Dr. Hageseth dates his first non-motor symptoms to 2004 when his sense of smell disappeared. In 2008 he developed severe constipation which he has had ever since. In 2011 he saw the emergence of a tremor in his right hand which progressed over the following year to involve his entire right side. It went on to include stooped posture, shuffling gait, and problems with balance. A neurologist confirmed his diagnosis in 2012. He tried three different medications over the next four months but discontinued each one due to side effects or lack of efficacy.
His neurologist gave him one piece of advice: EXERCISE, EXERCISE, EXERCISE.
A year later many of his symptoms had regressed. He attributed his improvement to the intensity of his exercise and taking up yoga. He established his first website: Sweating Out Parkinsons Disease. He intended to encourage other PWPs to follow his example.
By 2014 he was doing so well that he had a DAT scan to confirm the diagnosis of PD. It was positive.
Over the last year and a half, he explored why more people are not doing better with PD. It was then that he started to examine how the mind may influence the course of PD. Exercise is the key to living a full life with PD, But if the mind does not believe the degree of improvement that exercise can achieve. Then improvement will only go so far.
Because of the problem of dyskinesia developing after five years on levodopa, he thinks newly diagnosed should pursue a program of great intensity and focus and manage their minds, so they realize they can live with PD and not require levodopa.
Click the arrow below to hear my interview with Bill McAnalley PhD who discusses why food can fix things that drugs cant. His discussion focuses on explaining the causes of Parkinson’s and the right foods to treat each cause.
Information about Dr. McAnalley’s company, is accessed by visiting Aroga
Below are the talking points that Dr. McAnalley prepared for my interview with him on Parkinsons Recovery Radio where he explains why food can fix things drugs cant
Parkinson’s disease (PD), characterized with bradykinesia, static tremor, rigidity and disturbances in balance, is the second most common neuro-degenerative disorder. Alzheimer disease is first.
With the global trends in aging, the incidence of PD has increased year by year and the prevalence rate is up among the elderly over the age of 65 years. So far, there is still no exact cure for PD due to its diversity of etiology and complexity of symptoms.
Currently, Parkinson’s disease is treated with Levodopa and maybe Monamine, Oxidase Inhibitors (MOAs) or Acetylcholine inhibitors. Levodopa makes more Dopamine available for the dopamine receptor, MOAs increase the amount norepinephrine, dopamine and serotonin at their prospective receptors and acetylcholine inhibitors make more acetylcholine available to its receptor.
None of which address the physical cause of the disease.
The cause of PD has not been completely elucidated, but it has been generally acknowledged that the improvement of oxidative stress is one of the most important patho-physiological mechanisms.
Dr. Bill’s research has focused on stopping the causes of diseases like Parkinsons by:
The inhibition of oxidative stress:
PD patients are in a state of oxidative stress. Oxidative stress is caused by the increase of free radicals in the organism, while the ability to eliminate free radicals is decreased at the same time. A large amount of lipid peroxide, such as Malondialdehyde (MDA), hydroxyl, carbonyl, etc., will cause cell death, which leads to neuronal apoptosis ultimately.
The mitochondria is the power plant and energy conversion station of cells. It also regulates the process of gene expression and apoptosis. Recent reports have suggested that mitochondrial dysfunction is closely related to a variety of neuro-degenerative diseases including PD.
The reduction of toxic Excitatory Amino Acids (EAA):
Glutamate (Glu), Also, gamma-aminobutyric acid (GABA) and enkephalin can can produce excitotoxicity effects on nerve cells. Glutamate creates an excitatory effect on nerve cells, and is toxic when Dopa Amine neurons are fully or partially degenerated.
The inhibition of neuroinflammation:
Neuroinflammation is a common and important pathological mechanism in nervous system diseases and different neurological diseases are involved in neuroinflammation at some stage. At present, it is believed that neuroinflammation was involved in an important cascade reaction in neuronal degeneration of PD.
