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
Do You believe that all Parkinson’s Medication will slow down the PROGRESSION of Pd?
No! To the best of my knowledge, there is only one type of Pd Medication that the manufacturers claim CAN POSSIBLY slow down or even REVERSE the progression of your Pd!
ARE YOU ON THAT TYPE OF MEDICATION?
To find the only medication that the manufacturers have claimed to be proven, in scientifically controlled double-blind studies, to be able to SLOW DOWN or even REVERSE Parkinson’s Disease, all you have to do is place your order for this fascinating new book:
‘REVERSE PARKINSON’S DISEASE!’
This book has been written by me, John Pepper. My Parkinson’s disease started in the early 1960’s, when I was less than thirty years of age. I was only diagnosed in 1992, when I had started to shuffle, when walking, and this gave my doctor the final clue as to why my health was deteriorating.
I am NOT A DOCTOR!
What do the other types of medication do, if they don’t affect the progression of Pd?
Find the answers to these, and many other questions on medication, by ordering your copy of my book ‘REVERSE PARKINSON’S DISEASE’, NOW!
You are not in the position to decide what medication you should be on, but you do have the right to question your medication! If you have been diagnosed within the past five years, and you were not first put onto a medication, which can influence the progression of your Pd, then your doctor should give you the reason why not. Why would you start taking a medication, which has serious side effects, but does not slow the progression of your Pd? Those are the last resort medications to take, not the first.
Are you aware of the side effects of your medication? Has your doctor told you what you can do to avoid these side effects, if there is anything you can do about them?
You are the person with the Pd, not your doctor. His knowledge of your Pd is what he has read, and what he has been taught, while he was at college. He does not know the psychological effects that Pd has had on you, other than what you have told him, if you are aware of them. Don’t underestimate the value of your input, when it comes to the treatment of your Pd. No two people’s symptoms are the same.
There are thought to be at least four different types of Pd. Does your doctor know which type you have? Did you know that it is thought that at least 25% of all Pd diagnosis is wrong. Yes! Roughly 25% of people diagnosed with Pd, either don’t have Pd, or have a different type of Pd to the one they were thought to have. Frightening? Yes! This is not the fault of the medical profession, we just do not know enough about Pd. Period!
When I first wrote this book, because I felt that the world should know that I have been able to reverse my Pd, the reaction of the medical profession was, to say the least, very cool. Many neurologists took one look at me and, because I look so well, said I do not have Pd, without even carrying out any form of examination. I don’t blame them. They were taught that you don’t get better, when you have Pd. This has never happened before, at least, not to my knowledge.
This is something new. Why do I not claim to be cured, if I got better? Good question! I do know that if I stop my present regimen, my Pd gets worse again. I don’t know the answer to this. I do know that I was not the usual type of patient, when I was eventually diagnosed. I was physically very fit, due to a back problem I picked up in 1960, and for which, I had been advised to do lots of exercise, in order to strengthen my back muscles.
I was also prescribed a monotherapy of one of these medications, which can, according to the manufacturers, affect the progression of Pd.
For ten years, I took the only type of medication that can influence the progression of Pd, and I also did regular energetic exercise. in 2006, at the 1st World Parkinson’s Congress in Washington DC, we were told that exercise can also slow down or even reverse Pd.
Isn’t that a bit of luck?
How Does an MAO-b Inhibitor Work?
I repeat, I am not a doctor!
I am told that it inhibits the natural breakdown of Dopamine in the brain. That means that we get to keep more of the dopamine we already have in our brain, rather than take levodopa, with all the side effects that go with it.
In addition to the medication and exercise, I also got rid of all HARMFULL STRESS, out of my life, and I adopted a POSITIVE ATTITUDE towards my Parkinson’s Disease.
For Full Details, Order my Book Now!
