articles claimed that certain types of energetic exercise can and do affect the progression of Parkinson’s Disease
What has been my experience regarding exercise?
I spent twenty-two years, from 1970 to 1992, going to the gym, for one hour a day, six days a week, doing aerobic exercises and weight-training exercises.
For the next two years, after diagnosis, I increased the gym to 90 minutes - doing 60 minutes of aerobic exercise on the treadmill, step climbing and bicycle machines; and then, thirty minutes on various other weight-bearing machines.
During those two years, my condition continued to slowly get worse. After two years in 1994, I gave up the gym entirely, and gave in to my wife, Shirley's, request to join her at Run/Walk for Life. Within three months, my performance had improved quite noticeably. That was the first time it had shown any improvement for many years. That was the turning point in my Parkinson’s Disease!
What actually happened, since giving up going to the gym?
At Run/Walk for Life, I only did aerobic walking for three sessions a week, having started at twenty minutes a session, which increased by five minutes every second week. At the end of three months, I was walking for 45 minutes a session. The reason for doing only walking every second day was to give my muscles a chance to recover, after each exercise session. I was only allowed to walk every second day. In the past, I had been doing the same exercise every day, thus, not giving my muscles a chance to recover. They ended up eating up muscle tissue, in order to get the required energy they needed. The result was, my muscles got smaller and my fatty tissue grew larger. Not a good situation!
Energetic Walking Produces a substance Called GDNF!
What produces GDNF (Glial Derived Neurotrophic Factor) and why is it produced?
The body has a survival system, which is only activated when it thinks the body is under attack, or in danger. When we are under attack, or in danger, we either stand up to it and fight for our life, or we run away from it - the fight or flight syndrome - of which you must have heard.
The body produces this Growth Factor in every area of the body, which repairs the damaged tissue, if and when required. GDNF repairs damaged brain tissue, whereas the Growth Factor produced in the liver produces liver tissue etc. Our problem is that we have damaged Glial cells, which are neurons, that produce dopamine. When the GDNF repairs some of the neurons, we produce more dopamine and we start to get better. However, as we have not done anything to stop the Parkinson's from killing off more glial cells, we have to continually try to produce enough GDNF to stay ahead of the Parkinson's.
In other words, we have our own, built-in, repair kits!
What is the optimum time we should walk?
The optimum time for exercise has been found to be three, one-hour sessions, at maximum effort, per week, with a one day rest between sessions.
Why does more than one hour not produce more GDNF?
I don't know, but many tests have been done, and that was the result.
Why is walking or running the best form of exercise for this purpose?
It keeps our pulse-rate up to maximum level and maintains it there until we stop. Other forms of exercise tend to be stop-start, and cannot be sustained at any level, for the required one hour. If we were boxing, it would be just as good, but we could not sustain that for a full hour. As most Parkinson's patients have problems with balance, I would recommend walking, but running is just as good. Walking on the open road is better than walking on a treadmill, because we have to think about the surface on which we are walking and where we are going - whereas, on a treadmill, we merely have to put one foot in front of the other. This came out of many of the studies. The best results are produced when the brain is kept as active as the body. I assume that the condition required by the body to, produce the GDNF, would involve both the brain and the body.
Guess why I choose to walk?
I get lots of patients telling me that they don't like walking. It is boring! To me, it is not half as boring as the thought of being unable to move very well, or go anywhere, while living from one dose of medication to the next.
I have to concentrate so hard on walking properly, that I don't have time to get bored. It is so important to me, that I would not care if it got boring, as I enjoy my quality of life, even at the age of seventy-nine (2014).
We all have to make our own choices!
Either we do nothing, take our medication and put up with our Pd; or we exercise regularly and honestly, take the minimum medication and enjoy the benefits, by living a full life.
The choice is all yours!
Rhythmic beat may help Parkinson’s rehab
Copied from The Northwest Parkinson’s Foundation Weekly News Update
Walking to an audible beat may be useful in rehabilitation for people with Parkinson’s disease and similar disorders, a study shows.
futurity.org - Researchers studied the effects of various metronomic stimuli (a mechanically produced beat) on fifteen healthy adults, ages 18 to 30. Walkers participated in two sessions consisting of five 15-minute trials in which the participants walked with different cues.
In the first, participants walked at their preferred walking speed. Then, in subsequent trials, participants were asked to walk to a metronomic beat, produced by way of visuals, sound, or touch. Finally, participants were asked to walk with all three cues simultaneously, the pace of which was set to that of the first trial.
“We found that the auditory cue had the greatest influence on human gait, while the visual cues had no significant effect whatsoever,” says Ervin Sejdic, an assistant professor of engineering at the University of Pittsburgh, who reports findings in the journal PLoS One.
“This finding could be particularly helpful for patients with Parkinson’s disease, for example, as auditory cues work very well in their rehabilitation.”
With illnesses like Parkinson’s disease—a brain disorder leading to shaking (tremors) and difficulty walking, — a big question is whether researchers can better understand the changes that come with deterioration.
“tentimes, a patient with Parkinson’s disease comes in for an exam, completes a gait assessment in the laboratory, and everything is great,” says Sejdic. “But then, the person leaves and falls down. Why? Because a laboratory is a strictly controlled environment. It’s flat, has few obstacles, and there aren’t any cues (like sound) around us.
“When we're walking around our neighborhoods, however, there are sidewalks, as well as streetlights and people honking car horns: you have to process all of this information together. We are trying to create that real-life space in the laboratory.”
In the future, Sejdic and his team would like to conduct similar walking trials with patients with Parkinson’s disease, to observe whether their gait is more or less stable.
“Can we see the same trends that we observed in healthy people?” he says. “And, if we observe the same trends, then that would have direct connotations to rehabilitation processes.”
The team feels that visual cues could be considered as an alternative modality in rehabilitation and should be further explored in the laboratory. Additionally, they plan to explore the impact of music on runners and walkers.
Funding for this project was provided, in part, by the University of Pittsburgh, the University of Toronto, and Holland Bloorview Kids Rehabilitation Hospital.
More about Walking
My name is John Pepper. I was diagnosed with Parkinson’s disease in 1992.
Why can I walk properly, when I focus my full attention on each move?
Not having had any medical training and not being a scholar, I have to give my answer as a person with Parkinson’s disease - I don’t know!
Why is walking so important?
Here I am on safer ground! In 2006, the results of a lengthy scientific study, done in the USA, gave the answer to this question. These results were announced at the First World Parkinson’s Conference, held in Washington, DC. So why do we all not know about this important development?
Certain types of energetic exercise can slow down or even reverse Pd.
These results should be displayed on the walls of every neurologist in the world!
This was the reason why my Pd took so long to be diagnosed, in 1992, about twenty-nine years after my first symptom appeared in 1963.
Read all about this type of exercise and what I had been doing since 1970, which slowed down my Pd. My book, ‘Reverse Parkinson’s Disease’ tells my whole story, so that others can benefit from knowing what I did, in order to overcome my Pd. In a nutshell, I think that fast walking, MAO-b inhibitor medication, and stress control were responsible for my improved health! To tell the whole story in an article is just not possible.
This is the most exciting story for all Pd sufferers. It is the first story of REAL HOPE we have ever had!
The real question is:
Why don’t neurologists tell their patients about this good news? Why indeed!
Who is John Pepper?
I was born in 1934, in the English town of Harrow, which is famous for its public School. Harrow is now inside Greater London, but in those days, it was north of London. I started my schooling at the age of four, in Harrow. The Second World War started in 1939, before I turned five. I moved around a bit, due to the bombing, and had a narrow escape in 1940, when a landmine was dropped in the back garden of my home, and landed in a thick hawthorn hedge, and failed to explode. Had it exploded, I would not be here to tell the tale. My parents decided to leave Harrow in 1942, and moved to the country, away from the bombing. I went to nine different schools, before I gained entrance to another public school, in Winchester, at the age of ten, after passing a scholarship. I was then, at least two years younger than most of the boys in the class. That turned out to be a major mistake in my education. I found it impossible to settle amongst those, much older boys, and consequently became a loner, mainly due to the bullying I continuously endured for the first two years. I finished school at the age of sixteen, when my father thought that I was old enough to help support my family.
My first job was as an office boy in a bank in Winchester. After one year, I applied for a transfer to an overseas branch of the bank, which turned out to be in Johannesburg, South Africa. There I worked for a further four years, during which I passed all but two of the exams for my Institute of Banker’s Diploma. My elder brother persuaded me to join his employers, Burroughs Machines Ltd, selling adding machines. I did not enjoy selling, but finished up in that company, running the third branch I had established, in the city of Kimberley, which is famous for its diamonds. There I married Shirley Hitchcock, and we had two children. In 1963, I started a new printing business, in partnership with Eric Sulter. That business grew very quickly, until I moved to Johannesburg in 1970, where I started another continuous stationery printing business, while Eric continued to run the Kimberley company.
My Parkinson’s symptoms started in 1963, when I found that I was unable to throw a ball properly. I had never had this problem before, but did not talk to anybody about it. This was followed very quickly by other symptoms, such as the inability to write properly, constipation and chest infections. Then in the seventies I suffered from chronic depression and speech problems, together with other movement problems, such as dropping things and spilling my food. I was finally diagnosed with Parkinson’s in 1992, when I had started to walk badly, while dragging one leg and shuffling my feet.
