This Simple Remedy Changed My Life
Simple lifestyle improvements transformed my entire life. Its done exactly the same for thousands of other very ordinary people who thought theyd suffer their illness for life.
It requires a small initial effort. Not much. But a little more than unscrewing the lid on a jar of chemicals.
For the millions who see drugs as their only hope there are thousands like me who know for an absolute fact that theyre not.
Which is why we dont suffer those nasty symptoms anymore while they still do.
Brain Matters: Just Keep Moving
Patients with Parkinsons disease , a brain condition that affects movement and balance and can cause tremor, often have the same worry: Is my mind going to be affected?
While most patients have normal cognition at the start of the condition, unfortunately various aspects of thinking can be affected as PD progresses.
The most powerful treatment we can recommend is physical exercise. Many people are surprised to hear that exercise can literally change the brain both physically and chemically.
Exercise releases brain-derived neural factor , which supports and protects brain cells. It makes the brain cells use dopamine more efficiently , and it results in the formation of new synapses between brain cells.
Thus, exercise results in neuroplasticity, the brains way of healing itself in the face of a chronic condition. Clinically, exercise has been shown to improve global cognitive function, processing speed, sustained attention, and mental flexibility in PD patients.
So Why Is This Relevant To Parkinsons Disease
Parkinsons is a progressive, degenerative disease of the brain. The disease destroys cells in an area of the brain called the Substantia Nigra. This results then in typical Parkinsons symptoms such as a tremor, slow movement, and cognitive disturbances. It is because Parkinsons disease is a degeneration of part of the brain that we can use neuroplasticity principles as a method of managing the disease.
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Effects Of Exercise On Dendritic Spines
DA-depletion in the striatum leads to the loss of dendritic spines on striatal medium spiny neurons in both animal models8789 and in PD90. These morphological changes reflect the loss of synapses and hence reduction in neurotransmission not only in PD but a wide spectrum of brain disorders including Alzheimers disease and Fragile-X syndrome 91. Spine loss occurs predominantly on DA-D2R-containing MSNs of the indirect pathway, reflecting the dysfunction in neurotransmission in this circuitry 92, 93.
While an important question in exercise yet to be fully addressed in PD and its animal models, studies in healthy rodents subjected to different exercise paradigms have demonstrated experience-dependent increases in dendritic spine density in a number of regions including the hippocampus and cerebellum 70, 94. One hypothesis to be explored in models of PD is that exercise can reverse dendritic spine loss in DA-D2R containing striatal neurons.
Neuroplasticity And Parkinson’s Disease
|This PET scan reflects the decreaseddopamine activity of a Parkinson’spatient’s brain compared to a normal person’s brain.
|A synaptic view of dopamine levels in a normal and a Parkinson’s affected neuron.
|A deep brain stimulation device for treatment of symptoms of Parkinson’s disease.
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Why We Develop Parkinsons
Case study: Steve Peterson
I used to suffer from Parkinsons Disease
I still have Parkinsons Disease.
My specialist told me I always will.
But I dont suffer from the illness any more.
And thats the difference.
Despite everything medical that was going wrong for me then my life is now back to normal.
Actually, a little better than normal.
Im one of thousands who have learned to transformed their health. But I still feel blessed.
Let me tell you how this turnaround happened.
Want To Learn More About Exercise And Parkinsons
Significant research studies and anecdotal evidence highlight the critical importance of exercise for people with Parkinsons. In addition to neuroplasticity, regular physical exercise can improve mobility and coordination, boost your mood, reduce stiffness, and minimize soreness and fatigue. Find out more from this collection of resources. Want more Mike? You can watch his fabulous TEDx talk here.