Go to My WEBSITE: www.reverseparkinsons.net
SPRING Times No. 41, October 2006 Page 15:
By John Telford
Synapses connect nerve cells – so, in a sense, they connect thoughts. In this edition of ST, as in many others, articles written quite separately have born an unexpected relationship with each other. A discussion in one has serendipitously thrown light on another. The thoughts crossing the synapses in this edition relate to oxidative stress, neuroprotection and monoamine oxidase inhibitors such as selegiline
The article by Michael Kelly on exercise in the last edition prompted John Pepper to write in about how he believes regular, strenuous exercise has helped keep his Pd symptoms at bay. He happened to mention in correspondence that he had used selegiline (Eldepryl) as a monotherapy for many years (i.e. without any levodopa). I was not aware that there was any advantage in using selegiline on its own but another of our regular contributors had also used it in this way. But there should be no surprise about this mode of use. Monoamine oxidase type B inhibitors (MAO-b inhibitors) certainly slow down the degradation of the dopamine in the brain that has resulted from levodopa administered, as Pd therapy. But it will of course also extend the life of the dopamine produced naturally by the neurons. Therefore: in the early stages of the disease, when dopamine production has started to decline, an MAO-b inhibitor can help to conserve what dopamine is still being produced by the cells, not yet affected.”
The link between ideas relates to Flora Hill’s article above on alpha synuclein. In the model 2 that she describes, free dopamine is seen as harmful. Not in itself but because of the highly reactive oxygen species which are formed when excess of it is metabolized. The first stage of a major route in the metabolization of dopamine is the action of a monoamine oxidase – the very enzyme that compounds like selegiline act against. (The relatively new drug, rasagiline, which is marketed as Azilect is of the same class.) Model 2, then, suggests that such drugs may help with neuroprotection, by inhibiting the harmful degradation of any dopamine that has escaped being re-absorbed.
So the question is; has selegeline contributed to the slowness of PD progression that John Pepper has experienced? Well, we have to be cautious. One swallow does not make a summer, and conclusions cannot reliably be drawn from anecdotal evidence. After all, there still remains some question of whether John Pepper really has ‘standard’ Pd. Instead, the correct answer is what Flora proposes: that further research is done, firstly, to confirm the results of the trial she quotes, which point to MAO-b inhibitors being neuroprotective and second, to determine whether they are neuroprotective by the mechanism she outlines.
The following information was supplied by the Parkinson’s Post, Published by the Northwest Parkinson’s Foundation:
On May 16, 2006, the Food and Drug Administration (FDA) approved a new drug, rasagiline, for the treatment of Parkinson's disease (PD). Rasagiline, which will be sold under the name of Azilect® in the United States, is taken once a day. The manufacturer, Teva Pharmaceuticals, intends to have two strengths of this drug available for sale in the US later this year.
The FDA approved rasagiline as a stand-alone treatment for early PD and in combination with levodopa, a commonly used drug to treat PD, for the signs and symptoms of moderate to advanced PD. These approvals were based on the results of three clinical studies.
The first study included 404 participants who had early PD and were not taking any dopamine-like drugs for the treatment of PD. The study lasted for 26 weeks. The results showed that rasagiline was better than placebo at controlling the symptoms of PD, as measured by the Unified Parkinson Disease Rating Scale (UPDRS). The UPDRS is a tool that doctors often use in research studies to measure the effects of PD.
A total of 1,159 people with moderate to severe PD participated in the second two studies. These people were taking levodopa and had motor fluctuations, dyskinesias, or both. They kept a diary at home and recorded the amount of "off" time that they had each day. Both studies found that the addition of rasagiline to the subjects' usual medications reduced the amount of off time, as compared with before they started taking rasagiline. In addition, some people were able to decrease their dose of levodopa.
Additional studies will be conducted to evaluate the impact of dietary tyramine on people taking rasagiline (see the information below on monoamine oxidase (MAO-b inhibitors) and whether taking rasagiline increases a person's risk of developing melanoma. In the studies of rasagiline that have been completed, the rate of melanoma was slightly higher in those taking rasagiline, but it is not clear whether this was due to the drug or happened by chance and was not related to the drug. For now, people taking rasagiline should follow a diet that does not include foods that contain tyramine and should undergo regularly scheduled examinations of their skin to look for melanomas.
Azilect is in a class of drugs known as monoamine oxidase inhibitors (MAOIs). These drugs affect chemicals in the brain known as monoamines--serotonin, dopamine, and norepinephrine. Monoamines are involved in the transmission of messages between nerve cells. Dopamine is particularly important in regulating messages related to movement. People with PD have a decreased amount of dopamine in their brains.