When the central nervous system suffers from exogenous antigens stimulus, such as pathogenic microorganisms or foreign bodies, microglia will be rapidly activated. Then, the activated microglia cells can secrete various cytokines such as IL-1β, IL-2, IL-4, IL-6, TNF-α, and IFN-γ, etc. The cytokines cause is neuro-inflammation.
The inhibition of neuronal apoptosis:
Parkinsons is caused by the premature death of dopaminergic neurons by abnormal apoptosis activation. Energy for normal activities of brain cells comes directly from aerobic energy, and there is little energy storage. However once brain damage occurs, it will cause nerve cell apoptosis or death.
The Bcl-2 family of proteins regulate apoptosis. It is divided into two categories: anti-apoptosis gene (such as Bcl-2, Bcl-xL, Bcl-w, Bcl-1, etc.) and pro-apoptosis gene (such as Bax, Bak, Bad, Bid, etc.). Their ratio regulates apoptosis.
The inhibition of abnormal protein aggregation:
Misfolded and aggregated proteins play a key role in the pathogenesis of Parkinsons Disease. Protein aggregates differ from disease to disease. This common characteristic shows that protein deposition is toxic to neurons.
Studies confirmed that the activity of the proteasome dropped substantially in substantia nigra of patients with PD, which weakened the ability of the substantia nigra to degrade α-syn and other proteins.
Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration:
Nrf2 is a basic leucine zipper (bZIP) protein that regulates the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation. Several drugs that stimulate the NFE2L2 pathway are being studied for treatment of diseases that are caused by oxidative stress.
Listing of Core Food Ingredients that Address the Structure and Functional Causes of the Disease
The inhibition of oxidative stress:
Brahmi, Bacopa monnieri
Maca root powder, Lepidium meyenii (Walp.)
Tongkat Ali (Longjack), Eurycoma Longifolia
Turmeric root powder, Curcuma longa
The reduction of toxic Excitatory Amino Acids EAA:
Brahmi, Bacopa monnieri
The inhibition of neuroinflammation:
Turmeric root powder, Curcuma longa
Wild Yam root, Dioscorea villosa
The inhibition of neuronal apoptosis:
Noni Fruit, Morinda citrifolia
The inhibition of abnormal protein aggregation:
Amia powder, Emblica officinalis
Turmeric root powder, Curcuma longa
Targeting Nrf2 to Suppress Ferroptosis and
Mitochondrial Dysfunction in Neurodegeneration.
Chaga Mushroom, Inonotus Obliquus
Milk Thistle Seed Extract, Silybum marianum.
Tongkat Ali (Longjack), Eurycoma Longifolia
Aroga
Dr. Bill offered suggestions on the products he recommended for persons diagnosed with Parkinson’s. He recommended three
Aroga products: (1) the Core (2) the Plus Brain and Nerve and (3) the Bone, Joint and Endocrine (which supports hormones). At a minimum. the Core would take top priority.
Information about these products and the opportunity to order is available at:
How Natural Medicines Help Parkinson’s Disease. Barbara Frank uses Folk Medicine and Nature’s Medicines To Help Parkinson’s Patients. barbarafrank222.com
Parkinsons Recovery is dedicated to identifying promising new therapies that offer the promise of reversing symptoms of Parkinson’s disease. One such therapy, High-Dose Thiamine, was discussed on Parkinsons Recovery Radio by Italian neurologist Antonio Constantini MD. He has been prescribing High Dose Thiamine as a treatment for his Parkinson’s patients with good success. Click on the pointer to hear the replay.
Parkinsons disease (PD) is a systemic disease with motor and non-motor deficits. In July 2011, Dr. Costantini treated a 47-year-old man affected by spinocerebellar ataxia type 2 (SCA2). In this patient, fatigue as well as motor symptoms improved after parenteral high doses of thiamine (also this was our proprietary research).