In 1960, I had an accident, on-stage, lifting a dancer. I prolapsed a disc in my lower back. After ten years of pain and suffering, I was advised to do exercise to strengthen my back muscles. This helped me overcome the back problems, until 1977, when I had the offending disc removed. From then onwards, right up till today, I have done regular exercise, mainly aerobic walking these days. I also have been going to the gym, on and off for over forty years. I am not a lover of exercise, but I am very grateful for what it has done for me, since I started in 1970.
There were three unusual situations regarding my Pd history. I was bodily, very fit, which was not very common amongst Pd patients at the time of diagnosis; In 1994 I was prescribed a monotherapy of an MAO-b inhibitor, which stops the natural breakdown of dopamine, in the brain, which gives us the use of a greater amount of our own dopamine; I did not take any levodopa medication after the first two years of being diagnosed, which was extremely unusual; I gave up my high-powered job within three months of diagnosis, which relieved me of an enormous amount of stress; Many patients are not in the position to lose a large amount of their monthly income, as I was prepared to do.
All three of these circumstances have been responsible, in my opinion, for my good health today. Energetic exercise causes the brain to produce a substance called GDNF (Glial Derived Neurotrophic Factor), which repairs the damaged brain cells. This was proved by scientists and announced to the Parkinson’s world in 2006, in Washington DC, at the 1st World Parkinson's Cingress. The medication has also been independently proven to help slow down or even reverse Parkinson’s. From this you will see that doctors and scientists have known for many years that there is a lot we can do to help us overcome Pd. It does not appear to be in their interests to tell us this.
Because I no longer need to take any Patrkinson;'s medication and I live a normal life, I feel that I have to tell the world about my good fortune, and hope that others will follow in my footsteps. I am now seventy-nine, in 2014 and hope to live a normal life for many more years to come.
John Pepper 2014
Why did I Create This Website?
I’d like to think it is to make more people aware that there really is something we can all do to improve our quality of life, if we have Parkinson’s disease. I have spent many thousands of Rands, travelling all over the country, talking to other sufferers and Care-givers. I have always tried to make my visits part of a holiday. Sometimes I only spend a day in a place and move on, it depends how busy I am and how many people I really know.
I also want the website to bring about an awareness of my latest book, REVERSE PARKINSON’S DISEASE! Yes it really is possible to reverse Parkinson’s disease. I don’t know so much about those of us, who have had it for a long time. I don’t say that they cannot do anything to help themselves, but it is going to be a lot harder for them, than it was for me. Although my Parkinson’s started in 1963, it was only in 1992, that the neurologist was able to diagnose it, because of all the exercise I had been doing since 1970..
My symptoms started in 1963, when I found that I could not throw a ball properly. That was followed quite quickly by finding that nobody could read my handwriting, it got so bad. Then many of the other symptoms followed, one by one.
My neurologist said to me, “Parkinson’s disease is a neurological, degenerative disease, for which there is no cure. Get used to it, and get on with your life. You will continue to become more and more rigid, until you finally become bed-ridden and unable to move at all.” I did get on with my life, but I did not get used to the idea of becoming completely bed-ridden. That thought was too difficult for me to imagine. I fought hard to keep whatever movement I still had.
Unbeknown to me, at the time, I was already doing two things that definitely helped me to reverse my symptoms. It will take me many hours to tell you my whole story, so I wrote a book, and I hope you will want to know what I did, and what you can do, to bring about a reversal of your condition.
My website will tell you everything you need to know about what to do to reverse Parkinson’s Disease, but only you can do it for yourself. Nobody else can do it for you.
Knowing the facts, without knowing anything about why this or that works, isn’t good enough. You won’t be motivated to do what has to be done. There are no easy ways out. I have to make you want to do all the work, because, if you do, YOU WILL GET ALL THE BENEFIT, NOT ME!
The Five Most Important Actions Needed to Take Control of Parkinson’s Disease
I am not a doctor, I am a Parkinson’s Patient with 51 years of experience. These are the actions, which have helped me:
1. Regular Energetic Exercise
2. An MAO-b Inhibitor as the only Medication
3. Learn how to Take Conscious Control of all movements
4. Manage Stress Levels
5. Adopt a Positive Attitude
Power of the mind to move treatment further
Copied from The Northwest Parkinson’s Foundation Weekly News Update
Dr. Monique Giroux
PD Community Blog of NWPF - I have just completed a series of on mind-body medicine and the power of the mind in improving one’s outlook, treatment outcomes and perhaps life trajectory when living with a chronic condition. An experience at a recent lecture coupled with my own observations as a physician has led to the following observations:
1. You don’t need a lot of special props programs or techniques.
2. Be intentional. Identify what your intentions and goals are and how you are going to pay attention to the goal in the moment. This will help you identify and complete the steps needed to get there.
3. Find a moment. You may not need 20 or 40 minutes to get started. Simply taking two minutes for yourself, engaging your mind’s power on that very moment is the best way to get started
4. De-stress. Learn what works best for you – yoga tai chi, deep breathing exercises, aromatherapy, medication or guided imagery to name a few of the stress reduction techniques or activities available to you.
5. Learn to label your feelings or ideas. Science tells us that simply labelling our feelings or identifying the cause of our fears, concerns or reactions helps us deal better with distressing life events
6. Practice loving kindness. To others and equally important our selves.
7. Combine these stress reduction techniques and/or positive affirming techniques with medical care for the best response. What would happen if you couple a few minutes of guided imagery or meditation after taking a medication, exercising or any other treatment helpful for you condition. The additive effects may surprise you.
Add your own observation or activity you have found helpful to enhance the powerful effects of mind on body by replying with your own comment
The Dangers Of Toxic Metals
By Lawrence Wilson M.D.
Toxic metals comprise a group of minerals that have no known function in the body and in fact are harmful. Today mankind is exposed to the highest levels of these metals in recorded history, thanks to their industrial use and burning of coal, petroleum and incineration of waste material. They affect everyone and are a major cause of illness, aging and even genetic defects.
The study of toxic metals is part of nutrition and toxicology, areas not emphasized in medical schools. For this reason, these important causes of disease are accorded little attention in conventional mainstream medicine. This article focuses on the extent of toxic metal problems sources of toxic metals, symptoms and how to remove them.
INTRODUCTION TO THE MINERALS
Minerals are the building blocks of our bodies. They are required for body structure, fluid balance, protein structures and to produce hormones. They are a key for the health of every body system and function. They act as co-factors, catalysts or inhibitors of all enzymes in the body. Copper and iron, for example, along with other minerals are required for the electron transport system, and thus needed for all cellular energy production.
Minerals are classified into four groups: The macrominerals, or those needed in large quantity, include calcium, magnesium, sodium, potassium, phosphorus, sulphur, iron, copper and zinc. Required trace minerals include manganese, chromium, selenium, boron, bromine, silicon, iodine, vanadium, lithium, molybdenum, cobalt, germanium and others. Possibly required trace minerals include fluorine, arsenic, rubidium, tin, niobium, strontium, gold, silver and nickel. Toxic metals include beryllium, mercury, lead, cadmium, aluminum, antimony, bismuth, barium, uranium and others.
These categories overlap slightly because assessing minerals that are required by humans is problematic. Some may be needed in minuscule amounts. Clinical studies to prove this by depriving people of vital minerals would be cruel and possibly disastrous.
Also, note that minerals needed in lesser quantities are usually toxic in greater amounts. Examples are copper, iron, manganese, selenium and vanadium. Even calcium and sodium are quite toxic in excess.
TOXIC METAL DANGERS
Today mankind is exposed to the highest levels in recorded history of lead, mercury, arsenic, aluminum, copper, tin, antimony, bromine, bismuth and vanadium. Levels are up to several thousand times higher than in primitive man. In my clinical experience, everyone has excessive amounts of some or all of the toxic metals.
Toxic metals are also persistent and cumulative. The late Dr. Henry Schroeder, MD, who was a world authority on trace elements, wrote:
Most organic substances are degradable by natural processes. (However), no metal is degradable, they are here to stay for a long time.
Toxic metals replace nutrient minerals in enzyme binding sites. When this occurs, the metals inhibit, overstimulate or otherwise alter thousands of enzymes. An affected enzyme may operate at 5% of normal activity. This may contribute to many health conditions. Toxic metals may also replace other substances in other tissue structures. These tissues, such as the arteries, joints, bones and muscles, are weakened by the replacement process. Toxic metals may also simply deposit in many sites, causing local irritation and other toxic effects. They may also support development of fungal, bacterial and viral infections that are difficult or impossible to eradicate until this cause is removed.
The mineral replacement process often involves the idea of preferred minerals. For example, the body prefers zinc for over 50 critical enzymes . However, if zinc becomes deficient - and our soil and food are very low in zinc today - or exposure to cadmium, lead or mercury is sufficiently high, the body will use these in place of zinc. Cadmium, in particular, is located just below zinc in the periodic table of the elements, so its atomic structure is very similar to that of zinc. It almost fits perfectly in the zinc binding sites of critical enzymes such as RNA transferase, carboxypeptidase, alcohol dehydrogenase and many others or great importance in the body.
The ability to replace a vital mineral means, however, that toxic metals are not completely harmful. Indeed, they can extend life. They keep bodies functioning when vital minerals are deficient.
An analogy is to imagine taking an automobile journey. If one is far away from a repair shop when a key part like the fan belt breaks, if one had a spare piece of rope, one could tie it around the pulleys and continue the trip slowly. The rope would not function nearly as well as the original part, but would allow one to keep going. This is how toxic metals can function positively in the body. Many people limp along on grossly deficient diets, and are even born deficient and toxic. They do not realize their fatigue and other symptoms are due to the presence of incorrect replacement parts in their biological engine compartments. Depending on where toxic metals accumulate, the resulting effects may be given names such as hypothyroidism, diabetes or cancer.