After monoamines perform their jobs as messengers, they are broken down by a type of protein known as an oxidase. Rasagiline, like other MAOIs, limits, or is an inhibitor of oxidation, (which is the process of combining oxygen with some other substance). Because they inhibit oxidation, MAOIs increase the level of monoamines, including dopamine, in the brain.
Unfortunately, MAOIs also inhibit or prevent the breakdown of a naturally occurring substance known as tyramine. When tyramine builds up in the body, it can cause extremely high blood pressure, leading to rupture of blood vessels in the brain or even death. Many prescription and over-the-counter medications, such as antidepressants and cough-and-cold medicines, and dietary supplements contain tyramine or also interfere with the breakdown of tyramine. Therefore, if you are taking rasagiline, make sure that you are aware of these substances and that every healthcare provider who cares for you, including the person administering your anesthesia, if you are having an operation, knows that you are taking an MAOI.
A wide variety of foods also contain tyramine, and the level of tyramine increases in protein-based or processed foods as the protein breaks down. Eating the freshest possible meats and other protein-based foods is very important. Therefore, it's a good idea if you are taking an MAOI, to eat only food that is freshly prepared--let someone else finish off the leftovers, and you may want to steer clear of the buffet line at a restaurant. Some foods should be limited because they contain small amounts of tyramine, and others should be avoided completely. Be sure to check with your doctor for a complete listing of foods and medications that you should avoid. People with liver problems should also not take MAOIs. (Google Tyramine, for more information)
People who take MAOIs should be aware of the symptoms of high levels of tyramine, including severe headache, blurred vision, difficulty thinking, seizures, chest pain, unexplained nausea or vomiting, or signs or symptoms of a stroke. Patients and caregivers should seek immediate medical attention for patients who develop any severe headache or other atypical or unusual symptoms not previously experienced
Parkinson's Insights – My Story Part 1
There is no doubt that, contrary to established thinking, the progression of Parkinson’s disease, can be reversed. Although it has not been done by very many people, the fact remains that I've done it, and many others have followed, and will continue to follow.
My name is John Pepper and I have successfully reversed my Parkinson’s disease, to the point where I no longer need to take any Parkinson’s disease medication, since 2003, and nobody would ever know that I still have Parkinson’s disease.
How did I do this?
My case was quite unique, for the three following reasons:
My neurologist had prescribed a monotherapy of a unique type of Parkinson’s disease medication, which was the only medication that the manufacturers claimed - as a result of conducting extensive double-blind scientific studies on a wide range of patients – could possibly slow down or even reverse the progression of this condition. I know of nobody else, who has only been prescribed this type of medication and nothing else.
I was in the habit of doing regular energetic exercise, for over twenty years, before I was first diagnosed with Parkinson’s disease. I was therefore bodily very fit, which was not a unique occurrence amongst newly diagnosed patients, but it was, and is, not the norm; especially as it was accompanied by reason number one. I have continued to do rigorous exercise, since I was diagnosed, which is not common amongst Parkinson's patients at all.
I gave up my high-powered job, three months after I was diagnosed. I was aware that my job had become very stressful to me and I would have done anything at that stage to help me cope with the Pd. I also stopped singing in the church choir. It was not just the services that ate into my time it was all the rehearsals and the travelling to get there and back that was the problem. I wanted to simplify my life. I also left my Rotary club, which was not a burden, but I did not want to be amember who did nothing active in the club. Stress is one of the major triggers for many health issues. It affects many of my symptoms.
The combination of a Monotherapy of a special type of medication, regular energetic exercise and the management of stress, all urned out to be the crucial changes I had made in my lifestyle that have reversed the progression of my Pd, and they made my circumstances unique.
In addition to these three unusual circumstances, I made the following changes to my life style, during the next eight years, after diagnosis:
I decided to change my type of exercise.
I learned how to control my movements by focusing my full attention on controlling each movement!
I examined and changed my whole attitude.
After having given up my job, and having experienced the huge improvement in my health, I came to the realization that ‘Stress’ had played a major roll in the progression of my Parkinson’s disease.
Many people ask me about diet. I have found only one food item that must not be eaten by Parkinson’s disease sufferers and several other interesting substances that should be avoided.
Two years after my diagnosis, I realized that I had to learn to manage my sleeping problems.
The last change I made to my lifestyle was to start doing regular brain exercises.
I hope you have found this Insight helpful.