This clip is by Swiss medica clinic
youtu.be/n6yxkFl0olk
#q1 how this works with downers
they treat aa range of auto-immune conditions
say they helped 145 people
This clip is by Swiss medica clinic
youtu.be/n6yxkFl0olk
#q1 how this works with downers
they treat aa range of auto-immune conditions
say they helped 145 people
People who take immunosuppressants less likely to develop the disease
Prednison and other immunosuppressant effective for pre and early stage PD
pubmed.ncbi.nlm.nih.gov/32247373/
pubmed.ncbi.nlm.nih.gov/33409802/
1 completed research findings
www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)31585-4/fulltext
Exenatide had positive effects on practically defined off-medication motor scores in Parkinson’s disease, which were sustained beyond the period of exposure. Whether exenatide affects the underlying disease pathophysiology or simply induces long-lasting symptomatic effects is uncertain. Exenatide represents a major new avenue for investigation in Parkinson’s disease, and effects on everyday symptoms should be examined in longer-term trials.
Supplement alternative – Glutamine >>
A Report of 10 cases of Parkinson’s Disease cured by Xifengzhizhan pills and Xifengzhizhan capsules, Wang Weifan
treatment based on traditional Chinese herbal medicine
Low carb diets (LCDs starting at a young age are associated with an increased risk of subsequent coronary artery calcification (CAC) progression, particularly when animal protein or fat are chosen to replace carbohydrates.
The World Health Organization has come to the conclusion that a global ban on the use of amalgam will be problematic for economic and logistical reasons. So it has recommended a gradual decrease in the use of amalgam.
A document published on the FDA website, the U.S. Food and Drug Administration, describes the dangers of amalgam in an effort to encourage and persuade the head of the administration to ban the use of amalgam. The document specifically mentions amalgam as a cause of neurological diseases.
A review with an impressive scope (78 pages, about 500 references), on the FDA website, outlines the ways mercury from a dental source causes various chronic diseases.
Testimonials were given to the FDA on the harm caused by mercury from a dental source.
Studies on the toxicity of amalgam:
Review of 70 studies on toxicity of amalgam
Dental Amalgam Mercury Solutions
An information video explains several studies on the seepage of mercury from filling into the body. At minute 4:16 the video shows an experiment on monkeys. Fillings with mercury were marked with a radioactive isotope. Within about 30 days of the filings being inserted a significant accumulation of mercury in the kidneys, intestines, and other organs was demonstrated with the use of an MRI.
Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues.
Mercury detox, with and without infusion with chelating agent, here (H).
Mitochondrial dysfunction is common in PD. Mitochondria are organelle responsible for cellular energy production. Loss of function of mitochondria can lead to fatigue and other symptoms common in chronic diseases. A study in 2014 by Garth L. Nicolson, Ph.D. looked at how this can be avoided with natural supplements. Clinical trials have shown that using oral replacement supplements, such as L-carnitine, alpha-lipoic acid (α-lipoic acid [1,2-dithiolane-3-pentanoic acid]), coenzyme Q10(CoQ10 [ubiquinone]), reduced nicotinamide adenine dinucleotide (NADH), membrane phospholipids, and other supplements can naturally restore mitochondrial function. The study conducted regression analyses of data from participants using supplements to determine if fatigue was (1) consistent, (2) occurred with a high degree of confidence, and (3) could predict further reductions in fatigue.
The study concluded that oral natural supplements containing membrane phospholipids, CoQ10, microencapsulated NADH, l-carnitine, α-lipoic acid, and other nutrients can help restore mitochondrial function and reduce intractable fatigue in patients with chronic illnesses.
Guy: At this time I could find very few cases of trying carnivore for PD, actually none doing 100% carnivore.
According to Ronda Patrick below, Carnivore naturally includes caloric restriction, intermittent fasting, changes to the microbiome, low carb diet, and consuming more cholesterol those are 5 powerful tools which do not require a long term carnivore diet, which is a risk.
The one tool unique to a carnivore is eliminating all!! lectins (toxic molecules found in plants.
How significant is that in relation to the other tools and the diet outcome is yet to see.
another player to consider is MTOR high protein diet might shift it towards activation instead of deactivation
so, waiting for this to clear
P.M. :
In the following video, Dr. Ronda Patrick talks to Joe Rogan about the anecdotal evidence that suggests a carnivorous diet may be effective in alleviating the symptoms of autoimmune disorder, PD and other neurological conditions. She talks about her extensive 30-page work covering the trend towards a restrictive animal only diet. She discusses why someone would try this diet and how many immune disorder sufferers are trying low-carb high-protein diets because of the anecdotal reports they have heard.