MODERN DIETS AND TOXIC METALS
The danger of toxic metals is greatly aggravated today by the low mineral content of most of our food supply. An abundance of vital minerals protects against toxic metals. Vital minerals compete with toxic metals for absorption and utilization in enzymes and other tissue structures. However, when food is low in essential minerals, the body absorbs and makes use of more toxic metals. To continue the previous analogy, we are not stocking up sufficiently on factory parts, so we must use the greatly inferior replacement parts ≠ toxic metals. Causes for the low mineral content of almost all agricultural products are primarily:
Hybrid crops are bred for production or disease resistance, rather than superior nutrition.
Superphosphate fertilizers produce higher yields by stimulating growth, but do not provide all the trace elements.
Monoculture, the growing of just one crop over and over on the same piece of land, eventually depletes the soil.
Toxic sprays damage soil microorganisms needed to help plants absorb minerals from the soil.
Food refining and processing almost always reduce the mineral content of our food. Whole wheat flour, when milled to make white flour, loses 40% of its chromium, 86% of its manganese, 89% of its cobalt, 78% of its zinc and 48% of its molybdenum. Refining cane into sugar causes even greater losses. EDTA may be added to frozen foods to retain their color. However, this chelating agent removes minerals that otherwise would cause the surface minerals to ?tarnishπ, discoloring the vegetables.
According to Dr. Weston Price, author of Nutrition and Physical Degeneration, primitive man ate 5 to 11 times the amount of the essential minerals in his diet as modern man . The term 'empty calories' aptly describes most of our food today.
SOURCES AND DETECTION OF TOXIC METALS
For a more complete list of sources for each of the major toxic metals organized by the metal, see the Reference Guide at the end of this article.
Food Sources. Food grown near highways or downwind of industrial plants may contain lead and other toxic amounts of metals. Even organic home gardens may be contaminated if, for example, old house paint containing lead leaches lead into the soil.
Lead is considered the most widely distributed toxic metal due to its many uses in industry. However, mercury, arsenic, cadmium and particularly aluminum are just as widespread if not more, but are less well-studied.
Pesticides used on fruits, vegetables and many other foods may contain arsenic, lead, copper, mercury and other toxic metals.
Fish, especially those caught near the coast or in contaminated streams or lakes, are universally contaminated. Shellfish and bottom feeders in particular contain excessive cadmium, mercury and other toxic metals. Large fish concentrate mercury a million times or more. The federal government recently issued a warning that pregnant and lactating women should avoid tuna, shark, king mackerel and other large fish. I recommend everyone avoid these fish!
Table salt has aluminum added as an anti-caking agent. Sea salt is much better. Beverages in aluminum cans or food cooked in aluminum may contain elevated levels of aluminum. Ceramic plates and cookware from other nations often contain leaded glazes that come off onto the food.
Hydrogenated oils found in commercial peanut butter, margarines including soy margarine and vegetable shortening may contain nickel and cadmium used as catalysts.
Drinking Water. This is the most important source of toxic metals for most people. Aluminum, copper, toxic chlorides and fluorides are added to many municipal water supplies. Aluminum allows dirt to settle out of the water, while copper kills algae that grows in reservoirs. Chlorine is used to disinfect water, although ozone works very well and is a far more healthful treatment. Wells and even municipal water may also contain some lead, arsenic and other undesirable metals. Galvanized and black plastic pipes can be an important source of cadmium. Lead-soldered pipes and copper pipes may increase these metals in the drinking water if the water is soft. It is an uncommon problem in hard water areas.
Fluoride compounds added to drinking water are extremely toxic. They have found their way into ground water supplies, and thus into the food chain. Fluoride levels in foods processed with water may be very high, especially baby foods and reconstituted fruit juices. Health authorities who recommend fluoridating the water rarely if ever take into account fluorides already found in natural foods, foods processed with fluoridated water and fluoridated toothpaste. The combination adds up to overload in all cases.
Hydrofluosilicic acid, the chemical often used to fluoridate drinking water, is a smokestack waste that contains lead, mercury, cadmium, arsenic, aluminum, benzene and radioactive waste material .
Note that carbon and carbon block filters do not remove most toxic metals from water. Only distillation and reverse osmosis remove most toxic metals. Good quality spring water is probably best way to avoid the most common source of toxic metals and at the same time obtain vital minerals.
Airborne Sources of Toxic Metals. Most toxic metals are effectively absorbed by inhalation. Auto and particularly aircraft exhaust, industrial smoke and products from incinerators are among the airborne sources of toxic metals and other chemicals. Burned high in the atmosphere, aircraft fuel deposits everywhere and affects everyone on earth.
Burning coal can release mercury, lead and cadmium among other metals . Iranian and Venezuelan oil are high in vanadium. Other oil is excessive in toxic sulphur compounds. Tetraethyl lead was added to gasoline for many years. Residues are present on pavement and may settle on buildings, cropland and elsewhere. Today, manganese is added to gasoline. Uranium exposure is largely from airborne sources such as nuclear tests and accidental nuclear releases.
Older methods of incineration of electronic parts, plastics, treated fabrics, batteries and even diapers release all the toxic metals into the air. The use of scrubbers and newer methods of very high temperature incineration are much better.
Cigarette and marijuana smoke are high in cadmium, found in cigarette paper. Pesticides used on these crops may contain lead, arsenic and other toxic metals.
Medications. Many patented prescription and over-the-counter drugs contain toxic metals. Cipro (fluoquinolones) and Prozac (fluoxetine) are fluoride-containing chemicals, for example. Thimerisol, a mercury-containing preservative, is used in some vaccines, including all flu shots. Independent evaluation of a large study that is part of the Centers For Disease Control Vaccine Safety Datalink concluded that children are 27 times as likely to develop autism after exposure to three thimerisol-containing vaccines than those who receive thimerisol-free versions.
Thiazide diuretics contain mercury. These include Maxzide, Diazide and many others. Antacids such as Ryopan, Gaviscon, Maalox, Mylanta and many others are very high in aluminum. Antibiotics may also contain toxic substances including metals.
Direct Skin Contact. Almost all anti-perspirants and many cosmetics contain aluminum. Dental amalgams contain mercury, copper and other metals. Dental bridges and other appliances often contain nickel. Prostheses and pins used to hold bones together may contain nickel and other toxic metals. Copper intra-uterine devices, if left in place for years, release a tremendous amount of copper into the body. Soaps, body lotions and creams often contain toxic compounds. A few hair dyes contain lead. Selsun Blue shampoo contains selenium that is quite toxic in high doses.
Household lawn and garden chemicals may contain lead, arsenic and other compounds. Mercury treated seeds and arsenic-treated wood are other common sources of toxic metals.
Occupational exposure is important for plumbers, electricians, auto mechanics, printers, ironworkers, office workers and many other occupations. Workers need to wear gloves, masks and take other precautions when handling inks, metals and other toxic materials.
Congenital Toxic Metals. Today, all children are born with some toxic metals acquired in utero. All the toxic metals pass through the placenta from mother to child. This is seen clearly when reviewing mineral analyses of infants, such as that of Chloe, age 4 months, shown in the figure.
DETECTING TOXIC METALS
Toxic metals are not easy to detect as they lodge deep within tissues and organs. Serum tests are helpful at times, and not helpful for most chronic exposure. Toxic metals are removed from the blood rapidly and deposited in storage organs and tissues where they will do less damage.
Tissue tests such as hair mineral analysis are therefore more often helpful. The United States Environmental Protection Agency reviewed over 400 reviews of the use of hair for toxic metal detection and concluded that:
Hair is a meaningful and representative tissue for (biological monitoring for) antimony, arsenic, cadmium, chromium, copper, lead, mercury, nickel, vanadium and perhaps selenium and tin.
The author of a study of lead toxicity in Massachusetts school children, Dr. R. Tuthill, concluded:
Scalp hair should be considered a useful clinical and epidemiological approach for the measurement of chronic low-level lead exposure in children.
Skilled interpretation of the hair analysis is required. For example, when aluminum is elevated in the hair, iron and manganese are almost always elevated, but hidden as they do not accumulate in the hair.
Another method of detection is a challenge test in which one takes an injection of a chelating agent such as EDTA or DMPS. Then a 24-hour urine sample is analyzed for toxic metals. This will reveal some metals that are in the arteries, veins and kidneys, but misses most of the others.
No test can detect anywhere near all the toxic metals in the body. Often they are sequestered in hard-to-reach places such as the bones or poorly-perfused fatty tissues. They will be revealed, however, as they are excreted through the hair if one performs repeat hair mineral tests. As a clinician, I must assume everyone has toxic metals and any sound health program needs to be designed to remove them.
SYMPTOMS ASSOCIATED WITH TOXIC METALS
For a complete list of symptoms for each toxic metal, see the Reference Guide at the end of this article.
Toxic metals can contribute to any imaginable illness. For example, lead that replaces calcium in the bones can contribute to weakened bones and osteoporosis. Cadmium that replaces zinc in the arteries causes inflammation and hardening of the arteries. Iron that replaces zinc and other minerals in the pancreas, adrenals and elsewhere can contribute to impaired blood sugar tolerance and diabetes. Copper that replaces zinc in the brain is associated with migraine headaches, premenstrual syndrome, depression, anxiety, panic attacks and much more. Mercury and copper that replace selenium in various tissues impairs the conversion of T4 to T3, contributing to thyroid imbalances.