He formulated the hypothesis that in some inherited and degenerative diseases of the nervous system, the pathogenesis of the symptoms could be linked to a focal thiamine deficiency due to a dysfunction of the circulation of thiamine in the intracellular space or to structural enzymatic abnormalities. He speculated this dysfunction could be responsive to high-dose thiamine. Parkinson’s disease has also been related to mutations associated with SCA2. Applying the same approach to patients with Parkinson’s symptoms the observed results were nothing short of startling and never previously described in literature.
Now you may be able to prevent or reverse your Parkinson’s disease while you sleep…
Dr. Stasha Gominak MD received her medical degree from Baylor College of Medicine and completed her Neurology residency at the Massachusetts General Hospital in Boston.
Today I hosted a fascinating radio show interview with Natural Pharmacist Ross Pelton PhD and David Sage who discussed the impressive research documenting the effects of pulsed electromagnetic field therapy for treatment of a wide variety of symptoms. If your recovery program is stuck in the mud at the present moment, I encourage you to listen to the replay of this informative interview .
All About Pulsed Electromagnetic Therapy and the Bemer
This 2 1/2 minute video demonstrates the perfusion of capillaries during the course of a Bemer treatment. White white blood cells (leukocytes) are increased, red blood cells are disassembled and blood flow in dramatically increased.
Research on pulsed electromagnetic field therapy reports a series of positive outcomes including modulation of inflammation, reduction of pain, promotion of tissue repair and regeneration, improvement of neurological and cardiac functions, reduction of fatigue, acceleration of recovery from strokes and support of detoxification. These positive outcomes might clearly have a positive benefit for persons diagnosed with Parkinson’s disease.
Many people hold the belief near and dear to their heart that Parkinson’s disease is “degenerative.” Is this really true? Has anyone out there actually reversed their symptoms and if they have, how did they do it?
The radio show today answers these questions. First, I report results of a holiday survey which asks persons diagnosed with Parkinson’s disease whether they were better, the same or worse now when compared to the holiday season a year ago.As you will discover by listening to a detailed discussed of the results, a vast majority of respondents reported they were better or the same relative to one year ago. In other words, the first answer to the question is no. Parkinson’s is not “degenerative” for many people.
OK. What did people do to get better? I report and discuss each answer to the second question in the survey: What therapies were helping? You will be excited to learn that there are dozens of therapies that are making a big difference for people currently experiencing the symptoms of Parkinson’s disease.
Marty Hinz MD, known internationally for developing an amino acid protocol, discusses the following questions during the program today:
What is the primary cause of Parkinsons disease?
What the most effective Parkinsons disease treatment?
What is carbidopa?
Why is carbidopa used?
How does carbidopa deplete vitamin B6?
What happens when vitamin B6 depletes?
He is joined by Dr. Ross Stuart PhD who discusses the clinical experience with his patients using the amino acid protocol. And finally, Michael joins us to discuss his personal experience with using an amino acid protocol.
William Curtis talks about his efforts to understand how ketones have helped with his Parkinsons symptoms. He developed Parkinsons symptoms at the age of 45 in the year 2000 and has been instrumental in collaborating with NIH researcher Richard Veech in Washington DC..
What follows are the questions I ask Bill during the interview today on Parkinsons Recovery Radio.
How did Parkinsons affect your life?
What led you to experiment with ketosis?
After the ketogenic exercise, what did you do to find out more about how ketosis could help your Parkinsons symptoms?
What is the purpose of fasting?
What is the purpose of the morning fat and coffee mixture?
What happens when you eat too much carbohydrate?
What happens when you eat too much protein?
Can exercise take you out of ketosis?
Can stress take you out of ketosis?
What supplements do you take to support ketosis?
What do you think is causing the improvement in symptoms?
Have you been able to cut back on the Parkinsons medications?
What do you think is going on as far as the disease progression you personally are experiencing?
Where do you think the use of ketosis in Parkinsons is going?
