Gluten related PD

Gluten ataxia
File:Gluten ataxia eng.ogv
en.wikipedia.org/wiki/Gluten

Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten.[75] With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common. Myoclonus, palatal tremor, and opsoclonus-myoclonus may also appear.[76]

Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible.[76][77]

Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias.[76][78] Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% have intestinal damage.[76]

Other neurological disorders
In addition to gluten ataxia, gluten sensitivity can cause a wide spectrum of neurological disorders, which develop with or without the presence of digestive symptoms or intestinal damage.[13] These include peripheral neuropathy, epilepsy, headache, encephalopathy, vascular dementia, and various movement disorders (restless legs syndrome, chorea, parkinsonism, Tourette syndrome, palatal tremor, myoclonus, dystonia, opsoclonus myoclonus syndrome, paroxysms, dyskinesia, myorhythmia, myokymia).[13][79]

The diagnosis of underlying gluten sensitivity is complicated and delayed when there are no digestive symptoms. People who do experience gastrointestinal problems are more likely to receive a correct diagnosis and treatment. A strict gluten-free diet is the first-line treatment, which should be started as soon as possible. It is effective in most of these disorders. When dementia has progressed to an advanced degree, the diet has no beneficial effect. Cortical myoclonus appears to be treatment-resistant on both gluten-free diet and immunosuppression.[13]

Keto diet is a better mitochondrial therapy than ketones supplement in Parkinson’s disease

(2021). The therapeutic potential of ketone bodies in Parkinson’s disease. Expert Review of Neurotherapeutics: Vol. 21, No. 3, pp. 255-257.

Source: The therapeutic potential of ketone bodies in Parkinson’s disease

…Ketone supplementation combined with a regular carbohydrate-rich diet creates an unphysiological metabolic state that could undermine efficacy. A more promising approach may be to maintain a steady state of ketosis with a KD, while periodically boosting ketone concentration with supplementation. Progress will need to be made in developing a regimen that can be sustained for years, identifying individuals most likely to respond to ketone therapy, determining the threshold concentration for therapeutic ketosis, and managing other pharmacological treatments and social constraints. However, the bioenergetic potential of ketones and their wide-ranging pleiotropic effects indicate that ketone therapy holds considerable promise in PD and warrants further investigation.

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

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:

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

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

Could Coenzyme Q10 be Used as a Supplement for PD Patients?

A paper by Robert Alan Bonakdar, MD, and Erminia Guarneri MD, published by aafp.org in 2005 looks at coenzyme Q10 and its use in the treatment of a variety of disorders including PD, plus cardiac, immunologic, and oncologic conditions. Coenzyme Q10 appears to be a safe supplement with minimal side effects and low drug interaction potential. As yet, coenzyme Q10 has not been approved for the treatment of specific diseases in the USA. A randomized, double-blind, placebo-controlled, multicenter study of 80 patients found that 1,200 mg per day of coenzyme Q10 was associated with up to 44 percent less functional decline in patients with Parkinson’s disease, including activities of daily living. A study of 28 patients with Parkinson’s disease also demonstrated mild symptom improvement with daily oral dosing of 360 mg of coenzyme Q10. These results are awaiting confirmation.

Source: Coenzyme Q10 – American Family Physician

Fact Sheet: Dietary Supplements for Primary Mitochodrial Disorders

NIH publishes a fact sheet for health professionals on dietary supplements for primary mitochondrial disorders. The fact sheet summarizes published scientific trials, other studies, and reports on the use of dietary supplements to treat primary mitochondrial disorders. The most common ingredients in dietary supplements used in PMD therapy include vitamin C, vitamin E, and alpha-lipoic acid; electron donors and acceptors, such as CoQ10and riboflavin; compounds that can be used as alternative energy sources, such as creatine; and compounds that can conjugate or bind mitochondrial toxins, such as carnitine. A combination of these products is commonly called a mitochondrial cocktail. However, there are many combinations and dosages so the term is nonspecific and nondescriptive. Drug interaction needs to be taken into consideration as well as the level of evidence of efficiency, quality of ingredients, and dosage.

Source: Dietary Supplements for Primary Mitochondrial Disorders – Health Professional Fact Sheet

Review: The Role of Dietary Fat in Treatment of Brain Diseases

A review published in the Current Neuropharmacology journal in 2018 looked at the impact of dietary fats on brain function. It also examined gut-brain communication through microbiota; the impact of probiotics and prebiotics on brain functions; SCFA’s, microbiota, and neuroinflammation. It reviewed lipid sensing, satiety, and processing of hedonic food; the impact of diet on the hypo-thalamic control of reproduction; neuroprotective effects of N-3 PUFAs; dietary PUFAs, brain PUFAs and the role of PUFAs. The results of this review revealed that dietary fats are both friends and foes for brain functions. However, dietary manipulation for the treatment of brain disorders is not just a promise for the future, but a reality. In fact, the clinical relevance of the manipulation of dietary lipids, as for KDs, is well-known and currently in use for the treatment of brain diseases.

