Mitochondrial Dysfunction The Driving Force Behind Disease, What Can We Do?

Written by

Sabrina Freudenmann

An understanding of the role of mitochondria is the first step to comprehending how dysfunctional mitochondria actually affects us. The human body thrives on the energy produced within our cells. To produce this energy, our cells contain tiny organelles, which extract significant amounts of energy from ingested nutrients, in order to power each individual cell and the human body as a whole. These organelles are our mitochondria, often referred to as our cellular powerhouses.

All cells in the human body contain mitochondria, with the exception of red blood cells. The total number of mitochondria within cells varies from hundreds to thousands depending on the cell type and its energy requirements (muscle, liver and brain cells have higher levels). Mitochondria are actually bacterial in nature and likely arose from alphaproeobacteria, which have their own DNA and also RNA. Mitochondria are the only organelles that contain their own genome – the mitochondrial DNA (mtDNA). This makes them very special in comparison to all other cell organelles.

insights of mitochondria

The mitochondrial DNA encodes proteins essential to electron flow through a series called the respiratory chain (or electron transport chain). As its name applies, the respiratory chain consumes oxygen. Mitochondrial respiration channels high-energy molecular intermediates through a series of enzymatic reactions, transferring chemical energy from food substrates and oxygen. This stored energy is then used to power various mitochondrial functions, including adenosine triphosphate (ATP – energy) synthesis, calcium uptake, biosynthesis of macromolecules and hormones among others. Mitochondrial energy production powers growth and healing as well as the complex processes required for adaptation to the changing environment and stressors.

 

Role of mitochondria:

  • Energy regulation, production of ATP
  • Involved in the maintenance of intracellular calcium levels and calcium buffering (required for cellular signaling)
  • Regulates cell numbers and defends against unwanted or dangerous cells by triggering programmed cell death (apoptosis)
  • Signaling between the human (nucleus) and mitochondrial genome is also controlled by the mitochondria themselves via the production of Reactive Oxygen Species (ROS)
  • Mitochondrial biogenesis, fusion and fission have roles in aspects of immune cell activation
  • Mitochondria are critical for signaling major innate immune pathways

 

Causes of Mitochondrial Dysfunction

After toxic exposure or cell stress, mitochondria can be damaged, and increased free radical production may be followed by persistent mitochondrial dysfunction.

Cause_of_Mitochondrial_Dysfunction
  • Environmental impact

Without a doubt, there are vast amounts of scientific evidence linking environmental factors with damaged DNA. Increased exposure to heavy metals such as lead, nickel, cadmium and mercury as well as environmental chemicals as PCB, pesticides, xenoestrogens etc. have affected and interfered with mitochondrial function. Don’t forget, it is estimated that by the time the average women have their coffee, over 126 different chemicals in 12 different products have been applied to the face, body and hair (this also includes men and children).

  • Toxins

Thimerosal an ethylmercury found in certain Vaccines, has been associated with cellular / mitochondrial damage, reduced oxidative–reduction activity, cellular degeneration, and cell death.

Endogenous toxins from gut pathogens for example such as clostridia, which can be often found in dysbiosis influence mitochondrial and lipid metabolism.

Toxicity from pharmaceutical drugs is well documented causing mitochondrial disorders: Aspirin, Acetaminophen, Salicylates, Indomethacin/Naproxen, Lidocaine, Tetracycline, Statins, Metformin, HIV medications, Amiodarone, Citalopram, Fluoxetine, Haloperidol, Alprazolam/Diazepam and Phenobarbital

  • Nutritional deficiencies

Nutritional imbalances / deficiencies are leading to susceptibility for poor cellular function. This includes Vitamin B’s, Vitamin D, Vitamin C, CoQ10, Carnitine, zinc, selenium, iron, manganese……

  • Infection & Inflammation

Any kind of chronic infections such as bacterial, yeast and virus (candida or Epstein Barr virus) can suppress mitochondrial function.Chronic inflammation has a direct impact on mitochondrial function.

