Mitochondria: Essential Powerhouse for Brain & Vision

Cellular organelles called mitochondria produce energy.

Why are mitochondria essential to your health and well-being?

Mitochondria are the energy batteries of our cells. They are tiny organelles within most cells of the body that provide respiration and energy. Low metabolism develops in the brain as we age and is noticeable in brain regions where mitochondrial structure has changed. 1 The mitochondria attempt to replace themselves whenever they are damaged and destroyed. However, mitochondrial biogenesis can be disrupted. Mitochondrial disease, oxidative stress and free radical damage, drinking alcohol, eating a poor diet, and heavy metals can harm the mitochondria. Research on links between mitochondrial dysfunction and Alzheimer’s Disease are underway. The good news is that lifestyle and natural supplements can support healthy mitochondria functioning.

Mitochondrial Biogenesis

Mitochondrial biogenesis is the process by which cells increase mitochondria to replace damaged or non-functioning organelles. This process plays an essential role in maintaining an adequate functional neuronal mitochondrial mass by compensating for damaged mitochondria that have been eliminated. It is highly regulated and requires coordination and crosstalk between the complete set of DNA in a cell (nuclear genome) and mitochondrial genomes. While mitochondrial biogenesis occurs on a regular basis in healthy cells where mitochondria constantly divide and fuse with each other,  it also occurs in response to oxidative stress, increased energy demand, exercise training, and certain diseases.

Mitochondrial Disease

Some conditions are considered mitochondrial diseases. These are chronic and genetic disorders that can be inherited and which occur when mitochondria are altered and consequently can not produce sufficient energy for the body to function efficiently.

      • Examples are Lebers’, deafness, diabetes, and retinitis pigmentosa.

Other conditions are associated with mitochondria dysfunction.

      • Examples of eye disease are cataracts, optic nerve atrophy, eye muscle weakness, optic neuropathy, retinal damage, rod-cone dystrophy, and Stargardt’s disease.
      • Examples of brain disorders are Alzheimer’s, Parkinson’s, and possibly other dementia-related disorders where mitochondria problems appear to be critical factors.

Symptoms of mitochondrial diseases can include:

      • Poor growth.
      • Muscle weakness, muscle pain, low muscle tone, exercise intolerance.
      • Vision and/or hearing problems.
      • Learning disabilities, delays in development.
      • Autism spectrum disorder.
      • Heart, liver or kidney diseases.

Alzheimer’s and Neurodegenerative Diseases

In Alzheimer’s disease 2 brain mitochondria abnormalities

      • reduce membrane potential, the ability for ion transfer across membranes allowing the cell to act as a battery, and transmit signals to different parts of the cell,
      • increase permeability, reducing the membrane’s ability to act as gatekeeper, and
      • produce excess free radicals which damage proteins, lipids, and nucleic acids.

Growing evidence suggests that elevated amyloid beta levels (Aβ) related to Alzheimer’s disease (AD) contribute to these mitochondrial abnormalities and although the mechanism is not clearly established, both amyloid precursor protein (APP) and Aβ are found in mitochondrial membranes and interact with mitochondrial proteins. Overproduction of APP and Aβ may affect dynamics of mitochondrial fusion/fission,3  impair mitochondrial transport, disrupt the electron transfer chain, increase ROS (Reactive Oxygen Species) production,4  and impair mitochondrial function.

These findings build a strong case for mitochondrial dysfunction in AD and effective treatment will likely include targets that address mitochondrial function.

Issues that Negatively Affect Mitochondria

Oxidative Stress and Free Radicals

Oxidative stress develops when production of free radicals in cells exceeds the ability of antioxidants to stabilize them. Oxidative stress is probably at the root of most health conditions, because it has the capacity to damage all cell structures. It is implicated in a wide range of chronic and degenerative diseases.

Much of the free radical damage is done to mitochondria causing mutations or premature cell death. Within cell mitochondria, damage due to oxidative stress results in DNA strand breaks and lowered ability of DNA to replicate. Some forms of cancer are traced to this malfunction.