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Neuroplasticity In The Pathology Of Neurodegenerative Diseases
Editorial | Open Access
Jolanta Dorszewska, Wojciech Kozubski, Wioletta Waleszczyk, Matthew Zabel, Kevin Ong,”Neuroplasticity in the Pathology of Neurodegenerative Diseases”,Neural Plasticity,vol. 2020,Article ID 4245821,2pages,2020.https://doi.org/10.1155/2020/4245821
Overall Conclusions And Impact On Clinical Care
Over the last decade, a primary focus of neuro-rehabilitation has been to alleviate the motor deficits of PD through exercise 10, 125. The general idea is that exercise incorporating goal based motor skill learning improves motor skill performance in PD and that this may be enhanced through cognitive engagement. More importantly, studies suggest that combining goal based with aerobic training the possibility for improving automatic with cognitive motor control may be possible and thus reduce the attentional demands of consciously processing behaviors such as walking.126 Aerobic exercise may contribute to more general improvement in brain health and repair, through the recruitment of the immune system and/or increasing blood flow and trophic factor signaling as examples. These aerobic exercise benefits are likely to impact connectivity through priming the brain environment conducive for promoting synaptic neuroplasticity leading to altered circuitry. This review raises another fundamental question, which is can an individual learn themselves out of PD? Based on published studies, and current understanding of the detrimental effects of DA loss on brain circuitry, the most obvious response is no. However, exercise studies may be pointing towards potential and important neuroplastic mechanisms that through restoring some degree of basal ganglia circuitry provide a window of opportunity to improve motor learning and behavioral performance.
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And Now I Know Why We Dont
There are 8 main factors leading to Parkinsons. Some have a small effect. A couple are huge.
Together theyre essential in beating this horrible condition.
In truth, some of them my health-care center already acted on.
For example, they prescribed dopamine-enhancing drugs. For sure, I needed more dopamine.
I had tests and underwent occupational therapy. Again, good stuff it helped me manage my problems with balance, movement, stiffness.
But I also realized they were not helping me to avoid the worst symptoms of this disease. At best, they were just delaying it.
Yet thats what I wanted most to not end up with my own personal Parkinsons horror story.
Which is why I went headlong into my own research about my illness and, eventually, found my way out.
Neuroplasticity Exercise And Parkinsons
We recently sat down with Mike Studer, PT, DPT, MHS, NCS, CEEAA, CWT, CSST, FAPTA, to talk about neuroplasticity, exercise, sleep, and how important they are to living well with Parkinsons.
You can watch the full interview now and view the show notes below. Note that Mike is riding his trainer while we talk. He always walks his talk!
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The Effects Of Exercise On Dopamine Neurotransmission In Parkinsons Disease: Targeting Neuroplasticity To Modulate Basal Ganglia Circuitry
Issue title: Tracking Effects of Exercise on Neuronal Plasticity
Article type: Review Article
Affiliations: Department of Neurology, University of Southern California, Los Angeles, CA, USA | Department of Psychiatry and the Behavioral Sciences, University of Southern California, Los Angeles, CA, USA | Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, USA | Department of Psychiatry & Biobehavioral Sciences, Andrus Gerontology, University of Southern California, Los Angeles, CA, USA | Department of Psychology, CUNY, NY, USA
Correspondence: Correspondence to: Giselle M. Petzinger, MD, Department of Neurology, University of Southern California, Los Angeles,90033 CA, USA. Tel.: +1 323 442 1057
Keywords: Synaptic plasticity, basal ganglia, prefrontal cortex, glutamate, cognition
Journal: Brain Plasticity, vol. 1, no. 1, pp. 29-39, 2015
Why Does Modern Medicine Know This But Ignore It
Why dont we tackle the inflammation and toxins causes of those nerve cells continually dying in the substantia nigra?
My doctor told me: its cultural.
Most patients especially in western countries want a drug or a procedure for a problem.
Something thats a one-off fix like an operation.
Or an easy, regular thing like a course of tablets.
What they dont want to have to make an effort to heal themselves. So pills it is.
But most inflammatory diseases can be tackled more effectively by lifestyle changes than by drugs.
Whole classes of deadly modern illnesses can be changed by a small number of simple, targeted lifestyle tweaks.
But our medics push meds because they know that, mostly, their patients wont make lifestyle changes.
So they give their patients drugs knowing that theyll at least take them.
Frustratingly, the best solution addressing lifestyle factors isnt at all difficult. Its just that popping a pill is easier.