Toxic Metals and Aging. The slow, or not so slow, replacement of vital minerals with toxic metals is an important and neglected cause of aging due to deactivation of enzyme systems and the loss of organ and tissue integrity.
Toxic metal accumulation also feeds on itself. As one's energy production decreases with age, the body is less able to eliminate toxic metals, causing more metal accumulation.
Toxic Metals and Gene Expression. Genetic birth defects may be caused by faulty DNA or by faulty gene expression. Even if one's DNA is perfect, the synthesis of proteins from that DNA can be faulty. For example, zinc is required for a key enzyme in gene expression, RNA transferase. Not surprisingly, zinc deficiency is associated with conditions such as neural tube defects. A recent article in the American Journal of Clinical Nutrition discussed this hidden cause of genetic defects.
"An alternate form of a gene present in greater than 1% of the population is called a polymorphism".
While the article mainly discusses vitamin deficiencies as a cause for genetic defects, it gives the example that "mutations in Cu/Zn superoxide dismutase cause 25% of amyotrophic lateral sclerosis."
SOLUTIONS TO TOXIC METAL OVERLOAD
One should not fear toxic metals. They cannot be completely avoided, but one can minimize exposure with careful eating and a healthful lifestyle. Also, our bodies have a lot of evolutionary experience with them and effective mechanisms to eliminate them. These can be supported and enhanced by nutritional and other therapies. The following program, when followed faithfully, will lead to the safe removal of toxic metals.
1. Eat a varied, excellent-quality diet of mineralized foods. The body will absorb and utilize less toxic metals if it receives more preferred minerals. In a 1994 study in the Journal of Clinical Nutrition, food labelled "organic" selected randomly from Chicago food markets had an average of twice the mineral content of standard supermarket food. The famed people of Hunza who lived to 120 years or longer in excellent health drank glacial runoff that was so mineral-rich the water was cloudy.
Especially mineral-rich foods include kelp, sea salt, other sea vegetables, small fish and all root vegetables except potatoes and yams. Root vegetables must be cooked at least 45 minutes for their minerals to be most bio-available.
Adequate protein, especially animal protein, supplies sulphur-containing amino acids which help chelate toxic metals and support liver detoxification pathways.
Other high-sulphur foods include egg yolks and vegetables in the cabbage, radish, garlic and onion families. Sulphur is very helpful for detoxification in general, and for mercury and copper in particular.
Fibre is also helpful to reduce some toxic metals. It reduces bowel transit time, which can limit absorption of toxic metals. Certain fibres such as modified citrus pectin bind some toxic metals that reduces their absorption.
2. Improve Your Lifestyle and Habits of Living. Eat regular, sit-down meals. Also, eat quietly and slowly, and chew thoroughly. This can greatly enhance digestion and absorption of vital minerals. Most everyone needs to take digestive enzymes at least for a while to improve digestion. A relaxed and positive outlook also greatly facilitates digestion.
Sleeping 9 or 10 hours per night is most helpful to eliminate toxic metals. Most people do not sleep nearly enough. Six or seven hours per night is not sufficient for healing and detoxification. These are parasympathetic activities that occur mainly during the hours of sleep and rest.
3. Avoid all extreme or deficient diets. Strict vegetarian diets, for example, are always deficient in zinc and usually in many other essential nutrients. Raw food diets, while higher in some vitamins and other nutrients, are usually much lower in vital minerals. Cooking does not reduce the mineral content of food and usually makes minerals much more bio-available by breaking down fibre. Cooking also concentrates the food so that one ends up ingesting many more vital minerals.
Skipping meals or snacking on the run, eating the same foods every day or living on protein drinks also induce mineral deficiencies. For example, egg or whey protein powder is not a substitute for eating eggs or fresh goat milk. The latter are whole foods that are much richer in many minerals. Food supplements are never a substitute for an excellent diet.
Avoid refined foods such as white sugar, white flour, table salt and white rice. These are almost devoid of vital minerals and will cause the body to absorb and utilize more toxic metals.
4. Take Nutritional Supplements. Supplements can help reduce the absorption of toxic metals and facilitate their removal. Kelp supplements are one of the best. Kelp contains a wide range of vital minerals. It also contains some toxic metals, as do all products from the sea. However, they are tightly bound. Alginates found in kelp also help bind and remove radioactive minerals, another hidden and important health concern related to toxic metals.
One can use antagonists to help eliminate toxic metals. These compete specifically with toxic metals for absorption, transport and utilization in enzyme binding sites and in other tissue structures. For example, zinc and calcium are cadmium antagonists. Selenium and zinc are mercury antagonists.
I worked for a time at the National Institute of Occupational Safety and Heath. We investigated a factory in which workers were fed milk to help avoid lead poisoning. While a bit crude, the principle was sound, as calcium is a lead antagonist.
Specific minerals that most people need to add to their daily diet are more zinc, chromium, selenium and manganese. Most multivitamins do not contain enough. Other supplements that are helpful for toxic metals are N-acetyl cysteine, garlic, chlorella, cilantro extract and other sulphur-containing amino acid supplements. Chlorella, raw garlic, cilantro and NAC have a disadvantage in that they are extremely yin in Chinese medical terminology. This is not helpful for most people. The Life Extension Foundation offers a number of excellent mineral supplements, as well as Only Minerals and Phyto-food.
5. Reduce Airborne Exposure and Skin Contact. Avoid contaminated air as much as possible. City dwellers should use air filters in their homes and offices that can trap toxic metals. Unfortunately, even rural areas can experience pesticide drift, and auto and industrial fumes. If you must handle toxic materials at home or at work, wear gloves, masks and other protective gear.
Read labels carefully on skin care products. Most cosmetics and skin care products are somewhat toxic.
6. Improve your energy. This greatly enhances the body's ability to eliminate toxic metals. Nutritional balancing science using hair analysis is the key to this. It can assess metabolic rate, metabolic type, and exactly which supplements and how much of each are needed. Random supplementation does not work well.
Also, a combination of adequate rest and sleep, excellent diet and a healthful lifestyle are important. When needed, other natural therapies such as chiropractic, body work, energy work and others are also most helpful to restore and maintain an optimum energy level.
7. Improve your eliminative organs. In almost everyone, these do not function optimally. They are congested or sluggish due to glandular imbalances and the burden of toxic substances everyone must cope with. Nutritional support includes milk thistle and dandelion root for the liver, uva ursi and parsley for the kidneys, and fibre, digestive enzymes and other products for the bowel. Other excellent therapies include saunas, coffee enemas, colonic irrigation, massage, skin brushing and others.
Excessive sympathetic nervous system activity inhibits detoxification. Supplementary nutrients that inhibit excessive sympathetic activity include calcium, magnesium, zinc, choline, inositol, GABA, taurine and calming herbs. Other helpful therapies for this purpose include saunas, meditation, tai chi and biofeedback.
Saunas (hot air baths) have been used for thousands of years by many cultures. They are quite safe and very effective for detoxification. The New York Times recently reported on the success of saunas when nothing else was effective for the firemen who became ill at the World Trade Center disaster. Saunas draw blood to the surface, powerfully stimulate circulation and decongest the internal organs. Infrared saunas penetrate more deeply and are often more comfortable as they work at lower temperatures. Note that sweating during exercise is not as effective for detoxification as sweating when one is relaxed in a sauna. The best saunas I have experienced are those powered by infrared heat lamps.
8. Add Chelating Agents. To chelate means to bind to a metal. Certain substances bind tightly to toxic metals and assist their removal. Natural chelators include vitamin C, sulphur-containing amino acids, and some herbs including yellow dock and bugleweed. Molybdenum complexes with copper and is excellent when used sparingly.
Synthetic chelating agents include penicillamine and BAL (British anti-lewisite) for copper and deferoxamine for iron and aluminum. EDTA (ethylene diamine tetra-acetic acid) is a synthetic amino acid that binds to many minerals, toxic and essential. DMPS (sodium salt of 2,3-dimercapto-1-propane sulphonic acid) and DMSA (meso-2,3-dimercaptosuccinic acid) are synthetic agents used for mercury toxicity. Synthetic chelators are drugs that have more side effects, among which is their tendency to remove more good minerals along with the toxic ones. They may also accumulate in the body, along with the toxic metals they bind.
Toxic metals are in a delicate balance with other nutrients. Aggressive use of any chelator can have adverse and sometimes devastating health effects for this reason. This applies to high dose vitamin C, which powerfully lowers copper, and even moreso to the synthetic agents. For example, DMPS can dislodge mercury from fairly safe storage sites. It may then redeposit in more vital organs. It must be used with utmost caution.
Though chelation is the best known method to eliminate toxic metals, in my experience, synthetic chelators are hardly ever needed if one will undertake a complete healing program.
Toxic metal exposure is higher than ever before and an important cause of ill health. I predict that removing them will become recognized as a great secret for healing many health conditions. Unfortunately, few doctors test for or even consider searching for toxic metals.
Reducing our exposure is the simplest and most cost-effective way to prevent toxic metal problems. Efforts to clean up the water, food and air have advanced greatly, but more needs to be done. Governments can do their part, but the public must also learn about the dangers of toxic metals and how to avoid them. It should be a top priority in the education of the children.
Young men and especially young women can do much to help the next generation and themselves to avoid toxic metals by improving their health before having children. Dr. Weston Price discovered that in many primitive cultures, prenatal care for young women began at puberty by feeding the women special foods designed to maximize their vital mineral intake.
