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

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

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.

Cancer: The Metabolic Disease Unravelled.

The Cancer Industry

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

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

Migraine, like my patient Sarah had, also correlates closely to poor metabolic health. In the ENT otology clinic, we often saw this condition and had limited success in treating it. Sufferers of this debilitating neurological disease—about 12 percent of people in the United States—tend to have higher insulin levels and insulin resistance. A comprehensive review of fifty-six research articles identified links between migraine and poor metabolic health, pointing out that “migraine sufferers tend to have impaired insulin sensitivity.” The review supports the “neuro-energetic” theory of migraine. Additionally, evidence suggests that micronutrient deficiencies in key mitochondrial cofactors may also be a contributing factor of migraine. Research has suggested that migraines could be treated by restoring levels of vitamins B and D, magnesium, CoQ10, alpha lipoic acid, and L-carnitine. Vitamin B12, for instance, is involved in the electron transport chain responsible for the final steps of ATP generation in the mitochondria, and studies have indicated that high doses of B12 can help prevent migraine. These micronutrients usually have fewer side effects than other drugs used to treat migraines, making them a promising option for relief, which can be obtained through a diet rich in these micronutrients, or supplementation. Having high markers of oxidative stress, a key Bad Energy feature, is associated with a significantly higher risk of migraine in women, with some studies suggesting that migraine attacks are a symptomatic response to increased levels of oxidative stress. Less painful and more common tension-type headaches are also linked to high variability (excess peaks and crashes) in blood sugar. Hearing Loss The same story of metabolic ignorance in the ENT department unfolded for auditory problems and hearing loss, one of the most common issues presented to our ENT clinic. We’d typically tell our patients that their auditory decline was inevitable, due to aging and loud concerts in their youth, and we would suggest interventions like hearing aids. Yet insulin resistance is a little-known link to hearing problems. If you have insulin resistance, you are more likely to lose hearing as you age because of poor energy production in the delicate hearing cells and blockage of the small blood vessels that supply the inner ear. One study showed that insulin resistance is associated with age-related hearing loss, even when controlling for weight and age. The likely mechanism for this is that the auditory system requires high energy utilization for its complex signal processing. In the case of insulin resistance, glucose metabolism is disturbed, leading to decreased energy generation. The impact of Bad Energy on hearing is not subtle: A study showed that the prevalence of high-frequency hearing impairment among subjects with elevated fasting glucose levels was 42 percent compared to 24 percent in those with normal fasting glucose. Moreover, insulin resistance is associated with high-frequency mild hearing impairment in the male population under seventy years of age, even before the onset of diabetes. These papers suggest that assessing early metabolic function and levels of insulin resistance is essential in the ENT clinic and counseling individuals on the potential warning signs is paramount.

It’s the mark of an educated mind to be able to entertain a thought without accepting it.” – Aristotole

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

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.

It’s important to point out that the results of the Italian experiment and Dr. Racker’s predictions also jibe with the rules of chemistry we’ve already learned. Chemistry tells us that uncontrolled oxygen-PUFA reactions invariably generate free radicals and oxidative stress. When these reactions occur inside our mitochondria, our mitochondria can’t produce energy normally and will start leaking free radicals. This process of leaking free radicals consumes antioxidants, too—which the body can resupply, but it can take a while. Meanwhile, mitochondrial energy output will not be optimal, and the cell will be exposed to damaging oxidative reactions, toxin formation, and the general mayhem previously discussed. All of this is sometimes called mitochondrial oxidative stress, and mitochondrial oxidative stress is known to promote a variety of diseases for which medical science currently has no effective cures.

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.

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

Long COVID is believed to be related to Mitochondrial Disease.

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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

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

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.