Neural Plasticity In Human Brain Connectivity: The Effects Of Long Term Deep Brain Stimulation Of The Subthalamic Nucleus In Parkinsons Disease
Affiliations Center of Functionally Integrative Neuroscience , Aarhus University, Aarhus, Denmark, Department of Psychiatry, University of Oxford, Oxford, United Kingdom
Affiliations Department of Psychiatry, University of Oxford, Oxford, United Kingdom, Center of Brain and Cognition, Theoretical and Computational Neuroscience Group, Universitat Pompeu Fabra, Barcelona, Spain
Affiliations Center of Brain and Cognition, Theoretical and Computational Neuroscience Group, Universitat Pompeu Fabra, Barcelona, Spain, Institució Catalana de la Recerca i Estudis Avançats , Universitat Pompeu Fabra, Barcelona, Spain
Affiliation Center of Functionally Integrative Neuroscience , Aarhus University, Aarhus, Denmark
Affiliation Nuffield Department of Surgical Sciences, John Radcliffe Hospital, Oxford, United Kingdom
Affiliations Center of Functionally Integrative Neuroscience , Aarhus University, Aarhus, Denmark, Nuffield Department of Surgical Sciences, John Radcliffe Hospital, Oxford, United Kingdom
In Truth Its Not Magic At All
Of course, the kind of turnaround I experienced here does feel like magic.
Who wouldnt feel like theyve experienced something miraculous when an illness like this does an about-turn?
But everything I learnt from Jodi comes with sparkling scientific credentials.
Its researched knowledge from scientific establishments all over the United States, Europe and the world.
None of this program is controversial. There arent any scientists waiting to debunk any of this.
Because collectively this is their work. Jodi simply turned it into a set of 12 habits that thousands of us have used to treat a nightmare illness.
The only reason its not mainstream the only reason its only thousands of people who benefit from this rather than millions is because it involves some initial effort to take on these habits.
Yet once done its just so easy. And the reward?
Health. Pure and simple.
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Exercise Type Blood Flow And Neurogenesis
In rodent models of neurological disorders where reduced neurogenesis is evident, including mouse models of Alzheimers disease, exercise has been shown to elevate hippocampal neurogenesis and delay deficits in learning and memory . However, some studies have shown elevated or no effects of exercise in neurogenesis in the context of disease, such as Huntingtons disease . In animal models of PD, exercise may facilitate neurogenesis in the hippocampus and subventricular zone, similar to reports with wild-type animals, however, there are few reports showing enhanced neurogenesis within the damaged striatum or midbrain regions with physical activity . Clearly a major gap in our knowledge is whether exercise or the type of exercise influences different stages of neurogenesis in brain regions affected by disease.
Exercise Effects On Da Neurotransmission In Animal Models
In addition to its role in motor performance, preliminary studies in animals suggest that an exercise-induced increase in dorsal striatal DA-D2R expression may also contribute to the reported exercise related improvements in executive function, including behavioral flexibility . Specifically, studies have shown that 18 days of exercise can improve discrimination testing in a set-shifting, cross-maze task in healthy rodents. This exercise benefit was reversed through selective pharmacological blockade of the DA-D2R. Taken together animal studies support that exercise induced increase in DA availability along with increased DA-D2R expression in the dorsal striatum and its related cortical circuitry may contribute to exercise related effects in neuroplasticity and behavioral benefits in PD. Future studies in humans are clearly needed to confirm this relationship.
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Related Research Has Focused On Neuroprotection Not Neuroplasticity For Parkinsons
Much of Parkinsons research has mostly been on drug or surgical options to slow the rate of decline, or to protect the remaining brain cells and their connections. This is called neuroprotection. Neuroplasticity has to do with what you can do to change your own brain.1 Much neuroplasticity research has been about sensory circuitsfor example, to use movement or sensation, electrical stimulation, or other therapies to rewire to the brains receptor sites for sound, touch, or vision, even when there is sensory loss in the original circuits. Functional changes follow principles of the patients conscious effort, novelty, variety, appropriateness to age and ability, intensity, reinforcement, and reward. These principles are discussed by physical therapists in Umphred, et als Neurological Rehabilitation. Is it possible that those principles could stimulate neuroplasticity for Parkinsons?