One can greatly enhance the elimination toxic metals by reducing exposure, increasing vital minerals in the diet and avoiding mineral-deficient food. Assisting the eliminative organs, improving digestion, taking appropriate supplements, obtaining plenty of rest and using antagonists and perhaps chelators are also most helpful. The general use of inexpensive, infrared electric light saunas would be another excellent additional way to enhance toxic metal removal. These are excellent health insurance and well worth the effort.
SOURCES AND SYMPTOMS OF THE COMMON TOXIC METALS
Aluminum - cookware, beverages in aluminum cans, tap water, table salt, baking powders, antacids, processed cheese, anti-perspirants, bleached flour, antacids, vaccines and other medications and occupational exposure.
Arsenic - pesticides, beer, table salt, tap water, paints, pigments, cosmetics, glass and mirror manufacture, fungicides, insecticides, treated wood and contaminated food.
Beryllium - air pollution (burning fossil fuels), manufacture of plastics, electronics, steel alloys and volcanic ash.
Cadmium - cigarettes, (tobacco and marijuana), processed and refined foods, large fish, shellfish, tap water, auto exhaust, plated containers, galvanized pipes, air pollution from incineration and occupational exposure.
Copper - copper water pipes, copper added to tap water, pesticides, swimming in pools, intra-uterine devices, vegetarian diets, dental amalgams, nutritional supplements - especially prenatal vitamins, birth control pills, weak adrenal glands and occupational exposure.
Lead - tap water, cigarette smoke, hair dyes, paints, inks, glazes, pesticide residues and occupational exposure in battery manufacture and other industries.
Mercury - dental amalgams, large fish, shellfish, medications, air pollution, manufacture of paper, chlorine, adhesives, fabric softeners and waxes.
Nickel - hydrogenated oils (margarine, commercial peanut butter and shortening), shellfish, air pollution, cigarette smoke, plating and occupational exposure.
Aluminum - Alzheimer's disease, amyotrophic lateral sclerosis, anaemia and other blood disorders, colic, fatigue, dental caries, dementia dialactica, hypoparathyroidism, kidney and liver dysfunctions, neuromuscular disorders, osteomalacia and Parkinson’s disease.
Arsenic - abdominal pain, abnormal ECG, anorexia, dermatitis, diarrhea, edema, enzyme inhibitor, fever, fluid loss, goiter, hair loss, headache, herpes, impaired healing, interferes with the uptake of folic acid, inhibition of sulphydryl enzyme systems, jaundice, keratosis, kidney and liver damage, muscle spasms, pallor, peripheral neuritis, sore throat, stomatitis, stupor, vasodilation, vertigo, vitiligo and weakness.
Beryllium - adrenal insufficiency, arthritis, bone spurs, bursitis, depression, fatigue, osteoporosis and symptoms of slow metabolism.
Cadmium - hypertension, arthritis, diabetes, anaemia, arteriosclerosis, impaired bone healing, cancer, cardiovascular disease, cirrhosis, reduced fertility, hyperlipidemia, hypoglycemia, headaches, osteoporosis, kidney disease, schizophrenia and strokes.
Copper - acne, adrenal hyperactivity and insufficiency, agorophobia, allergies, hair loss, anaemia, anxiety, arthritis, autism, cancer, chronic candida albicans infection, depression, elevated cholesterol, cystic fibrosis, depression, diabetes, dyslexia, elevated estrogen, failure to thrive, fatigue, fears, fractures of the bones, headaches, heart attacks, hyperactivity, hypertension, hypothyroidism, infections, inflammation, insomnia, iron storage diseases, kidney and liver dysfunctions, decreased libido, multiple sclerosis, nervousness, osteoporosis, panic attacks, premenstrual syndrome, schizophrenia, strokes, tooth decay and vitamin C and other vitamin deficiencies.
Lead - abdominal pain, adrenal insufficiency, anaemia, arthritis, arteriosclerosis, attention deficit, back problems, blindness, cancer, constipation, convulsions, deafness, depression, diabetes, dyslexia, epilepsy, fatigue, gout, impaired glycogen storage, hallucinations, hyperactivity, impotency, infertility, inflammation, kidney dysfunction, learning disabilities, diminished libido, migraine headaches, multiple sclerosis, psychosis, thyroid imbalances and tooth decay.
Mercury - adrenal gland dysfunction, alopecia, anorexia, ataxia, bipolar disorder, birth defects, blushing, depression, dermatitis, discouragement, dizziness, fatigue, headaches, hearing loss, hyperactivity, immune system dysfunction, insomnia, kidney damage, loss of self-control, memory loss, mood swings, nervousness, numbness and tingling, pain in limbs, rashes, excessive salivation, schizophrenia, thyroid dysfunction, timidity, tremors, peripheral vision loss and muscle weakness.
Nickel - cancer (oral and intestinal), depression, heart attacks, hemorrhages, kidney dysfunction, low blood pressure, malaise, muscle tremors and paralysis, nausea, skin problems, tetany and vomiting.
 Schroeder, H., Trace elements and Man, The Devin-Adair Company, CT, 1975.
 Ibid, p. 154
 Braunwald, E. et al, editors, Harrisonπs Principles of Internal Medicine, McGraw-Hill, Professional, 15th edition, 2001.
 Pfeiffer, C., Zinc and Other Micronutrients, Keats Publishing, CT, 1978.
 Kutsky, R., Handbook of Vitamins, Minerals and Hormones, 2nd edition, Van Nostrand Reinhold Company, NY, 1981.
 Ibid., Schroeder, H., Trace Elements and Man.
 Hall, R.H., Food For Naught, The Decline in Nutrition, Vintage Books, NY, 1974.
 Anderson, M. and Jensen, B. Empty Harvest; Understanding the Link Between Our Food, Our Immunity and Our Planet, Avery Penguin Putnam, 1993.
 Price, W., Nutrition and Physical Degeneration, Price-Pottenger Nutrition Foundation, CA, 1949.
 Stannard, J., Shim, Y.S., Kritsineli, M., Labropoulo, P.,Tsamtsouris, A., Fluoride levels and fluoride contamination of fruit juices, J Clin Ped Dentistry, 1991;16(1).
 From the warning label on hydrofluosilicic acid, Cargill Corporation, FL.
 Casdorph, H.R. and Walker, M., Toxic Metal Syndrome, Avery Publishing, NY, 1995.
 National Autism Association, Press Release, Feb. 9, 2004.
 Eck, P. and Wilson, L., Toxic Metals in Human Health and Disease, Eck Institute of Applied Nutrition and Bioenergetics, Ltd., AZ, 1989, p. xiv.
 Shamberger, R.J., Validity of hair mineral testing, Bio Trace Element Res, 2002, 87:1-28.
 Muir, M., Current controversies in the diagnosis and treatment of heavy metal toxicity, Alternative and Comp Ther., June 1997:170-178.
 Environmental Protection Agency, Research and Development, Toxic Trace Metals in Human and Mammalian Hair, EPA-600, 4.79-049, August 1979, p. 3.
 Tuthill, R., Hair lead levels related to childrenπs classroom attention-deficit behavior, Arch Env Health, 1996, 51(3)214-220.
 Ames, BN, Elson-Schwab, I., Silver, EA, High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity: relevance to genetic disease and polymorphisms, Am J Clin Nut. April 2002;75(4):616-658.
 1993, J Applied Nut, 45(1).
 Mortensen, M.E. and Watson, P., Chelation therapy for childhood lead poisoning: The changing scene in the 1990s, Clin Ped., 1993;32:284-291.
 Committee on Drugs, American Academy of Pediatrics Treatment guidelines for lead exposure in children, Pediatrics, 1995, 96:155-159.
Dr. Lawrence Wilson specializes in mineral analysis and the removal of toxic metals, and has done so for 23 years. He consults for Analytical Research Laboratories, a mineral testing facility, where he apprenticed for 14 years with a brilliant biochemist, Dr. Paul C. Eck. He wrote a text about his work, Nutritional Balancing and Hair Mineral Analysis.
He has reviewed some 15,000 hair mineral analyses and followed some 5000 patients as they removed their toxic metals and balanced their minerals. He has also experimented extensively with sauna therapy, an emerging treatment modality for toxic metal removal.
Dr. Lawrence Wilson
P.O. Box 54
Prescott, AZ 86302-0054
Visit http://www.drlwilson.com/ for books, and audio tapes from Dr. Wilson.
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‘Reverse Parkinson's Disease!’
Do you want to find the best ways to improve your quality of life, if you have Parkinson's disease...?
Contrary to the thoughts and advice of most of the medical profession, and the established way of treating Parkinson’s disease, the progression of this terrible condition, can be reversed! It is being done right now.
Find out how I, John Pepper, managed to reverse my Parkinson's and how you can possibly do it too?
I have successfully reversed my Parkinson’s disease, to the point where I no longer need to take any medication. It has now been over twelve years (as at 2014) since I last took any Parkinson’s disease medication.
I was diagnosed with Parkinson's disease in 1992, and stopped taking Parkinson’s disease medication in 2002. My Parkinson’s disease symptoms began in 1963, when I found that I could not throw a ball properly.
My physical and mental condition has improved so much that other people, even my close friends, have no clue that I still have Parkinson's disease. I even had to convince an international research scientist, that I have Parkinson’s disease. After convincing himself, through exhaustive investigations, he could only stand in absolute amazement.
Fellow Parkinson's sufferers come up to meet me, when I’m travelling on my Parkinson's awareness seminars and are in awe of the miracle they see.
YES! There is HOPE...
Dear friend I’m telling you this because I have lived in the clutches of Parkinson's disease for over fifty years.
ñ I can now WALK, without shuffling!
