…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.
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.
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.
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.
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.
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.
A 2020 trial looks at the anti-aging effects of niacin. The key is to promote not only a longer life but a healthier life. As we age our NAD molecules decrease so that there is not enough fuel for Sirtuins enzymes that can help reverse DNA damage and signs of aging. One of the main reasons our NAD+ decreases is the enzyme CD38. CD38 is also involved in the degradation of the precursor to NAD, nicotinamide mononucleotide (NMN). As we age our CD38 levels increase and NAD+ go down. The less we activate our Sirtuins the more CD38 we have, so NAMPT suppresses CD38 expression via SIRT1. We can break this vicious circle by taking niacin which can create NAD+ so Sirtuins will have the fuel they need. The study notes that increased NAD+ levels remarkably improved disease hallmarks and mitochondrial mass. This is interesting for treating high cholesterol cases and chronic disease.
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.
high-fat, low-carb keto diet. Being in ketosis, the state where your body uses fat instead of glucose for energy, increases the NAD+ to NADH ratio. You want higher NAD+, because it protects cells from oxidative stress[20][21] — an imbalance between free radicals and antioxidants in your body that contributes to aging.[22][23]
Practice intermittent fasting. Restricting your eating increases NAD+ levels.[24][25] Though calorie-restriction diets and periods of fasting will do it, those aren’t sustainable for the long term. Intermittent fasting is, if you do it right. Here’s how to get started with intermittent fasting.
Take 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.
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
Resveratrol – 1g/daily – mornings with yogurt (see where to buy)
Nicotinamide Mononucleotide (NMN) – 1g/daily – mornings (see where to buy)
Metformin (prescription drug) – 1g/daily in the evenings – except on days when exercising
Multivitamins? Only vitamin D3 with K2, he aims to get the rest from his diet
Statin (prescription drug) – taken since his early 20s due to family history of cardiovascular disease
Aspirin – 83mg daily
make a list according to this guy
checkout Uleic vs resveratrol
Risk:
Metformin may increase risk of PD and other neurodegenerative disease
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