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

 

mutant (A53T) α-synuclein exhibit impaired autonomic regulation of heart rate characterized by elevated resting heart rate

Mutations in α-synuclein cause some cases of familial PD. Several lines of transgenic mice that overexpress wild type or mutant human α-synuclein exhibit progressive accumulation of α-synuclein in neurons, motor dysfunction and death (). Mice expressing mutant (A53T) α-synuclein exhibit impaired autonomic regulation of heart rate characterized by elevated resting heart rate associated with accumulation of α-synuclein aggregates in the brainstem and reduced parasympa-thetic (cardiovagal) tone (). Maintenance of the α-synuclein mutant mice on ADF reversed the autonomic deficit, whereas a high fat diet exacerbated the autonomic deficit (). Consistent with the latter findings, a high fat diet hastened the onset of motor dysfunction and brainstem pathology in another line of α-synuclein mutant mice, which was associated with reduced activity of kinases known to be involved in neurotrophic factor signaling (). In addition to enhancement of neurotrophic factor/BDNF signaling, IF may counteract PD-related pathogenic processes by stimulating autophagy. Indeed, inhibition of mTOR with rapamycin, which stimulates autophagy, reduced oxidative stress and synaptic damage, and improved motor function in a α-synuclein accumulation-based mouse model of PD ().

full article intermittent fasting >> 

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 

 

Forced exercise 35% improvement, motor learning ? upregulate dopamine

www.ncbi.nlm.nih.gov/pubmed/19131578/

www.ncbi.nlm.nih.gov/pmc/articles/PMC4744893/#s002

motor learning activated by stressor – speed, to adapt to the stressor,result is speed and performance when in speed

i assume it goes both ways and e.g. Zen meditation will slow onedown, also depresion/LH/static job

possible treatment -external speed (treadmill),external speed  /pulse measurement

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I speculate that high intensity over continues period of time develops (up regulate) dopamine secretion. that includes brain games

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/

 

neuroprotective effect of nicotine and coffee in PD and AD

Dr Andrue Huberman – Nicotine can hold off certain types of PD and AD, and it also increase neuroplacticity

www.youtube.com/shorts/P1I-gHB8Ucc

more information:

Neuroprotective effect of nicotine
 
A meta-analysis of coffee drinking, cigarette smoking, and the risk of Parkinson’s disease. 

 

Modifiable Risk Factors of Parkinson’s Disease (multiple studies)
byu/magic-theater inCholinergicHypothesis

Infection by Prion-like infection α-synuclein

from food:

www.ncbi.nlm.nih.gov/pmc/articles/PMC5701169/

  • so human source probably also possible
  • leaky gut probably a factor

According to research from John Hopkins, Duke University, and Utah State University, caregivers of someone with neurodegenerative disease are six times more likely to develop the condition themselves. Neurodegenerative disease is a spectrum disease.

Resection of the vagus nerve before rotenone treatment stopped the spread of PD-like pathology.13 Taken together, these data support the intriguing Braak and prion hypotheses of PD development.

 

 

Longevity diet + Long fast (fmd), Intermintent fasting 5:2 16:8

vegetarian, no sugar, good oils, low protein, small fish

FMD see >>

see chapter 4 in the book

FMD –  file 28 longevity diet audiobook

research by longo regarding many conditions that benefit from periodic fasting

homemade FMD:

My Experience with the 5-Day Fasting Mimicking Diet

Dr Mattson research and recommendations 5:2 and 16:8

According to research conducted by neuroscientist Mark Mattson and others, cutting your energy intake by fasting several days a week might help your brain ward off neurodegenerative diseases like Alzheimer’s and Parkinson’s while at the same time improving memory and mood.

5:2 diet…every time you eat, glucose is stored in your liver as glycogen, which takes about 10 to 12 hours to be depleted. After the glycogen is used up, your body starts burning fats, which are converted to ketone bodies, acidic chemicals used by neurons as energy. Ketones promote positive changes in the structure of synapses important for learning, memory, and overall brain health. But if you eat three meals a day with snacks between, your body doesn’t have the chance to deplete the glycogen stores in your liver, and the ketones aren’t produced. Mattson says exercise can also get your body to lower its glycogen levels, and not coincidentally, exercise has been shown to have the same positive effects on brain health as fasting.

5:2 diet…when the brain is challenged by physical exertion, cognitive tasks, or caloric restriction, the body produces a protein called BDNF (brain-derived neurotrophic factor), which not only strengthens neural connections and increases the production of new neurons but can also have an anti-depressive effect.

see also Dr Fung on treating insulin resistance with low carb + fasting

IDM Program

 

 

 

Autophagy

Although autophagy fails to degrade large protein aggregates once they are formed in the cytoplasm, drug-induced activation of autophagy is effective in preventing aggregate deposition, indicating that autophagy significantly contributes to the clearance of aggregate-prone proteins. The pivotal role of autophagy in the clearance of aggregate-prone proteins has been confirmed by a deductive approach using a brain-specific autophagy-ablated mouse model.

Abstract –

onlinelibrary.wiley.com/doi/pdf/10.1002/mds.26477