ñ I can now bring a GLASS of WINE to my mouth, without spilling it!
ñ I can now SPEAK, without slurring my words.
ñ I can now SING, without stopping, because I cannot think of the next words!
ñ I can now DRAW a STRAIGHT LINE, without any squiggles!
ñ I can now SMILE, with the same old facial expression I had before the Parkinson’s disease took over my life!
I am well aware of the terrible side effects of Parkinson’s disease medication:-
ñ Dyskinesia. (Unwanted, embarrassing movements of the arms and legs, sometimes quite violent)
ñ On/Off periods of effectiveness of the medication. When you are in the ‘On’ condition, you feel as if you never had Parkinson’s disease. But quite suddenly, you go into the ‘Off’ condition, which is often worse than you would feel if you did not take any Parkinson’s disease medication at all.
ñ The need to take more and more medication, just to get the same effect you got in the beginning.
ñ The inevitability of getting to the stage, where the medication has no effect, leaving you with nowhere to go, other than having invasive brain surgery.
ñ The need to regiment your life into taking this and that medication at fixed times of the day and night; otherwise face the consequences of not having done so.
ñ Other common side effects, including nausea, giddiness, Hallucinations and discomfort.
Could you possibly do the same, and reverse your Parkinson's disease?
YES! I urge you to follow this path!
I've seen the results of many others, who have followed this path – Look at 'Endorsements' on this website. There have been dozens more!
They have improved the quality of their lives tremendously. We have only one life to lead and we can enjoy it, if we choose to embark on this new lifestyle, in order to reverse our Parkinson’s disease.
ñ Your family and loved one's could see you at your best for much longer.
ñ You could well be able to do all the travelling you thought you'd have to give up. At the age of 79, I have just come home from a cruise up into the Baltic Sea for two weeks. I need no walking aids and I am still able to walk all day long on guided tours. In 1992, I could not have donw any of this.
ñ You could well be able to do so much more, when you have learned how to control your movements, without the need for medication.
ñ You could well regain your self-confidence again.
ñ You could well feel comfortable in the company of others.
ñ You could well speak properly again, without becoming flustered and self-conscious
ñ You could well be able to smile again, when you look in the mirror at that new YOU!
I offer you my effective solution to reverse your Parkinson's disease, right here today, because I want you to reverse your Parkinson's disease, exactly as I have, and many others are doing.
1. Follow my unique lifestyle modification protocol.
2. Discover the unique Brain exercises you need to do.
3. Practice the exact exercises I used, to reverse my Parkinson's disease.
4. Change your attitude towards life and your Parkinson’s disease.
5. Avoid food items you shouldn't eat, and learn how you should change your eating habits.
6. Manage your harmful stress levels, which seriously affect your Parkinson's disease.
7. Improve your sleeping habits.
8. Learn how to focus your mind on all those movements, which Parkinson's disease has made so difficult for you.
I found the 8 steps above, the only way to reverse Parkinson's disease. In my search for ways to improve my quality of life, this was the only way I have found to effectively reverse my Parkinson's disease. My original prognosis for my quality of life with Parkinson's disease was very bleak, but it has turned out to be no worse than anybody else without Parkinson’s disease, because of the solutions I discovered. I am not offering to sell you any 'Snake Oil' or fancy 'Water'. I am not asking you to pay me so much every month to help you get better. I offer you all the information on this website, free of charge! It will stay up to date for as long as I live, and hopefully after I have gone.
I offer every one of you the exact Blue Print to reversing your Parkinson's right now.
Download it here - on the Home Page
4 Morning Tips for a Calm and Joyful Day!
Copied from The Northwest Parkinson’s Foundation Weekly News Update
Psychcentral.com - How we start the morning often sets the stage for how the rest of the day unfolds. Of course life throws us curve balls in the middle of the day, maybe you get a stressful email or someone rear ends you with their car or you lost that deal that you were looking forward to. Anything can happen in the present moment, but how we start our day can often affect how we greet those challenges.
Here are four tips to start your day that will help you with the inevitable ups and downs that you get handed.
1. Mindful Check-In – It’s good to begin the day simply noting where you are starting the day from. How is your body, what emotions are present, is your mind calm or already racing off to work? If you’re lying in your bed, you just note that, getting a sense of the body feels comfortable or tense. Are you feeling calm, anxious, annoyed, or maybe neutral? What is on your mind?
2. Prime Your Mind for Good – After a brief mindful check-in, one way of inclining your mind toward resiliency and even opening up to the good of the day is to consider an intentional gratitude practice. What in your life right now do you have to be grateful for? It could be something simple, like waking up on the right side of the bed, to having a roof over your head, to having a good cup of coffee in the morning. Just practice inkling your mind to the good in life.
3. Bring Presence to the Morning Activities – When you’re in the shower, be in the shower, not solving problems at work already. When you’re making breakfast for you or your family, consider the intention of that being to take care of yourself and others through the day. Put some love into your food. If there are pets or other family members in the house, before you leave make sure to say an intentional goodbye, looking into their eyes
4. Red Light Practice – As you drive to work use red lights as an opportunity to just check in, pressing the reset button if traffic has got you flustered or just using it as an opportunity to get centered and focus on what matters. You can make the choice to listen to your favorite music, intentionally plan the day out in your mind, or just have a quiet drive for a change. If you take public transportation you can do the same thing every time the bus, train, or subway stops. If you work from home, try this before turning on your computer. Exposing yourself to choices and acting on them just feels good and primes your mind for the rest of the day that you have choices in how you want to respond to situations.
Try these four things each morning as an experiment to see how your life changes.
As always, please share your thoughts, stories and questions below. Your interaction creates a living wisdom for us all to benefit from.
Vaccine for Parkinson’s Disease Enters Phase 1 Clinical Trial
Copied from The Northwest Parkinson’s Foundation Weekly News Update
Brain Blogger - The word “vaccination” generally brings to mind the prevention of infectious disease. However, significant advances have recently been made in the field of therapeutic vaccination for the treatment of chronic human disorders including neurological conditions and cancer.
Simply put, a vaccine is a mixture of compounds (most often proteins) that are selected for their ability to activate the immune system. These compounds, also known as antigens, are then injected into the body where they prepare the immune system for a future assault. The result of such prophylactic vaccination is either complete immunity to the illness, or at least a significant reduction in disease severity.
While a prophylactic vaccine is administered as a preventative measure, therapeutic vaccines are intended to help fight a disease that has already taken root. For example, a therapeutic vaccine might be given to a patient with cancer in order to enlist the patient’s own immune system in the fight against the disease.
The problem with this kind of approach is ensuring that the antigen used in the vaccine does not induce an immune response against healthy parts of the body. Again, using cancer as an example, diseased cells often contain mutated proteins, or proteins that are not usually expressed in adult tissue (known as onco-fetal genes). This means that vaccines using these antigens specifically target cancer cells.
Recently, a therapeutic vaccine for Parkinson’s disease developed by Austrian pharmaceutical company Affiris entered a clinical trial, a landmark move in the management of a disease that is currently only treated at a symptomatic level.
Patients with Parkinson’s disease suffer from a number of debilitating symptoms that are the result of the loss of a particular class of neurons in the brain. These neurons are involved in the control of muscle function and are particularly sensitive to the neurotransmitter dopamine. It is for this reason that current treatments revolve around modulation of the levels of this chemical.
The underlying molecular cause of the disease is a protein called alpha-synuclein. Ordinarily this protein is found throughout the neocortex, hippocampus, thalamus, substantia nigra, and cerebellum, although its precise function remains unknown. Importantly, this protein is very unusual in that it does not fold up like the majority of proteins. Its “floppy”, unfolded appearance means that it is particularly susceptible to getting tangled up and forming protein aggregates within brain cells, thus sentencing the affected cell to death. The formation of protein aggregates also underlies other brain disorders, including Alzheimer’s disease and Creutzfeld-Jacob disease.
It is the alpha-synuclein protein tangles that are targeted by the vaccine currently in trials, PD01A. The study, funded by the Michael J. Fox Foundation to the tune of $1.5 million, will assess the safety of the vaccine in both men and women with Parkinson’s disease, with the results expected in July of 2014.
Given the prevalence of protein aggregates in brain diseases, therapeutic vaccination might therefore represent a promising future treatment for several neurological conditions.
Procedure Could Help Local Patients Beat Parkinson's Disease
Copied from The Northwest Parkinson’s Foundation Weekly News Update
NBC 7 San Diego - Researchers hope a procedure using patients' own stem cells will cure Parkinson's Disease, or at least eliminate symptoms for decades.
Eight patients have joined the project at Scripps Research Institute in La Jolla to take part in the initial trial. Before they are able to proceed, they must get funding and obtain approval from the Food and Drug Administration.
"We're all treading water until the funds can be found and the hoops that the FDA give us can be jumped through," said Cassandra Peters, who was a paralegal at a law firm until 2005, when the symptoms of Parkinson's made it too difficult to work. She was diagnosed at age 44, 13 years ago.
The planned procedure entails taking a skin sample from the patients, then creating pluripotent stem cells with the genetic material. Millions of stem cells will then be injected into the brain to create dopamine neurons, which are destroyed by Parkinson's disease.
It's a technique discovered by Japanese researcher Shinya Yamanaka who won the Nobel Prize in Medicine in 2012.
Jeanne Loring, Ph.D., Director of the Center of Stem Cell Research at the Scripps Research Institute said similar work has been done in the past.
"There was work done in the 1980s and early 1990s in which fetal tissue was transplanted into the brains of people with Parkinson's disease," Loring said.