Why Do We Get This Illness
Parkinsons Disease is a degenerative brain illness.
Why does our brain health start to degenerate?
It degenerates due to a loss of nerve cells in a part of the brain called the substantia nigra.
These nerve cells in the substantia nigra manufacture a neurotransmitter called dopamine. But as the nerve cells die off less dopamine is created.
We need dopamine.
The loss of dopamine leads to the loss of body control and leads to a whole cascade of other physical and mental symptoms that combine to steadily ruin a persons life.
Theres a simple, well-understood trail from good health to Parkinsons:
Nerve cells dying off in the substantia nigra > reduced dopamine production > Parkinsons Disease
However, almost all modern-day medical treatments start at step 2 reduced dopamine. Were trying to increase dopamine.
Which sounds sensible at first. But the problem is that were tackling a disease that has already started.
And were not addressing it at the point of its underlying cause.
Its like being in a sinking boat and constantly bailing out the water instead of fixing the leak.
We can bail for so long. And then we sink.
The reason why most people eventually get so ill with this condition is because almost no treatments tackle step 1 the dying of the substantia nigra cells.
Yet doesnt it make sense to address the initial cause of this dreadful condition?
Of course it does.
Ive learnt a lot about this disease..
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We Have Choices About How This Condition Plays Out
In fact, medical scientists have proved that many people with a genetic disposition to this never get it.
While others with no genetic disposition at all still get full-on Parkinsons that ravages their mental health quickly and remorselessly.
Its not genetics. Its a basic illness with recognized causes.
Remember: the substantia nigra produces dopamine. Its the loss of substantia nigra nerve cells that leads to the loss of dopamine.
And that loss of dopamine leads to Parkinsons Disease.
So the big question is:
Why on earth is the substantia nigra losing those dopamine-producing cells in the first place?
I was shocked to discover that we already know why were losing those priceless, life-giving substantia nigra cells.
Yet still do almost nothing about it
I Feel Wonderful And Theres A Reason Why
Actually, there are three fantastic reasons:
First and foremost: I have tackled the loss of dopamine by working on the underlying cause of that loss.
We know that cell loss in the substantia nigra is the direct cause of dopamine loss. I address that cell loss in gentle but powerful ways and so protect dopamine levels.
Second, I increase dopamine production in my brain using non-drug methods. Increasing dopamine fights this condition head-on leading to wonderfully quick improvements.
Third, I have taken each of the symptoms of my illness stiffness, shaking, anxiety and so on and addressed them directly. Ive enacted specific daily habits that make those symptoms reduce to almost nothing.
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Exercise And Blood Flow
Exercise increases blood flow in the healthy brain in a wide range of animal species undergoing various exercise regimens 96, 97. Thus exercise may facilitate neuroplasticity by influencing the vasculature of the central nervous system through angiogenesis and altered blood brain barrier permeability. The delivery of peripheral signaling molecules originating from muscle or adipose tissue including insulin, angiogenic factors such as vascular endothelial growth factor , hypoxia mediated factors such as hypoxia-induced factor 1 , leptin, and neurotrophic factors including BDNF98 can be promoted.
Memory Consolidation And Continued Practice
Mixed ANCOVA for offline gains revealed no significant main effect for Block or Condition . However, a significant Condition x Block interaction effect indicated that offline learning differed between groups. Subsequent separate ANCOVA for 1-day offline change scores revealed no significant difference . In contrast, a significant ANCOVA for change scores to 7-day retention test suggested better offline learning in the EX group .
We additionally analyzed skill improvement with continued practiced during 7-day retention session in a separate ANCOVA. The absence of a statistically significant main Block , Condition , or Condition x Block interaction effect indicated that participants did not improve performance with continued practice irrespective of group.
Motor skill data. Mean motor skill performance during acquisition and retention offline skill learning illustrated as mean percentage change from last acquisition block to 1-day retention block offline skill learning illustrated as mean percentage change from last acquisition block to first 7-day retention block * indicates p < .05 error bars indicate 1 standard error of the mean.
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