      • Inflammation is both a cause and result of oxidative stress. Oxidative stress and inflammation easily induce each other.
      • Free radical accumulation and restriction of the ability to move electrons via mitochondrial pathway (known as the respiratory chain enzyme complex) causes damage to mitochondria in the brain,5 leading to the onset of neurodegenerative diseases, such as Parkinson’s, Alzheimer’s, and Huntington’s disease.
      • Too many free radicals react with fatty acids and proteins within cells and impair their function.
      • Membranes of lipids are highly vulnerable to oxidative stress, and damage to them in the brain may be important in understanding Alzheimer’s disease where accumulation of beta amyloid may be a protective response to oxidative stress.


In the last few years researchers have determined that not only does alcohol negatively impact mitochondria in the liver, but that brain mitochondria are particularly vulnerable.6 Research in both animal and human models have shown that alcohol intake changes mitochondrial structure and function by impairing mitochondrial biogenesis and causing mitochondrial DNA damage.7

Poor Diet

A poor diet with large amounts of refined carbohydrates, fats, sugars, and various additives, flavorings and preservatives contributes to development of free radicals, inflammation, and oxidative stress, which, in turn negatively affect mitochondria function. “Mitochondria are the powerhouse of the cell and mainly responsible for nutrients metabolism, but they are also the main source of oxidative stress and cell death by apoptosis. Unappropriated nutrients may support mitochondria to become the Trojan horse in the cell. “8

Heavy Metals

The accumulation of heavy metals in the body may induce various detrimental intracellular events, including oxidative stress, mitochondrial dysfunction, DNA fragmentation, protein misfolding,  cell cleansing/removal, and premature cell death.9

Promote Healthy Mitochondrial Function

Researchers have identified several methods to improve mitochondrial functioning.

Caloric restriction involves consuming 20-40% lower calories than normal, and has been reported to protect against age-related mitochondrial dysfunction10 and to reduce mtDNA damage.11

Exercise, alone or in combination with caloric restriction may also represent an efficient strategy to delay mitochondrial aging and age-related as it improves oxidative capacity, protein quality control, and has been shown in aging men to promote mitochondrial biogenesis.12, 13

Diet. try to avoid all refined carbohydrates, trans fatty acids found in many processed foods, baked goods, margarine, crackers, avoid fried foods, sugary drinks and diet sodas, artificial sweeteners, all sugar particularly high fructose sugar. Eat lots of green, leafy vegetables, colored foods such as berries, carrots and purple cabbage.

The ketogenic diet increases production of specific mitochondrial uncoupling proteins (UCPs)14 and may also protect against various forms of cell death. [iii] 15

Foods.  Favor green leafy vegetables, blueberries, mulberries, green and black tea.

Herbs.16 Acetyl-L-Carnitine, L-carnosine, Alpha Lipoic Acid, Ashwagandha, Astaxanthin, Baicalein,  CoQ10, Curcumin, D-Ribose, Ginseng, Glutathione, Gotu Kola, Grapeseed Extract, Lutein, Lycopene, Pyrroloquinoline quinone (PQQ), Resveratrol, Vitamin C.

Supplement Recommendations

PPQ. Pyrroloquinoline quinone helps support mitochondria function, the power supply of the cells, and is a powerful antioxidant. This formula is non-GMO

L-Carnosine. Carnosine is a molecule (containing two amino acids) that has antioxidant properties to fight free radicals.

Dr. Grossman’s Vitamin C – (plant-based). Organic Amla supplies vitamin C content of this formulation, along with bioflavonoids that synergistically support vitamin C.

Dr. Grossman’s Advanced Eye and Dr. G’s Whole Food Superfood Multi120 Vcap Combo – 2 months supply

Advanced Eye and Vision Support Formula

Mitochondria Support Package – any one of the products in this package can be ordered individually as well.


