Action items that may improve PD status

  • evidence-based
  • Root causes may play a role in many conditions, in all causes listed below, a link to PD was found
  • Key items in the list include: Keto, Fasting, Intermittent fasting, FMD, mitochondria support,  micronutrient optimization/supplementation, macro’s, pathogens, poisons, mind-body, motor learning, masticking, vibration therapy, diet, exercise, EMF radiation dysbiosis & licky gut. cold/ heat exposure,   hormetic stressors, sleep optimization.
  • The goal of the list is to map causes and available treatments relevant to the condition.
  • This is a work in progress, adding new items all the time (sign up for updates)
  • Visit https://healthlinks.cc/list/meds/pd-meds/ for the meds related

 

Oral Glutamine Increases Circulating GLP-1, Glucagon and Insulin Levels in Lean, Obese and Type 2 Diabetic Subjects

Glutamine effectively increases circulating GLP-1, GIP and insulin levels in vivo and may represent a novel therapeutic approach to stimulating insulin secretion in obesity and type 2 diabetes.

Keywords: GLP-1, GIP, glucagon, insulin secretion, glutamine

Source: Oral Glutamine Increases Circulating GLP-1, Glucagon and Insulin Levels in Lean, Obese and Type 2 Diabetic Subjects

Adequate Vitamin B12 and low Homocysteine Levels may slow  progression of PD

Source: Vitamin B12 and Homocysteine Levels Predict Different Outcomes in Early Parkinson’s Disease

Background: In moderately advanced Parkinson’s disease (PD), low serum vitamin B12 levels are common and are associated with neuropathy and cognitive impairment. However, little is known about B12 in early PD.

Objective: To determine the prevalence of low vitamin B12 status in early PD and whether it is associated with clinical progression.

Methods: We measured vitamin B12 and other B12 status determinants (methylmalonic acid, , and holotranscobalamin) in 680 baseline and 456 follow-up serum samples collected from DATATOP participants with early, untreated PD. Borderline low B12 status was defined as serum B12 <184 pmol/L (250 pg/mL), and elevated homocysteine was defined as >15 µmol/L. Outcomes included the UPDRS, ambulatory capacity score (sum of UPDRS items 13-15, 29&30), and MMSE, calculated as annualized rates of change.

Results: At baseline, 13% had borderline low B12 levels, 7% had elevated homocysteine, whereas 2% had both. Elevated homocysteine at baseline was associated with worse scores on the baseline MMSE. Analysis of study outcomes showed that compared with the other tertiles, participants in the low B12 tertile (<234 pmol/L; 317 pg/mL) developed greater morbidity as assessed by greater annualized worsening of the ambulatory capacity score. Elevated homocysteine was associated with greater annualized decline in MMSE (−1.96 vs. 0.06; P = 0001). Blood count indices were not associated with B12 or homocysteine status. Conclusions: In this study of early PD, low B12 status was common. Low B12 at baseline predicted greater worsening of mobility whereas elevated homocysteine predicted greater cognitive decline. Given that low B12 and elevated homocysteine can improve with vitamin supplementation, future studies should test whether prevention or early correction of these nutritionally modifiable conditions slows development of disability. © 2018 International Parkinson and Movement Disorder Society Supporting Informatio

probiotics Bacillus subtilis PXN® 21® eliminates alpha-synuclein aggregates, possible PD treatment

Article in Cell megazine:
www.cell.com/cell-reports/fulltext/S2211-1247(19)31743-7?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124719317437%3Fshowall%3Dtrue

where to buy:

www.bio-kult.com/aboutmigrea

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.

Supplement alternative – Glutamine >> 

 

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

 

 

Rehabilitation of Mitochondria by Lipid Replacement

According to Dr. Garth Nicholson, with prolonged mycoplasma viral infections, the pathogen penetrates cells and causes mitochondrial damage. The phenomenon is typical in a number of chronic diseases (for the infection as a cause of chronic diseases go here), as a result of cancer treatments, and as a result of aging. Declined mitochondrial function causes fatigue and other damage.

For the role of mitochondria in idiopathic Parkinson’s go here, and here.

The above treatment was originally developed for anti-aging.

LRT – Lipid Replacement Therapy

Treatment is by capsules containing lipids needed to repair the mitochondria. Capsules contain a higher concentration of lipids than found in food. The capsules preserve their integrity as they travel through the digestive system. In essence, it is a nutritional supplement.

A short explanation of LRT:

As discussed in the video, it can be assumed that a diet based on unprocessed and uncooked organic food will have good results.

Here is a study showing a significant improvement in mitochondrial function after taking an NT Factor supplement pack for 12 weeks.

NT Factor Contents:

NTFactor® is a nutrient complex that is extracted and prepared using a proprietary process that protects lipids from oxidation. In addition, nutrients, vitamins and probiotic microorganisms are added to the preparation. It contains the following ingredients: Glycophospholipids: polyunsaturated phosphatidylcholine, other polyunsaturated phosphatidyl lipids, glycolipids and other lipids such as cardiolipin and sterol lipids. Probiotics: Bifido bacterium, Lactobacillus acidophilus and Lactobacillus bacillus in a freeze-dried, microencapsulated form with appropriate growth nutrients. Food Supplements, Vitamins and Growth Media: bacterial growth factors to support probiotic growth, including defatted rice bran, arginine, beet root fiber extract, black strap molasses, glycine, magnesium sulfate, para-amino-benzoate, leek extract, pantethine (bifidus growth factor), taurine, garlic extract, calcium borogluconate, artichoke extract, potassium citrate, calcium sulfate, spirulina, bromelain, natural vitamin E, calcium ascorbate, alpha-lipoic acid, oligosaccharides, vitamin B-6, niacinamide, riboflavin, inositol, niacin, calcium pantothenate, thiamin, vitamin B-12, folic acid, chromium picolinate.

Additional Information and Purchase:

Caloric vestibular stimulation (CVS) relieved motor and non-motor symptoms(PD)

repeated sessions of caloric vestibular stimulation (CVS) relieved motor and non-motor symptoms associated with Parkinson’s disease (PD).

www.prd-journal.com/article/S1353-8020(19)30252-4/fulltext

Caloric vestibular stimulation involves the transmission of either warm or cool temperature, usually via water or air, from the external ear canal to the vestibular organs located in the adjacent labyrinth

 

Future: The A1 astrocyte paradigm: New way for pharmacological intervention in neurodegeneration – PubMed

We recently demonstrated that NLY01, a novel glucagon-like peptide-1 receptor agonist, exerts neuroprotective effects in two mouse models of PD in a glia-dependent manner. NLY01 prevented microglia from releasing inflammatory mediators known to convert astrocytes into a neurotoxic A1 reactive subtyp …

Source: The A1 astrocyte paradigm: New avenues for pharmacological intervention in neurodegeneration – PubMed

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 Disorders e.g 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