She said the problem was that fetal tissue produced inconsistent results.Loring believes using pluripotent stem cells derived from the same patient in which the cells will be transplanted will be much more reliable.
"The thing about Parkinson's Disease is there's really only one nerve cell type that needs to be replaced, and we know exactly where to put it," Loring said.
That confidence has been passed to the patients in this project who, unlike many other research projects, have been very involved in the process-- meeting with scientists and researchers in the laboratory.
"If this procedure works, and I know that it will, it will be the answer to so many people's prayers," Peters said.
Funding for the procedure remains a challenge as the government has not provided any grants for the project. Patients have been taking matters into their own hands, raising money for the non-profit Summit 4 Stem Cell, which hopes that Parkinson's victims' hike to Mount Everest base camp can help raise money for this initial procedure.
Edward Fitzpatrick, who was diagnosed with Parkinson's nearly seven years ago, said the group has raised nearly one million dollars and needs to raise $1.5 million more to perform the procedure on the initial test group.
The Food and Drug Administration must also give its approval. Dr. Loring said there were no set requirements from the regulatory group, but researchers are working closely with the FDA to reach a solution.
Pig cell treatment for Parkinson's cleared for trial
Copied from The Northwest Parkinson’s Foundation Weekly News Update
radionxz.co.nz - A new treatment that injects cells from a pig's brain into the brains of people with Parkinson's disease is one step closer to being used.
New Zealand company Living Cell Technologies has been given clearance from the Ministry of Healthy to trial the treatment called NTCELL.
In a world first, the brain cells of a piglet bred in Southland could soon be transplanted into people suffering from the disease.
The neurodegenerative condition stems from a lack of a chemical in the brain, dopamine, which causes a loss of coordination and uncontrolled movements.
The principal investigator for the trial, Barry Snow, says the pig cells keep nerves healthy and stop tremors.
"What we anticipate these growth factors will do from the pig cells is help the dying back nerve cells from Parkinson's disease start to regrow again. In fact, we know these cells from the pigs work really well in animal models."
Living Cell Technologies has tested the transplant on rats and monkeys and says both species had fewer tremors and better control of their movements.
A professor at the company, Bob Elliot, says they plan to test the transplant on four people with severe Parkinson's. He says if successful, it will be a better option compared with deep brain stimulation used now which uses electric currents to probe the brain.
"The electrical treatment doesn't do anything about regenerating the damaged part of the brain, it just stirs the brain up in that sort of general area. Whereas this treatment is actually getting right at where the cause of the problem is and replacing those dead brain cells with new ones."
Parkinson's New Zealand chief executive Deidre O'Sullivan says their members are excited and fully supportive.
"People always talk about a cure, however, slowing down progression or preventing progression is almost as good as a cure. In terms of impact on quality of life of people living with Parkinson's, it will have a massive impact."
But Ms O'Sullivan says they will remain cautious, as with any new treatment.
The Anti-Vivisection Society, which opposes experiments on animals, says that caution is warranted. Director Phil Clayton says humans do not react to treatments in the same way as animals.
"Experiments on other species like that don't give predictive results of what would happen in humans - so if that's all that's been relied on, they should stop and think again and find some either better evidence or not do the trials."
The trial will have to be assessed and approved by a health ethics committee before it can go ahead.
Living Cell Technologies' chief executive Andrea Grant says a similar trial that involved transplanting cells from a pig's pancreas into people with Type 1 diabetes was approved in New Zealand in 2008. A fourth trial is about to be held in Argentina.
Ms Grant says they will do what it takes to ensure that this trial is approved also.
"We've taken this technology platform now into appoximately 35 patients around the world and there's been no issue with viral or microbiological transfer in any of those patients.
"So in terms of the safety aspects - which is what ethics is mainly concerned with - we're feeling that we've ticked all the boxes."
Ms Grant says the company hopes to have its application approved by the end of this year so it can begin in 2013.
If all goes to plan, the NTCELL treatment could be available to the public in 2016.
Copyright © 2012, Radio New Zealand
Parkinson's extended-release drug fails to win FDA approval for U.S.
Copied from The Northwest Parkinson’s Foundation Weekly News Update
www.nj.com - Impax Laboratories failed to win U.S. approval for a new version of an extended-release drug used to relieve spasms in patients with Parkinson’s disease.
The Food and Drug Administration requires a re-inspection of a plant involved in the development of the medicine called Rytary, which combines standard Parkinson’s medications in a new sustained release formulation, the Hayward, California-based company said today in a statement. A warning letter was issued in May 2011, Impax said.
“We will work with the FDA on the appropriate next steps for the Rytary application,” said Larry Hsu, president and CEO of Impax, in the statement. “We remain committed to resolving the warning letter and bringing this new treatment option to patients who are suffering from Parkinson’s disease.”
The medication would likely be used most among patients for whom the standard medicines, levodopa and carbidopa, have stopped working as reliably, said David Amsellem, an analyst with Piper Jaffray & Co. in New York. Rytary could generate peak sales of $200 million to $300 million, Amsellem said.
“A controlled-release product is something that has been elusive over the years,” Amsellem said in a telephone interview.
Impax, which specializes in controlled-release drugs, will develop and sell Rytary in the U.S. and Taiwan while GlaxoSmithKline, based in London, will market it in other regions throughout the world. Impax already markets a generic version of a longer-acting combination called Sinemet, sold by Merck & Co.
Merck’s Sinemet extended-release carbidopa-levodopa tablet received approval in 1991 though it’s not widely used, Amsellem said. People who use it are more likely to suffer impairment of voluntary movement than those who use the immediate-release version, according to the label for the medication.
Patients with advanced Parkinson’s disease who used Rytary experienced a 34 percent decrease in the amount of time during waking hours when the medication wore off and involuntary muscle movements returned, the companies said in an August 2011 statement. This was compared with a decrease of 10 percent for those who used the immediate-release generic drugs combined with entacapone, a medicine that helps more of the other treatments reach the brain.
The starting point was 5.9 hours, improving to 3.8 hours of “off time” when Rytary wore off compared with 5.2 hours for the generics.
Parkinson’s is a progressive neurological disorder that causes body tremors, the loss of muscle control and impaired movement, according to the National Institutes of Health. There is no cure. A variety of medicines provide relief from symptoms for the estimated 10 million people worldwide with the disease.
‘Sunlight’ found to lower blood pressure
There’s abundant evidence linking sunlight exposure with a reduced risk of chronic diseases including heart disease, several forms of cancer, multiple sclerosis and diabetes. If the sun is bright enough and high enough in the sky, sunlight can stimulate the product of vitamin D (actually, a hormone) in the skin. Higher levels of vitamin D in the body are also associated with a reduced risk of chronic disease. This supports the idea that sunlight’s apparent benefits are mediated through the production of vitamin D.
However, the nature of such so-called ‘epidemiological’ evidence proves little. All it tells us is that both higher levels of sunlight exposure and higher levels of vitamin D are associated with better health. None of this actually tells us whether sunlight is beneficial to health and even if it is, that these benefits are brought through higher levels of vitamin D.
However, it’s perhaps worth considering the fact that vitamin D receptors exist widely around the body including fat tissue, the adrenal gland, bone, brain, breast, cartilage, colon, hair follicles, intestine, skeletal muscle (muscles connected to bones such as those in the legs and arms), cardiac (heart) muscle, kidney, liver, ovary, pituitary gland, retina, sperm, thyroid and uterus (womb). The presence of a receptor for a substance can be taken as a sign that this substance exerts some influence over the structure and/or function of that tissue.
Another piece of evidence which points to a direct effect of vitamin D on health is the fact that vitamin D has been found to have the capacity to bind to about 3,000 sites within DNA . This research also found that vitamin D could affect the activity of 229 genes, including several the influence conditions that are linked to vitamin D.
However even if vitamin D directly affects health, this does not mean that the benefits attributed to sunlight are necessarily only related to its ability to boost vitamin D levels. We know, for instance, that light exposure can have a profound influence on mood and sleep during months when no vitamin D will be made in the skin at all.
Also, in an animal model, light exposure has be found to help multiple sclerosis and that this benefit could not really be explained by changes in vitamin D levels. .
I was interested to read about a piece of research announced today in which the impact of light and vitamin D on blood pressure was assessed. You can read a report of this research here. http://www.sciencedaily.com/releases/2013/05/130507195807.htm
This research, conducted in Edinburgh, UK, involved exposing individuals to a 20-minute session under lamps that gave off ultraviolet light as well as heat. The impact on blood pressure was compared to another session in which the individuals were exposed to similar lamps that gave off heat but no UV light.
According to the report, the UV light exposure led to a significant reduction in blood pressure compared to exposure to heat alone. And, it seems, there was no appreciable change in vitamin D that might explain the difference in effects. The benefits appear to have been put down to an increased production of nitric oxide, which has blood vessel relaxant and blood pressure lowering effects.
Without access to the actual paper (due to be presented at a scientific meeting on Friday) it’s difficult to say much more about this research. But it adds to the idea that the benefits of sunlight are likely to come from mechanisms that go beyond vitamin D. Also, it was interesting to note recognition from the authors of this study that whatever impact sunlight has on skin cancer risk needs to be balanced with whatever benefits may be had in terms of improved cardiovascular health. And that’s before we begin to consider any other benefits sunlight has in terms of chronic diseases such as cancer, diabetes and multiple sclerosis.