Natural Eye Care: Your Guide to Healthy Vision and Healing

Natural Brain Support: Your Guide to Preventing and Treating Alzheimer’s, Dementia, and Other Related Diseases Naturally

Natural Parkinson’s Support: Your Guide to Preventing and Managing Parkinson’s


  1. Hirai K, Aliev G, Nunomura A, Fujioka H, Russell RL, et al. (2001). Mitochondrial abnormalities in Alzheimer’s disease. J Neuro-sci. May 1; 21(9):3017-23.
  2. Moreira PI, Siedlak SL, Wang X, Santos MS, Oliveira CR, et al. (2007). Increased autophagic degradation of mitochondria in Alzheimer disease. Autophagy. Nov-Dec; 3(6):614-5.
  3. Manczak M, Calkins MJ, Reddy PH. (2011). Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer’s disease: implications for neuronal damage. Hum Mol Genet. Jul 1; 20(13):2495-509.
  4. Manczak M, Anekonda TS, Henson E, Park BS, Quinn J, et al. (2006). Mitochondria are a direct site of A beta accumulation in Alzheimer’s disease neurons: implications for free radical generation and oxidative damage in disease progression. Hum Mol Genet. May 1; 15(9):1437-49.
  5. Trushina E, McMurray CT. (2007). Oxidative stress and mitochondrial dysfunction in neurodegenerative diseases. Neuroscience. Apr 14; 145(4):1233-48.
  6. Tapia-Rojas C, Mira RG, Torres AK, Jara C, Pérez MJ, Vergara EH, Cerpa W, Quintanilla RA. (2017). Alcohol consumption during adolescence: A link between mitochondrial damage and ethanol brain intoxication. Birth Defects Res. Dec 1;109(20):1623-1639.
  7. Hoek JB, Cahill A, Pastorino JG. (2002). Alcohol and mitochondria: a dysfunctional relationship. Gastroenterology. Jun;122(7):2049-63.
  8. García-García FJ, Monistrol-Mula A, Cardellach F, Garrabou G. (2020). Nutrition, Bioenergetics, and Metabolic Syndrome. Nutrients. Sep 11;12(9):2785.
  9. Wright RO, Baccarelli A. (2007). Metals and neurotoxicology. J Nutr. Dec; 137(12):2809-13.
  10. Sohal RS, Ku HH, Agarwal S, Forster MJ, Lal H. (1994). Oxidative damage, mitochondrial oxidant generation and antioxidant defenses during aging and in response to food restriction in the mouse. Mech Ageing Dev. May; 74(1-2):121-33.
  11. Gillette-Guyonnet S, Secher M, Vellas B. (2013). Nutrition and neurodegeneration: epidemiological evidence and challenges for future research. Br J Clin Pharmacol. Mar;75(3):738-55.
  12. Menshikova EV, Ritov VB, Fairfull L, Ferrell RE, Kelley DE, et al. (2006). Effects of exercise on mitochondrial content and func-tion in aging human skeletal muscle. J Gerontol A Biol Sci Med Sci. Jun; 61(6):534-40.
  13. Viña J, Gomez-Cabrera MC, Borras C, Froio T, Sanchis-Gomar F, et al. (2009). Mitochondrial biogenesis in exercise and in age-ing. Adv Drug Deliv Rev. Nov 30; 61(14):1369-74.
  14. Sullivan PG, Rippy NA, Dorenbos K, Concepcion RC, Agarwal AK, et al. (2004). The ketogenic diet increases mitochondrial un-coupling protein levels and activity., Ann Neurol. Apr;55(4):576-80.
  15. Noh HS, Kim YS, Lee HP, Chung KM, Kim DW, et al. (2003). The protective effect of a ketogenic diet on kainic acid-induced hippocampal cell death in the male ICR mice. Epilepsy Res. Feb;53(1-2):119-28.
  16. Additional research on these herbs and other information in this article is included in much more detail in the Natural Brain Support book.