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.

Ridding Cells of Harmful Protein Aggregates by Inducing Autophagy

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.

ApoE4 Information for Alzheimer’s, and Chronic Diseases Including PD

The Wiki page, Apoe4 offers a collection of resources and information that can help you prevent and address health problems related to APOE -ε4 allele. APOE, short for Apolipoprotein E, is both a protein and a gene. As a protein, ApoE is involved in the metabolism of fats (lipids) in the body and comes in different isoforms. In our modern environment, the ε4 allele of the gene confers a higher risk for Alzheimer’s disease and other medical conditions. It is possible to be tested to see if you carry the E4 gene which would mean you are more likely to develop Alzheimer’s, although many other factors also determine vulnerability to Alzheimer’s. E4 is also associated with other chronic diseases including dementia, brain disorders, high cholesterol, infectious diseases susceptibility, gallstones, and cardiovascular disease.

Source: ApoE4.Info Wiki

Review of Possible Use of a Keto Diet in PD Treatment

A review focused on the role of ketogenic diets in neurodegenerative diseases (including PD) was published in the MDPI journal Nutrient in 2019. The goal of the review was to assess the effectiveness of ketogenic diets as part of therapy for neurodegenerative diseases. In PD, dopaminergic neurons in the substantia nigra are affected by a degeneration process leading to motor and non-motor disturbances. The available results of research projects dealing with the use of the KD and ketone bodies in neurodegenerative diseases are fairly promising. At the same time, the majority of studies reviewed were employed in vitro or by using animal models. The number of studies with human participation is rather small, and those that exist feature relatively short therapy duration periods.

Source: Role of Ketogenic Diets in Neurodegenerative Diseases (Alzheimer’s Disease and Parkinson’s Disease)

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

Vitamin D

#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 Source7Trusted 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 of 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).

does vit D cause calcification of arteries?
according to one articles, it could in some settings, not clear when, many other sources point out the benefits of vit d
www.ncbi.nlm.nih.gov/pmc/articles/PMC5986531/

Vitamin D is critical for brain health…

Magnesium

www.naturalstacks.com/blogs/news/magnesium

www.naturalnews.com/046401_magnesium_dietary_supplements_nutrient_absorption.html

magnesium deficiency can cause hreart palpatation and also calcification of heart and blood vessle

general association between magnesium and heart health www.ncbi.nlm.nih.gov/pmc/articles/PMC3957229/

 magnesium salts  could reduce the progress of aortic valve stenosis 

 

Insulin Resistance, GLP-1 analogues, Incretin Mimetics for AD and PD

Brain
AD – See Bredesen

PD –
A pilot study in PD patients testing a GLP-1 receptor agonist that is currently on the market as a treatment for type 2 diabetes (exendin-4, Byetta) also showed encouraging effects. Several other clinical trials are currently ongoing in AD patients, testing another GLP-1 analogue that is on the market (liraglutide, Victoza). Recently, a third GLP-1 receptor agonist has been brought to the market in Europe (Lixisenatide, Lyxumia), which also shows very promising neuroprotective effects. This review will summarise the range of these protective effects that those drugs have demonstrated. GLP-1 analogues show promise in providing novel treatments that may be protective or even regenerative in AD and PD, something that no current drug does.
Drugs developed for treatment of diabetes show protective effects in Alzheimer’s and Parkinson’s diseases.
 
Drugs developed for treatment of diabetes show protective effects inAlzheimer’s and Parkinson’s diseases – full text review

www.ncbi.nlm.nih.gov/pubmed/28927992

חקייני אינקרטין (Incretin Mimetics)

Heart:

Gut
See Ronda Patrick

 

related treatment option for PD  see https://1.getmanaged.online/nly01-halts-pd/