Mitochondrial Disease Quotes

This is the mitochondrial DNA.” Bowers nodded back to the cryo-case. “It’s the genetic material that actually makes the energy that powers our cells. Think of it like this. Each of our cells has the usual 23 pairs of chromosomes that make us human and determine our physical appearance, how we fight off disease, and other physical characteristics. Now think of the mitochondria as little organisms within our cells. Like cells within a cell. It’s those little organisms that make energy for our cells. And they have their own DNA.” “I

This brings us to the latest area being explored in connection with low-intensity lasers: Alzheimer’s disease, the commonest kind of dementia. The Alzheimer’s brain is also inflamed, and the mitochondria have difficulty functioning and show signs of aging called oxidative stress, which is a kind of “rusting” of the molecules. Lights, which improve general cellular functioning in the brain, can improve all three conditions—inflammation, mitochondrial problems, and oxidative stress.* The hallmark of Alzheimer’s is that the neurons build up excess misshapen proteins, called tau proteins and amyloid proteins, to form plaques that lead to degeneration.

Infectious diseases cause a rise in oxidative stress, which is largely responsible for coordinating our genetic response to the infection. As we age, mitochondrial respiration also causes a rise in oxidative stress, which activates essentially the same genes through a common mechanism that involves transcription factors like NFΚB. Unlike infections, however, ageing is not easily reversed: mitochondrial damage accumulates continuously. The stress response and inflammation therefore persist, and this creates a harsh environment for the expression of ‘normal’ genes. The expression of normal genes in an oxidized environment is the basis of their negative pleiotropic effects in old age

At the most basic level, scientists are discovering that nearly all of the chronic diseases that cause so much suffering and are steadily driving up the cost of health care all share mitochondrial dysfunction, excessive inflammation, high cortisol levels, and other markers of broken biochemistry. In a very real sense, we all have the same disease because all diseases begin with broken, incorrect biochemistry and disordered communication within and between our cells. For health to return, the chemistry must revert to normal, and communication within and between our cells must be restored. This is true for every disease.

Nearly every disease state known to man has been linked to low mitochondrial activity.  Understanding which foods and factors enhance metabolism, and which inhibit it are paramount for successfully preventing or reversing disease.

In this more nuanced view, aging and the diseases that come with it are the result of multiple “hallmarks” of aging: • Genomic instability caused by DNA damage • Attrition of the protective chromosomal endcaps, the telomeres • Alterations to the epigenome that controls which genes are turned on and off • Loss of healthy protein maintenance, known as proteostasis • Deregulated nutrient sensing caused by metabolic changes • Mitochondrial dysfunction • Accumulation of senescent zombielike cells that inflame healthy cells • Exhaustion of stem cells • Altered intercellular communication and the production of inflammatory molecules Researchers began to cautiously agree: address these hallmarks, and you can slow down aging. Slow down aging, and you can forestall disease. Forestall disease, and you can push back death.

The root cause of all chronic degenerative diseases is a dysfunctional metabolism.

Long COVID is believed to be related to Mitochondrial Disease.

The Cancer Industry

Cancer: The Metabolic Disease Unravelled.

Doctors put drugs of which they know little into bodies of which they know less for diseases of which they know nothing at all.

Activate adenosine monophosphate-activated protein kinase (AMPK). AMPK is an enzyme that stimulates mitochondrial autophagy (mitophagy) and mitochondrial biogenesis as well as five other critically important pathways: insulin, leptin, mammalian target of rapamycin (mTOR), insulin-like growth factor 1, and peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PPAR⊠). It also increases nerve growth factor and helps protect against the type of oxidative stress that leads to Parkinson’s disease. Your AMPK levels naturally decline with increasing age. Following a cyclical ketogenic diet will help you maintain healthy AMPK levels.

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It’s not difficult to see why the World Health Organization has added methylene blue to its list of Essential Medicines.

Oxidation burns things gradually and steadily. Just as oxidation causes metal to rust and apple flesh to brown, it damages cells throughout the body by zapping DNA, scarring the walls of arteries, inactivating enzymes, and mangling proteins. Paradoxically, the more oxygen we use, the more we generate reactive oxygen species, so theoretically vigorous physical activities that consume lots of oxygen should accelerate senescence. A related driver of senescence is mitochondrial dysfunction. Mitochondria are the tiny power plants in cells that burn fuel with oxygen to generate energy (ATP). Cells in energy-hungry organs like muscles, the liver, and the brain can have thousands of mitochondria. Because mitochondria have their own DNA, they also play a role in regulating cell function, and they produce proteins that help protect against diseases like diabetes and cancer.29 Mitochondria, however, burn oxygen, creating reactive oxygen species that, unchecked, cause self-inflicted damage. When mitochondria cease to function properly or dwindle in number, they cause senescence and illness.30

Mitochondrial degradation and damage to stem cells probably account for 95% of degenerative disease.

existing metabolic disease, the resumption of an active lifestyle can significantly improve preexisting cellular damage and promote gains in muscle mass. Regular endurance exercise, by itself—independent of changes in diet—can normalize age-related mitochondrial dysfunction by stimulating mitochondrial biogenesis. (20