Dr. Patrick talks about various studies related to high-protein diets and studies related to resetting your immune system through diet. This fascinating podcast brings up the anecdotal evidence and studies of various diets and their effect on autoimmune disorders and PD neurological conditions. She also discusses the effect of fasting, the potential damage of various diets, the modified Ketogenic diet, and the mechanisms that happen in the body when you restrict your diet or fast.
In examining the hypothesis that PD could stem from an influenza virus infection that develops into encephalitis lethargica the role of bacterial and viral infections as a possible cause of Parkinsonism is questioned. The paper compares the clinical, histological, and structural features of Parkinsonism in infectious diseases and looks at the influenza virus and why and how it became associated with PD. Herpes Simplex Virus 1; Epstein-Barr Virus; Varicella-Zoster Virus; Hepatitis C; the Japanese Encephalitis Virus and the West Nile Virus are discussed in connection with PD. The review also examines the Human Immunodeficiency Virus (HIV) and Parkinsonism. In conclusion, the synergistic effect of infectious pathogens in inducing neuroinflammation leading to PD development has been observed. However, it cannot be established that all cases of PD are associated with increased inflammation and underlying chronic infection. Further research is necessary to examine the involvement and extent to which pathogens and inflammatory cytokines play in the pathomechanism of PD.
Source: Infectious Etiologies of Parkinsonism: Pathomechanisms and Clinical Implications
This review was written by Dr. Mark P. Mattson of the John Hopkins University School of Medicine and published in the 2014 Journal of Parkinson’s Disease. It examines whether lifestyle changes that increase insulin sensitivity such as increased exercise and intermittent energy restriction (intermittent fasting) could counteract neurodegenerative processes and improve functionality. Various studies on animal models seem to indicate that peripheral insulin resistance and midlife diabetes may increase the risk of PD. This review examines whether improved peripheral and brain energy metabolism, exercise, GLP-1 analogs, and intermittent energy restrictions (IER) could boost neuronal adaptive stress response pathways and ultimately enhance neurotrophic signaling, DNA repair, mitochondrial biogenesis, and proteostasis.
Interventions that Improve Body and Brain Bioenergetics for Parkinson’s Disease Risk Reduction and Therapy by Dr Mark Mattson
Mark Mattson in TED: fasting/caloric restriction/ intermittent fasting…help against neurodegenerative conditions
The latest invention from Neuralink is ultra-thin “threads” that could be injected into the brain to examine neuron activity. These brain-chip interfaces could hopefully be used to treat chronic conditions like PD. One of the goals of this new technology is to allow humans to keep up with the constant leaps and bounds of AI tech. So far there have only been animal trials of Neuralink’s new technology but with astounding results. Neuralink president, Max Hodak said that the company is close to clinical trials in neurological disorders.
The first human trials will focus on paralysis patients and will involve installing four of the new devices into the patient’s brains. If successful, Neuralink will probably release some developer API. The new technology has the potential for use on PD patients and could be used to improve deep brain stimulation therapy. Deep brain technology already exists but not at the level that Neuralink will hopefully be offering.
Source: Musk’s Neuralink close to clinical trials of “brain interface” device –
This 2018 report from the Journal of Parkinson’s Disease examines the association between the gut bacteria Helicobacter pylori and PD. H. pylori is a common gut bacterium that causes ulcers, gastritis, and can lead to stomach cancer. The majority of PD cases are caused by unknown environmental factors, and bacterial infections could be one of them. This has led doctors to look at the link between H. pylori and PD. After reviewing past studies on the subject four important points were noted: H. pylori-infected PD patients experience worse motor function issues than those not infected; people with PD are more prone to be infected by H. pylori and eradication of H. pylori could improve motor function and levodopa absorption in people with PD.
Source: Eradicating Helicobacter pylori Infections May Be a Key Treatment for Parkinson’s Disease
Mike Mutzel from High Intensity Health (author of Belly Fat Effect) talks to Frank Llosa of KetoneAid. KetoneAid produces a Ketone Ester (raw beta-hydroxybutyrate (BHB) ketone) supplement that can get you into a deep state of ketosis within 30 minutes. You would have to fast or go on an intense ketogenic diet to reach the same ketosis state. There are different types of Keto testing, blood glucose testing, and different types of exogenous Ketones. Ketosis is influenced by BHB salts; Ketone supplements. There have been many discussions about the link between PD and the ketogenic diet. In one study PD patients were put on a ketogenic diet for a month and the results showed a 43% improvement in the Unified Parkinson’s Disease rating scale. There is no doubt that PD is affected by diet and nutrition so the ketogenic diet may offer relief from some symptoms.
