Exenatide, a GLP-1 receptor agonist licensed to treat type 2 diabetes, and recently shown to be associated with reduced severity of 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.

LSVT voice therapy

we suggest that LSVT encourages acceptance of and comfort with increased loudness and the ability to self-monitor vocal loudness. Addressing this apparent sensory mismatch between vocal effort and vocal output may contribute to generalization and maintenance of treatment effects. Finally, treatment that is simple, redundant, and intensive may help accommodate the processing speed, memory, and executive function deficits observed in some individuals with IPD. It may also promote overlearning and internalization of the vocal effort required for normal loudness

pubs.asha.org/doi/full/10.1044/1058-0360%282002/012%29

Our 15 years of research have generated the first short- and long-term efficacy data for speech treatment (Lee Silverman Voice Treatment; LSVT/LOUD) in Parkinson’s disease. We have learned that training the single motor control parameter amplitude (vocal loudness) and recalibration of self-perception of vocal loudness are fundamental elements underlying treatment success. This training requires intensive, high-effort exercise combined with a single, functionally relevant target (loudness) taught across simple to complex speech tasks. We have documented that training vocal loudness results in distributed effects of improved articulation, facial expression, and swallowing. Furthermore, positive effects of LSVT/LOUD have been documented in disorders other than Parkinson’s disease (stroke, cerebral palsy). The purpose of this article is to elucidate the potential of a single target in treatment to encourage cross-system improvements across seemingly diverse motor systems and to discuss key elements in mode of delivery of treatment that are consistent with principles of neural plasticity.

www.thieme-connect.com/products/ejournals/abstract/10.1055/s-2006-955118

 

 

The use of vitamin K to reduce high INR

The use of vitamin K in patients with warfarin over-anticoagulation lowers excessively elevated INR faster than withholding warfarin alone; however, it has not been clearly demonstrated that vitamin K treatment does, in fact, lower the risk of major hemorrhage. As vitamin K administration via the intravenous route may be complicated by anaphylactoid reactions, and via the subcutaneous route by cutaneous reactions, oral administration is preferred. A dose of 1-2.5mg of oral phytomenadione (vitamin K(1)), reduces the range of INR from 5.0-9.0 to 2.0-5.0 within 24-48 hours, and for an INR >10.0, a dose of 5mg may be more appropriate.

Source: The use of vitamin K in patients on anticoagulant therapy: a practical guide – PubMed

Mycoplasma (and bacteria in general) as a Cause of Narrowing of the Cardiovascular Valves

Cause of Cardiovascular Calcification

Research shows a connection between the level of valve calcification and the presence of mycoplasma pneumoniae and chlamydia pneumoniae in the affected tissue. The study speculates that the calcification is not an age-related degenerative phenomenon, but rather a reaction to the presence of bacteria.

Culture-negative Endocarditis: Mycoplasma hominis Infection

Presence of mycoplasma and viruses in damaged heart tissue and arteries (but also in normal tissue)

Bacteria in Calcific Aortic Valve Stenosis

Treatment of Mitochondrial Dysfunction with Natural Supplements

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.

Source: Nicolson GL. Mitochondrial Dysfunction and Chronic Disease: Treatment With Natural Supplements. Integr Med (Encinitas). 2014;13(4):35-43.

Could a Carnivore Diet Help with Autoimmune Disorder and PD


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.

Cholesterol Provides Some Protection Against PD 

Michael E. McEvoy the founder of Metabolic Healing gives a summary of studies on the connection between cholesterol, Parkinson’s Disease, and statins. Cholesterol plays an important role in PD, yet it is very controversial for different reasons. A 2018 cohort study found higher total cholesterol and LDL was associated with a decreased risk of PD over time for men, but not for women. The 2008 Honolulu-Asia Aging study found PD incidence increased with decreasing LDL-C levels in a dose-dependent manner for men aged 71-75. A 2006 Rotterdam-based study found higher total cholesterol associated with a significantly decreased risk of PD in women only. A 2017 study of 2,322 PD patients found high cholesterol associated with lower PD risk. These studies establish that higher cholesterol is associated with lower PD risk.

Studies that have found statins were protective have been criticized for having significant population bias. As yet no study which has shown statin protection against PD has accounted for patients with hyperlipidemia (these studies have excluded patients with hyperlipidemia). A 2017 study investigating the possibility of statins used in association with PD suggested that statin use may facilitate the onset of pre-clinical PD.

Parkinson’s Pilot Program

Related research presented in the video

Toxic Chemicals, Plants, and Organic Elements that may Trigger Development of PD

Viartis is a UK-based group of independent, self-funded medical researchers specializing in Parkinson’s Disease. They have compiled a list of toxic elements that may cause or partially cause PD. The list includes plants and flowers like Annonaceae; chemical elements like Carbon Disulfide, copper, and cyanide; pesticides like Dieldrin; organic compounds like Hydrocarbons and industrial chemicals like N-Hexane. Each toxic element is given a brief description and a list of where you might be exposed to the dangerous element. It includes mention of consumer products that may contain the chemicals and where they come from. High exposure to these toxic substances has been found to increase the chances of developing PD.

Source: Toxic Causes of PD

Detox options, click here

Toxins used in labs to generate PD model

Could Parkinson’s be Caused by Infection?

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

Could Intermittent Fasting/ Caloric Restriction/ Exercise Improve PD Status

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

In Development: Neuralink’s Brain Implants , to Treat PD

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 –

What is the Link Between Helicobacter Pylori and PD?

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

Keto for PD: The William Curtis Story

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/

Could Fasting Help Control PD Symptoms?

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.

Source: Neuroprotection of Fasting Mimicking Diet on MPTP-Induced Parkinson’s Disease Mice via Gut Microbiota and Metabolites – PubMed

Interaction of Mitochondria, a-Syn, and the Endo-lysosomal System

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.

Source: The Overcrowded Crossroads: Mitochondria, Alpha-Synuclein, and the Endo-Lysosomal System Interaction in Parkinson’s Disease