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

 

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

All About mTOR, mTOR Inhibitors and mTOR Activators

SelfHacked published an article by Puya Yazdi, MD in September 2020 about mTOR and natural mTOR inhibitors and activators. mTOR responds to signals from nutrients, growth factors and cellular energy status and controls cell growth and proliferation based on regulating protein syntheses. mTOR is one of those things that’s good to have cycled. Sometimes we want to increase it to grow muscle and improve certain aspects of cognition, while the rest of the time we want to have low levels to increase longevity, decrease the risk of cancer, and reduce inflammation. Too much mTOR activation is associated with many diseases including neurodegeneration. There are mTOR inhibitors mainly used as immunosuppressants to prevent transplant rejection and in anticancer therapy and strategies such as ketogenic diets. mTOR activators include a variety of amino acids and the hormone insulin as well as proteins, excess carbs, Orexin, and more. For health and longevity, we’d want systemic mTOR levels to be low most of the time, with occasional periods of activation. Research suggests it’s preferable to have mTOR more active in your brain and muscles rather than in your fat cells and liver. Exercise is ideal because it does exactly this.

Source: All About mTOR + Natural mTOR Inhibitors & Activators – SelfHacked

New treatments for PD, in trials

direct administration to the brain (that’s new) of GDNF  (also new)

The FDA granted approval of Nourianz to Kyowa Kirin, Inc.

  • A universal feature of Parkinson’s is aggregation, or clumping, of the protein alpha-synuclein in the brains and body cells of people with the disease (similar to the amyloid clumps seen in Alzheimer’s disease). Multiple drug companies are conducting clinical trials to try to prevent or break up synuclein clumps, which scientists believe could stop PD in its tracks.
  • Several potentially disease-modifying therapies continue to advance via “repurposing” — scientifically evaluating drugs approved for various conditions for their benefit in PD. Isradipine (a hypertension drug) and inosine (an antioxidant supplement) are now in Phase III trials. The field also has seen promise in the diabetes drug exenatide and the cancer drug nilotinib.

New meds, in trial

 

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

Keto for PD, Some Evidence

…What are the benefits of Ketosis?
Achieving a state of ketosis can have many benefits from treating chronic illnesses to optimizing performance. While the benefits are well documented, the underlying mechanism of action is not entirely known. The diet seems to enhance the ability of mitochondria, the power plants of our cells, to deliver our bodies’ energy needs in a manner that reduces inflammation and oxidative stress. Through optimizing the way our body uses energy, we fortify our bodies’ ability to take on the ever-growing stressors of our modern way of living.

some results:
charliefoundation.org/keto-for-parkinsons/

Vitamin D

does vit D cause calcification of arteries?
according to one article, it could in some settings, not clear when, many other sources point out the benefits of vit d

Vitamin D in Vascular Calcification: A Double-Edged Sword?

#q
How much sun exposure is needed for vit D instead of supplements?

answer from https://www.healthline.com/nutrition/vitamin-d-from-sun#time-of-day

At noon, the sun is at its highest point, and its UVB rays are most intense. That means you need less time in the sun to make sufficient vitamin D (5Trusted Source).

Many studies also show that the body is most efficient at making vitamin D at noon (6Trusted Source, 7Trusted Source).

For example, in the UK, 13 minutes of midday sunlight exposure during summer three times per week is enough to maintain healthy levels among Caucasian adults (5Trusted Source).

Another study found that 30 minutes ttof midday summer sun exposure in Oslo, Norway was equivalent to consuming 10,000–20,000 IU of vitamin D (8Trusted Source).

The commonly recommended daily dose of vitamin D is 600 IU (15 mcg) (3).

Vitamin D is critical for brain health…