1. Ramagopalan SV, et al. A ChIP-seq defined genome-wide map of vitamin D receptor binding: Associations with disease and evolution. Genome Res. 2010 Aug 24. [Epub ahead of print]
Psychiatric Treatment Crucial for Many Parkinson’s Patients
Copied from Northwest Parkinson’s Foundation Weekly News Update
Psychiatric News - A decade or so ago, psychiatrists would have been hard pressed to provide evidence-based psychiatric treatments to Parkinson’s patients. Thanks to research advances, that situation has improved considerably.
Not just the public, but many clinicians, believe that Parkinson’s disease is exclusively a neurological disorder—that is, that it only entails tremors, stiffness, and difficulty with balance.
Yet there are many psychiatric aspects to the illness as well, psychiatrists who specialize in Parkinson’s disease stressed during recent interviews with Psychiatric News.
Parkinson’s patients can experience a raft of psychiatric symptoms, Daniel Weintraub, M.D., an associate professor of psychiatry and neurology at the University of Pennsylvania and a psychiatrist with the Parkinson’s Disease Research, Education, and Clinical Center at the Philadelphia Veterans Affairs Medical Center, reported. These symptoms include anxiety, depression, personality changes, memory problems, sleep problems, impulse control difficulties, psychosis, and dementia.
And these symptoms can occur at different stages of the disease and have different causes, Parkinson’s researcher Laura Marsh, M.D., pointed out. She is a professor of psychiatry and neurology at Baylor College of Medicine and director of the Mental Health Care Line at the Michael E. DeBakey Veterans Affairs Medical Center.
Among individuals with Parkinson’s, anxiety disorders develop at a higher rate than in the general population, Marsh indicated, and can have their onset up to 20 years or so before tremors and other motor aspects of the disease are apparent. Also, several studies show a high rate of a family history of anxiety conditions in such individuals. Thus it looks as if there could be genetic links between anxiety and Parkinson’s in some individuals.
As for depressive symptoms, they can also occur before the motor symptoms of Parkinson’s surface, Marsh noted, but closer than anxiety symptoms to the time that the motor symptoms appear. “I have seen a number of patients who had never had a mood disorder earlier in their life, but who developed a depressive disorder around age 55, followed by the motor symptoms of Parkinson’s three years later,” she said. And here too, it looks as if the depression may be an early sign of the parkinsonian disease process, not a reaction to the motor symptoms of the disease.
According to psychiatrist and Parkinson’s expert Laura Marsh, M.D., even though Parkinson’s is a chronic, progressive disease with no cure, actor Michael J. Fox is an example of how people with it can still live rich lives.
Indeed, “patients with depression will often say, ‘Why wouldn’t I be depressed? I have Parkinson’s,’ when in fact disability due to Parkinson’s motor symptoms is not correlated with depressive symptoms,” William McDonald, M.D., a professor of psychiatry at Emory University and a Parkinson’s researcher, told Psychiatric News. “Clinically we have found that some of the most disabled Parkinson’s patients are not depressed, and some of the most depressed Parkinson’s patients have only minor motor disabilities.”
The reason that anxiety and depression may be precursors of the appearance of Parkinson’s motor symptoms, Marsh suggested, may be due to the discovery, a few years ago, that the parkinsonian disease process starts in the brainstem and then advances to the midbrain. The brainstem contains serotonin and adrenergic neurons that could contribute to anxiety and depression, whereas the midbrain contains dopaminergic neurons that contribute to the motor symptoms of Parkinson’s, she explained.
The pathological gambling or hypersexuality that some Parkinson’s patients experience appears to be due, however, largely to the dopaminergic medications that patients are prescribed for their motor symptoms—not to the disease process itself, Marsh noted.
And the same is true for the hallucinations or delusions that some Parkinson’s patients experience, Weintraub added. However, as Marsh noted, “the evidence suggests that they are due not just to dopaminergic medications, but also to the disease process.”
Since psychiatric problems can be a significant part of Parkinson’s disease, what can psychiatrists do to help Parkinson’s patients? “Until relatively recently I couldn’t have answered this question very definitively,” Matthew Menza, M.D., chair of psychiatry at the Robert Wood Johnson Medical School and a Parkinson’s expert, said during an interview. “But I think that over the past decade, there have been a number of reasonably good studies that have begun to address the question.”
Regarding anxiety, for example, “One of the more interesting things that has been demonstrated recently is that exercise, which is a well-validated treatment for anxiety disorders in general, also appears to benefit Parkinson’s patients who are anxious,” Menza said.
Several randomized, double-blind, placebo-controlled trials have shown that antidepressants can help Parkinson’s patients who are depressed, Menza also pointed out. One of these was conducted by McDonald and his colleagues and is in press with Neurology. The trial has demonstrated that “Parkinson’s depression is very treatable using standard antidepressants and [these medications] can be remarkably effective in improving quality of life and even motor symptoms, with few adverse effects,” McDonald said.
Cognitive-behavioral therapy (CBT) can also benefit depressed Parkinson’s patients, Roseanne Dobkin, Ph.D., along with Menza and other colleagues at the Robert Wood Johnson Medical School, reported in the October 2011 American Journal of Psychiatry. Eighty depressed Parkinson’s subjects participated in a randomized controlled trial in which CBT was compared with clinical monitoring. CBT was modified to meet unique needs of the Parkinson’s population and was provided for 10 weeks. Assessments were completed by blind raters at baseline, midway through treatment, at the end of treatment, and finally four weeks later. The CBT group experienced significantly less depression by the end of treatment than the control group did, and these gains were maintained four weeks later.
Most people with Parkinson’s have some sleep problems. “It looks as if many of the drugs that we psychiatrists use for sleep disorders probably have some [positive] effect in people with Parkinson’s disease,” Menza observed.
Regarding the memory problems that are common later in Parkinson’s disease, the drugs available to treat Alzheimer’s disease “can help a bit,” he said.
“So psychiatrists, I think, have available to them a variety of medications and nonmedication therapies that may be useful for people with Parkinson’s,” he noted.
And still more psychiatric tools to help Parkinson’s patients may be emerging in the near future, Marsh indicated. For example, when most antipsychotic medications are given to Parkinson’s patients for hallucinations or delusions, the antipsychotics may eliminate the symptoms, but they may also block the action of the dopaminergic drugs given to control motor symptoms. As a result, the patients’ motor symptoms can get worse. New antipsychotics in the development pipeline might be able to treat psychotic symptoms successfully without increasing the patients’ motor symptoms.
“One of the great things about taking care of individuals with Parkinson’s disease, of all the neurodegenerative disorders, is that it has very effective treatments,” Marsh declared. “So even though it is a chronic, progressive, neurodegenerative disease, and even though it has no cure, people can live with it and do well despite its challenges, especially if the psychiatric problems are treated.”
How Many Psychiatrists See Parkinson’s Patients?
Not that many, Laura Marsh, M.D., a professor of psychiatry and neurology at Baylor College of Medicine and a Parkinson’s researcher, told Psychiatric News. “And when they do, it is often because the problems have gotten out of hand—say, someone is really depressed or suicidal.”
And do neurologists ever seek out psychiatrists to help them with Parkinson’s patients’ psychiatric problems? “It really depends,” said Daniel Weintraub, M.D., an associate professor of psychiatry and neurology at the University of Pennsylvania. “If you are in a place such as I am, which is a large academic medical center, I do work closely with neurologists…. At other places where there may not be the same access to psychiatrists, where Parkinson’s care may not even be provided by movement-disorders neurologists but by a general neurologist, then I think that the collaboration is less likely to exist.”
Thus “in Parkinson’s disease, the psychiatric complications remain underrecognized or undertreated,” Marsh asserted.
So how might psychiatrists reach out to help Parkinson’s patients?
One way is to become involved in interdisciplinary care teams and learn about the motor and other somatic and cognitive features of the disease, Marsh suggested. “It is a rewarding condition to treat psychiatrically because treatment works.”
Also, psychiatrists should stay alert for Parkinson’s in older adults who are depressed, George Grossberg, M.D., a professor of psychiatry and neurology at St. Louis University and a geriatric psychiatrist with an interest in Parkinson’s, advised during an interview. “Often we psychiatrists may be the first ones to suspect Parkinson’s in such patients,” he said.
Moreover, psychiatrists who consult to assisted-living facilities or nursing homes should be especially vigilant for Parkinson’s disease in patients, Grossberg said, since neurologists who specialize in Parkinson’s rarely provide such consultation.
Search Is On for New Treatments
“There is an energetic effort right now to find treatments that slow the progression of Parkinson’s,” Matthew Menza, M.D., chair of psychiatry at the Robert Wood Johnson Medical School and a Parkinson’s expert, said during an interview. The effort is focused on neuroprotective treatments such as nonsteroidal inflammatory drugs, since there is substantial evidence that inflammation is involved in the Parkinson’s disease process.
“Many of the disorders that we deal with in psychiatry start early in life—in childhood or adolescence—and some of them appear to get worse over the years,” he said. “So if we had a treatment that was neuroprotective, it might have application in psychiatric disorders. True, nothing is ready for prime time right now. But it is certainly something that people are thinking about.”
“Parkinson’s disease is in many ways the prototypical neuropsychiatric disorder in that it causes clear damage to the brain, but also has many psychiatric aspects to it,” Menza observed. “The hope of those of us who work in this interface between psychiatry and neurology is that if we understand more about Parkinson’s, it’s going to lead to a better understanding of many other diseases that we believe are based in the brain, such as attention-deficit/hyperactivity disorder, bipolar depression, and schizophrenia….[And] if we understood Parkinson’s better, we might have better insights into how to treat these other purely psychiatric disorders.