Symptoms / Diseases associated with mitochondrial dysfunction

  • Most age-linked degenerative neurological disease (Alzheimer disease, Parkinson’s disease)
  • Malignant tumours and premalignant states
  • Congestive heart failure and cardiomyopathy
  • Muscular dystrophy
  • Motor neuron disease (ALS)
  • Metabolic syndrome, insulin resistance and type 2 diabetes, obesity, fatty liver
  • Chronic fatigue syndrome and fibromyalgia
  • Nervous system injury / neuropathies, including multiple sclerosis and cancer chemotherapy induced neuropathy
  • Hypothyroidism, clinical and especially subclinical
  • Increased risk of infections
  • Chronic kidney disease, hypertension
  • Schizophrenia and bipolar disorder; other conditions linked to neuro-inflammation including depression
  • Migraine headache prevention
  • Chronic stress response
  • Insomnia due to hypothalamic suppression
cell stress, abnormal inflammation and immunity

So what can we do?

Addressing the underlying causes of mitochondrial dysfunction

  • Avoiding too much free radical production
  • Increasing oxygenation
  • Getting excellent and sufficient sleep so that mitochondrion can repair themselves
  • Excellent nutrition in respect to micronutrients.
  • Addressing poor digestive function (Leaky gut, dysbiosis)
  • Protection of mitochondrial function by Nrf2, increasing reduced glutathione production, increasing mitochondrial antioxidants.
  • Stabilising blood sugar levels
  • Identifying allergies, intolerances and food sensitivities
  • Detoxifying to unload heavy metals, pesticides, drugs, (alcohol, tobacco etc) and volatile organic compounds, all of which negatively influence mitochondrial function.
  • Reducing Stress
  • Balancing hormones
where Mitochondria is found?

Some self-caring tips for improving mitochondrial function and energy:

 

  1. Swim in the ocean: sea water stimulates mitochondrial function and biogenesis.
  2. High intensity interval training (HIIT): stimulates mitochondrial biogenesis in skeletal muscle. A sedentary lifestyle leads to reduced muscle aerobic capacity and mitochondrial apoptosis which leads to muscle atrophy. An active lifestyle can reverse this.
  3. Yoga: Intense muscle stretching and conditioning stimulates mitochondrial biogenesis.
  4. Turn off your climate control in your home and car. Exposure to heat and cold is known as hormesis which also stimulates our mitochondria. Alternatively, try an infrared sauna.

Nutrient cofactors needed for healthy mitochondrial function:

  • Krebs cycle – B1, B2, B3, B5, Fe, Mg, Mn and lipoic acid (all of the B vitamins are necessary for mitochondrial function)
  • CoQ10 (Ubiquinol)- Coenzyme Q10 supports mitochondrial energy production in the electron transport chain by carrying electrons from cytochrome to cytochrome in order for ATP to be produced in the mitochondria. Without CoQ10, there is no electron transfer
  • Alpha-Lipoic acid– Alpha-Lipoic Acid (ALA) is a mitochondrial fatty acid that is highly involved in energy metabolism. It is a potent anti-oxidant compound and works with mitochondria and the body's natural anti-oxidant defenses.
  • OzoneOzone is a powerful mitochondrial stimulant. The fundamental underlying cause behind all degenerative disease from diabetes to heart disease to cancer is decreased mitochondrial energy production. Ozone can often correct this problem. Ozone also increases antioxidant protection by activating Nrf2 more than any other therapy. Under conditions of stress or growth factor stimulation, activation of Nrf2 counteracts the increased reactive oxygen species production in mitochondria. Any Nrf2 activator, was found to promote mitophagy, thereby contributing to the overall mitochondrial homeostasis.
  • Acetyl-L-Carnitine– Acetyl-L-Carnitine is well-known for its ability to protect the mitochondria. Acetyl-L-carnitine (ALC) is derived from the acetylation of carnitine in the mitochondria. Carnitine acetylation helps eliminate oxidative products from the body.
  • MelatoninMelatonin is a potent antioxidant protecting mitochondria, which are exposed to abundant free radicals. It also increases reduced glutathione, SOD and GPx.
  • ResveratrolResveratrol is a naturally occurring polyphenol found in more than 70 species of plants, including grapes, cranberries and peanuts, which was shown to confer diverse physiological effects such as cancer protection, microvascular protection, neuroprotection, cardioprotection, antidiabetic protection and mitochondrial function support.
  • NAC – N-Acetyl Cysteine (NAC) is the precursor for the powerful antioxidant glutathione, has also been effective in treating mitochondrial dysfunction.