Source: Impact of Dietary Fats on Brain Functions
LGIT safe (see 305)

2020 Clinical Trial: Mannitol for PD

The NIH Clinical Trial published information on a study provided by Arkadir David of the Hadassah Medical Organization. The study took 60 participants and ran a phase II single center, randomized, double blind and placebo controlled study assessing the safety, tolerability, and effects of progressively increased dose of oral mannitol in PD. The study began in November 2018 and will end in December 2020. There were 60 Participants of both genders and aged 40 to 75 years. The study assessed the safety of mannitol by the number of treatment-related adverse events and significant changes in vital signs. Tolerability was tested by the level of discomfort. Other changes in participants that were monitored included changes in constipation assessment; Montreal Cognitive Assessment; Brief Smell Identification; change in levodopa-equivalent dose units; change in non-motor symptoms of PD scale and the change in the ratio of total-to-proteinase K-resistant a-syn in red blood cells measured by enzyme-linked immunosorbent assay. Results of this study have not yet been posted.

Source: Safety, Tolerability and Effects of Mannitol in Parkinson’s Disease – Full Text View – ClinicalTrials.gov

 

Vitamin D | Linus Pauling Institute | Oregon State University

n a randomized, double-blind, placebo-controlled study, 112 PD patients (mean age, 72 years) on standard PD treatment were supplemented with 1,200 IU/day of vitamin D or a placebo for 12 months. Vitamin D supplementation nearly doubled serum 25-hydroxyvitamin D concentration (from mean of 22.5 ng/mL to 41.7 ng/mL) in supplemented subjects and limited the progression of PD, as indicated by a greater proportion of patients who showed no worsening (as assessed by the Hoehn and Yahr stage and the United Parkinson Disease Rating Scale part II) in the supplemented group compared to the placebo group (243). It is not known whether vitamin D insufficiency has a role in the pathogenesis of the disease, but the repletion of vitamin D may provide health benefits that go beyond the prevention and/or the treatment of PD. For example, vitamin D deficiency may contribute to the increased risk of osteoporosis and bone fracture in individuals with neurologic disorders, including PD and multiple sclerosis (244-246). Interestingly, sunlight exposure was found to be associated with improved vitamin D status, higher bone mineral density of the second metacarpal bone, and lower incidence of hip fracture in a prospective study conducted in 324 elderly people with PD (247).

Source: Vitamin D | Linus Pauling Institute | Oregon State University

Sleep Master Class by Dr. Mark Hyman

Mark Hyman offers a 8-part Sleep Master Class to help you reclaim your sleep and support your immune system. In the course he walks you through the root causes of poor sleep and how to take practical steps to regain sleep and achieve better health. quality sleep can keep you lean, keep your blood sugar balance, keep you happy and even improve your sex drive. Sleep challenges have been associated with heart disease, diabetes, insulin resistance, weight gain, depression, anxiety, brain fog, and even neurological problems like Alzheimer’s. On the course, five experts discuss how we are sabotaging our sleep and how poor sleep can make us grumpy, stressed, and even sick. Learn how, what and when you eat, your light exposure, hormones, gut health, nutrient status, exposure to toxins, and other factors can affect your quality of sleep. Most importantly the course covers steps you can take to optimize your sleep.

Source: Sleep Course

NADD+ and NADH

NADH for PD:

(NADH) has been used as medication in 885 PD patients in an open label trial. About half of the patients received NADH by intravenous infusion, the other part orally by capsules. In about 80% of the patients a beneficial clinical effect was observed

NADH for brain issues
www.ncbi.nlm.nih.gov/pubmed/29634344

older research
pdfs.semanticscholar.org/ed59/9c8a4b6e45592c8da1099103c5797e82f87b.pdf

NAD+ vs NADH
www.elysiumhealth.com/en-us/knowledge/science-101/whats-the-difference-between-nad-and-nadh

NR+?

Most sources say boost  NAD+ using precursors or NAD+ supplement (NMN, NR)

also oxaloacetate :

oxaloacetate. A higher ratio of NAD+ to NADH helps you make more energy and makes your cells work better. Oxaloacetate activates the longevity pathway in a similar way that calorie restriction does. It converts to malate, which raises your NAD+ to NADH ratio,[26] which makes more NAD+ available for your cells to use. Try: KetoPrime, a highly bioavailable form of oxaloacetate

see also https://onlinelibrary.wiley.com/doi/full/10.1111/j.1474-9726.2009.00527.x

NAD+

Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes

NADH for PD:

short history of NAD related work from 2016, anecdotal evidence suggest its a game changer
measuring NAD is hard to do
precursors taken orally – do they surviv? NADD patched, iv,supossitory…

liposomal NMN ?

all precursors will be tested soon
NAD deficit might be high so that 2x increase in NAD level is not significant