Mike Mutzel from High-Intensity Health (author of Belly Fat Effect) talks to William Curtis about his PD journey and how a ketogenic diet changed his life. Curtis suffered from PD for over 17 years before he started exercising, fasting, and following a low-carb, ketogenic diet that remarkably improved his PD symptoms. Through trial and error, Curtis found the right balance in his diet. The William Curtis’ program for easing PD symptoms is not appropriate for everyone. For example, PD patients that have balance problems could do more harm to themselves if they followed Curtis’ diet. After 12 hours of fasting through the night, Curtis has a bulletproof coffee in the morning prepared with butter, heavy cream, coconut oil, and Stevia. This helps his PD symptoms and increases the ketone D-betahydroxybutyrate (BHB).
good results in rats
www.ncbi.nlm.nih.gov/pmc/articles/PMC4912670/
keto vs low fat
8 weeks
both diets had good results, keto was better
pubmed.ncbi.nlm.nih.gov/30098269/
some ways Keto help are not well understood
www.ncbi.nlm.nih.gov/pmc/articles/PMC5790787/
Curtis has a website
ketonesforparkinsons.com/
This 2019 report in the National Library of Medicine (National Center for Biotechnology Information) looks at lifestyles and dietary habits associated with PD. A fasting mimicking diet (FMD), fasting 3 days followed by 4 days of refeeding for three 1-week cycles, which accelerated the retention of motor function and attenuated the loss of dopaminergic neurons in the substantia nigra in 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced PD mice. Levels of brain-derived neurotrophic factor (BDNF), known to promote the survival of dopaminergic neurons, were increased in PD mice after FMD, suggesting the involvement of BDNF in FMD-mediated neuroprotection. The findings showed that FMD also inhibited neuroinflammation and modulated the shifts in gut microbiota composition.
A 2019 study published in the International Journal of Molecular Sciences looked at the interaction of mitochondria, a-synuclein and the endo-lysosomal system. PD is characterized by dopaminergic neuronal loss and the alpha-synuclein-containing Lewy body inclusions in the substantia nigra. Genetic investigations have revealed evidence of the involvement of mitochondrial function, alpha-synuclein (α-syn) aggregation, and the endo-lysosomal system, in disease pathogenesis. Although familial parkinsonism makes up less than 10% of adult parkinsonism, the findings generated from genetic studies have enhanced the understanding of the neuron degeneration processes. These include mitochondrial dysfunction, disruption of network integrity, and α-syn accumulation; the functions of the proteasome and endo-lysosomal pathways in cellular degradation. Mitochondrial dysfunctions, endo-lysosomal disruptions, and α-syn aggregation mutually interact within neurons, while α-syn prion-like propagation may also be associated with PD in an inter-neuronal manner. Both mitochondria and endo-lysosomal dysfunction contribute to the development of α-syn pathology, however, the specific organelle playing the most important role might be decided by genetic and environmental factors. Most likely, a vicious cycle may develop once one system becomes dysfunctional. Further elucidation of the precise molecular mechanisms involved in the pathogenesis of PD may lead to the development of future therapeutic targets to treat PD.
A 2020 publication in the MDPI journal, Biomolecules looks at targeting a-syn for PD therapeutics. PD is characterized by the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy Bodies (cytoplasmic inclusions). The Lewy Bodies are clumps of protein that can build up and create problems in the brain. The Lewy Bodies contain the aggregated a-synuclein protein that can propagate throughout the brain. Many PD studies have looked at ways of inhibiting a-synuclein accumulation to ease PD symptoms. There are various approaches to a-syn inhibition and multiple clinical trials that examine the link between PD and a-syn, with the hope that a treatment may be found for PD using a-syn. Given the central role of α-syn in PD pathology and progression, α-syn met the criteria to be a tantalizing and evident therapeutic target for PD. Promising strategies include predominantly immunization, anti-aggregative molecules, and an increase in α-syn clearance.
Source: Targeting α-Synuclein for PD Therapeutics: A Pursuit on All Fronts
This short, enlightening video clip is an extract from a FoundMyFitness interview with Dr. Guido Kroemer. PD is characterized by protein aggregation of a-synuclein and mitochondrial dysfunction, partly due to mitophagy failure. A recently proposed strategy in preventing (or perhaps treating) neurodegenerative diseases like PD is to starve the cells or use biochemical methods to induce general autophagy and thus help the cell rid itself of protein aggregates. Here Dr. Kroemer describes how mitophagy contributes to the pathophysiology of neurodegenerative diseases like PD and Alzheimer’s and how autophagy might mitigate these processes.