calcium metabolism disorders that cause hypercalcemia (too much calcium in the blood)
genetic or autoimmune disorders affecting the skeletal system and connective tissues
According to Harvard University, a common misconception is that calcifications are caused by a calcium-rich diet. However, researchers haven’t found a link between dietary calcium and a higher risk for calcium deposit
avoid TUMS andacid
avoid supplements which include calcium carbonate
This is also true for kidney stones. Most kidney stones are made of calcium oxalate. People who get calcium oxalate stones release more calcium in their urine than those who don’t. This disparity happens no matter how much calcium people have in thei
Low carb diets (LCDs starting at a young age are associated with an increased risk of subsequent coronary artery calcification (CAC) progression, particularly when animal protein or fat are chosen to replace carbohydrates.
The World Health Organization has come to the conclusion that a global ban on the use of amalgam will be problematic for economic and logistical reasons. So it has recommended a gradual decrease in the use of amalgam.
A document published on the FDA website, the U.S. Food and Drug Administration, describes the dangers of amalgam in an effort to encourage and persuade the head of the administration to ban the use of amalgam. The document specifically mentions amalgam as a cause of neurological diseases.
A review with an impressive scope (78 pages, about 500 references), on the FDA website, outlines the ways mercury from a dental source causes various chronic diseases.
Testimonials were given to the FDA on the harm caused by mercury from a dental source.
An information video explains several studies on the seepage of mercury from filling into the body. At minute 4:16 the video shows an experiment on monkeys. Fillings with mercury were marked with a radioactive isotope. Within about 30 days of the filings being inserted a significant accumulation of mercury in the kidneys, intestines, and other organs was demonstrated with the use of an MRI.
Research shows a connection between the level of valve calcification and the presence of mycoplasma pneumoniae and chlamydia pneumoniae in the affected tissue. The study speculates that the calcification is not an age-related degenerative phenomenon, but rather a reaction to the presence of bacteria.
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.
Viartis is a UK-based group of independent, self-funded medical researchers specializing in Parkinson’s Disease. They have compiled a list of toxic elements that may cause or partially cause PD. The list includes plants and flowers like Annonaceae; chemical elements like Carbon Disulfide, copper, and cyanide; pesticides like Dieldrin; organic compounds like Hydrocarbons and industrial chemicals like N-Hexane. Each toxic element is given a brief description and a list of where you might be exposed to the dangerous element. It includes mention of consumer products that may contain the chemicals and where they come from. High exposure to these toxic substances has been found to increase the chances of developing PD.
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.
If you’re dealing with a chronic disease or you know someone who is then Chris Kresser’s Health Solutions Library can provide you with resources. Among the resources are books and ebooks that cover preventing and reversing chronic illness and guides for living a healthier life. There are also courses you can take in health care and articles focused on health written by leading specialists. Kresser offers an easy-to-use index to help you find the resources for your particular ailment.
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.
Xylitol is a chemical compound and can be classified as a polyalcohol and sugar alcohol, specifically alditol. Xylitol is used as a food additive, often replacing sugar in foods. It occurs in several fruits and humans and animals naturally make trace amounts during the metabolism of carbohydrates. Xylitol is also produced commercially by fermentation of discarded biomass. Xylitol is water-soluble and like most sugar alcohols, xylitol is achiral. Xylitol has negligible effects on blood sugar because it is metabolized independently of insulin. There are no serious health risks for normal consumption. Increased xylitol consumption can increase oxalate, calcium, and phosphate excretion in urine. About 50% of eaten xylitol is not absorbed by the intestines in humans. Instead, 50–75% of this amount is fermented by gut bacteria to short-chain organic acids and gases. The liver metabolizes 50% of absorbed xylitol. The main metabolic route in humans is: in cytoplasm, nonspecific NAD-dependent dehydrogenase (polyol dehydrogenase) transforms xylitol to D-xylulose. Specific xylulokinase phosphorylates it to D-xylulose-5-phosphate. This then goes to pentose phosphate pathway for further processing.
the SEM data show that the protein-protein cross-linking bonds are the starting sites of calcification. In addition, substitution of Ca2+ cations by Mg2+ cations leads to the formation of amorphous hydroxyapatite, preventing aortic valve stenosis, which suggests that treatment with magnesium salts may reduce stenosis of aortic valves… iv.iiarjournals.org/content/28/1/91.full
Studies showed that a calcium to magnesium intake ratio <2.8 is critical for optimal health, supporting a long-held but non–evidence-based recommendation that the calcium to magnesium ratio should be close to 2. Increasing calcium intakes in the United States since 1977 have resulted in a calcium to magnesium ratio >3.0 since 2000, coinciding with increasing rates of T2D and colorectal cancer. US studies assessing oral magnesium therapy or dietary magnesium intakes showed beneficial effects of dietary magnesium in CVD, T2D, and cancers, although similar studies in populations with lower calcium to magnesium ratios (≥1.7) reported the opposite… www.ncbi.nlm.nih.gov/pmc/articles/PMC4717874/
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 — an imbalance between free radicals and antioxidants in your body that contributes to aging.
Practice intermittent fasting. Restricting your eating increases NAD+ levels. 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, which makes more NAD+ available for your cells to use. Try: KetoPrime, a highly bioavailable form of oxaloacetate.
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