References:

Fonslow, B. R., Stein, B. D., Webb, K. J., Xu, T., Choi, J., Kyu, S., & Iii, J. R. Y. (2013). NIH Public Access. Curr Treat Options Neurol ., 10(1), 54–56. http://doi.org/10.1038/nmeth.2250.Digestion

Fonslow, B. R., Stein, B. D., Webb, K. J., Xu, T., Choi, J., Kyu, S., & Iii, J. R. Y. (2013). NIH Public Access. Curr Treat Options Neurol ., 10(1), 54–56. http://doi.org/10.1038/nmeth.2250.Digestion

Neustadt, J., & Pieczenik, S. R. (2008). Review Medication-induced mitochondrial damage and disease, 780–788. https://doi.org/10.1002/mnfr.200700075

Lagouge, M., Argmann, C., Gerhart-Hines, Z., Meziane, H., Lerin, C., Daussin, F., … Auwerx, J. (2006). Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1?? Cell, 127(6), 1109–1122. http://doi.org/10.1016/j.cell.2006.11.013

Alcaín2, J. M. V. and F. J. (2013). Sirtuin activators and inhibitors, 38(5), 349–359. https://doi.org/10.1002/biof.1032.Sirtuin

Fonslow, B. R., Stein, B. D., Webb, K. J., Xu, T., Choi, J., Kyu, S., & Iii, J. R. Y. (2013). NIH Public Access. Curr Treat Options Neurol ., 10(1), 54–56. http://doi.org/10.1038/nmeth.2250.Digestion

Liu, J. (2008). The effects and mechanisms of mitochondrial nutrient ??-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: An overview. Neurochemical Research, 33(1), 194–203. http://doi.org/10.1007/s11064-007-9403-0

Lee, C. P. (1999). Following Traumatic Brain Injury in Rats, 16(11).

Dinkova-kostova, A. T., & Abramov, A. Y. (2015). Free Radical Biology and Medicine The emerging role of Nrf2 in mitochondrial function. Free Radical Biology and Medicine, 88, 179–188. https://doi.org/10.1016/j.freeradbiomed.2015.04.036

Herst, P. M., Rowe, M. R., Carson, G. M., & Berridge, M. V. (2017). Functional Mitochondria in Health and Disease, 8(November). https://doi.org/10.3389/fendo.2017.00296

Kurochkin, I. O., Etzkorn, M., Buchwalter, D., Leamy, L., & Sokolova, I. M. (2011). Top-down control analysis of the cadmium effects on molluscan mitochondria and the mechanisms of cadmium-induced mitochondrial dysfunction. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 300(1), R21–R31. http://doi.org/10.1152/ajpregu.00279.2010

Schmidt, C. W. (2010). Unraveling environmental effects on mitochondria. Environ Health Perspect, 118(7), A292–A297. http://doi.org/10.1289/ehp.118-a292

Geier, D. a., King, P. G., & Geier, M. R. (2009). Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds. Toxicological & Environmental Chemistry, 91(4), 735–749. http://doi.org/10.1080/02772240802246458

Neustadt, J., & Pieczenik, S. R. (2008). Medicationinduced mitochondrial damage and disease. Molecular Nutrition & Food Research, 52(7), 780–788. http://doi.org/10.1002/mnfr.200700075

Vernon, S., Whistler, T., Cameron, B., Hickie, I., Reeves, W., & Lloyd, A. (2006). Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus. BMC Infectious Diseases, 6(1), 15. http://doi.org/10.1186/1471-2334-6-15

Mills, E. L., Kelly, B., Logan, A., Frezza, C., Murphy, M. P., Neill, L. A. O., … Bryant, C. E. (2016). Succinate Dehydrogenase Supports Metabolic Repurposing of Mitochondria to Drive Inflammatory Article Succinate Dehydrogenase Supports Metabolic Repurposing of Mitochondria to Drive Inflammatory Macrophages, 457–470. https://doi.org/10.1016/j.cell.2016.08.064

Robert B. Cameron1,2, Craig C. Beeson1, and Rick G. Schnellmann2. (2017). Development of Therapeutics That Induce Mitochondrial Biogenesis for the Treatment of Acute and Chronic Degenerative Diseases. J Med Chem, 59(23), 10411–10434. https://doi.org/10.1021/acs.jmedchem.6b00669.Development

 

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