The “battery” of the cell, the mitochondria, is crucial to good health. However, when mitochondrial function is compromised, it can lead to a host of health issues, ranging from neurodegenerative disorders to cardiovascular diseases. Understanding the intricate relationship between mitochondrial health and overall well-being is essential, particularly when it comes to brain and eye health. What roles do mitochondria play in memory, cognition, and the pathogenesis of Alzheimer’s Disease? How do chronic stress and oxidative stress impact mitochondrial function? Do certain nutrients and dietary habits support these vital organelles? Can exercises help to maintain optimal mitochondrial health and, therefore, overall health?
How Mitochondria Work
Mitochondria are present in nearly every cell in the body and are often referred to as the “powerhouses of the cell.” They generate the majority of the cell’s energy through aerobic respiration and the breakdown of carbohydrates and fatty acids, storing this energy in the form of adenosine triphosphate (ATP). ATP then serves as a chemical energy source throughout the cell.
When mitochondria don’t function properly, it can lead to the development of various diseases, including heart disease, cancer, neurodegenerative disorders, and cardiovascular conditions such as stroke. Mutations in mitochondrial DNA, which is inherited maternally, can result in the absence or malfunction of crucial mitochondrial proteins, contributing to these diseases. However, regular exercise can enhance mitochondrial function, particularly in older adults, by promoting mitochondrial biogenesis and reducing oxidative stress.
Alzheimer’s Disease (AD) and Mitochondrial Dysfunction
Mitochondria act as the energy generators for our cells, producing ATP that fuels various metabolic processes. Dysfunction in these organelles is a significant factor in the development of Alzheimer’s Disease (AD). 1 As the brain ages, it tends to experience hypometabolism (reduced metabolic activity), particularly in regions where mitochondrial structures become altered. 2
In Alzheimer’s Disease, abnormalities in brain mitochondria lead to reduced membrane potential, increased permeability, and an overproduction of free radicals, which in turn damage proteins, lipids, and nucleic acids. Research indicates that higher levels of amyloid beta in AD patients contribute to these mitochondrial issues. Although the exact mechanism is not fully understood, both amyloid precursor protein (APP) and amyloid beta (Aβ) are found in mitochondrial membranes and interact with mitochondrial proteins. Excessive APP and Aβ can disrupt mitochondrial fusion and fission, 3 impair mitochondrial transport, interfere with the electron transfer chain, increase the production of reactive oxygen species (ROS), and further impair mitochondrial function. 4 These insights underline the critical role of mitochondrial dysfunction in AD, suggesting that effective treatments will likely need to target mitochondrial health. 5 6
Chronic and Oxidative Stress
Chronic stress can lead to diminished mitochondrial function.7 A significant portion of free radical damage targets the mitochondria, causing mutations or premature cell death.8 Oxidative stress within mitochondria results in DNA strand breaks and a reduced ability for DNA replication, which can contribute to the development of certain cancers. 9
Factors such as oxidative stress, elevated homocysteine levels (a neurotoxin for mitochondria), and glucocorticoid receptor trafficking all impact mitochondrial function under chronic stress. High levels of reactive oxygen species (ROS) like superoxide, hydrogen peroxide, and hydroxyl radicals further damage mitochondrial function. 10
Oxidative stress occurs when the production of oxygen-free radicals surpasses the body’s antioxidant capacity to neutralize them. 11 Antioxidants counteract free radicals by donating an extra electron, thus preventing damage to healthy cells. Glutathione, a master antioxidant, can neutralize a wide range of free radicals throughout the body and is the most abundant antioxidant in the brain. Alzheimer’s patients often have significantly lower levels of glutathione, making its replenishment crucial for natural treatment.
Brain lipids are particularly susceptible to oxidative stress, which can induce lipid peroxidation and degrade polyunsaturated fatty acids (PUFAs).12 Collectively, evidence suggests that oxidative damage from chronic stress can lead to mitochondrial dysfunction and decreased lipid production, including PUFAs.
Sleep Deprivation and Brain Health
Growing research indicates that sleep deprivation acts as a neurobiological stressor, leading to oxidative damage in the brain. 13 Certain nutrients have been shown to protect mitochondria and lipids in neuronal circuits from oxidative damage, which is crucial for maintaining cognitive and emotional health.
Nutrients That Promote and Support Mitochondrial Health
Maintaining adequate levels of specific nutrients is crucial for optimal mitochondrial function, as several micronutrients play key roles in energy production and overall cellular health. Here are some important nutrients that support mitochondrial health:
B Vitamins: Essential for the tricarboxylic acid cycle (Krebs Cycle), which includes eight enzymes critical for mitochondrial function.
Taurine: Supports mitochondrial function and energy production.
Selenium, α-Tocopherol (Vitamin E), Coenzyme Q10, Caffeine, and Melatonin: These nutrients enhance the electron transfer system, promote mitochondrial biogenesis (the creation of new mitochondria), and protect against oxidative damage.
Ascorbic Acid (Vitamin C): Helps reduce oxidative stress and supports overall mitochondrial health.
Zinc: Plays a role in maintaining mitochondrial function.
Carnitine: Essential for fatty acid beta-oxidation and mitochondrial transport of fatty acids, crucial for normal mitochondrial function.
Nitrate and Lipoic Acid: Support various aspects of mitochondrial function.
Berberine: Protects against light-induced retinal degeneration by reducing oxidative stress in the retina and shows promise for brain disorders by restoring proper mitochondrial function.
UBQH (CoQ10): An essential electron transporter that acts as a fat-soluble antioxidant, protecting lipid membranes and lipoproteins from oxidative damage and preventing DNA damage. 14
NMN (Nicotinamide Mononucleotide): A precursor to NAD+ (nicotinamide adenine dinucleotide), critical for metabolism, DNA repair, cell growth, and survival.
PPQ (Pyrroloquinoline Quinone), Resveratrol, and Quercetin: Improve mitochondrial respiratory control and stimulate mitochondrial biogenesis, offering benefits like increased longevity, improved energy utilization, and protection from reactive oxygen species.15 16
Essential Fatty Acids (EPA and DHA): DHA is concentrated in neuronal membranes and synapses, regulating neurotransmission and signal transduction, 17 18 and interacting with membrane-bound enzymes.
Vitamins C & E: Help reduce lipid peroxidation, preventing oxidative lipid deterioration and maintaining membrane permeability and fluidity.
These nutrients collectively support mitochondrial health, enhance energy production, and protect against oxidative damage, contributing to overall cellular and metabolic well-being.
Foods to Avoid
Limit Sugar and Refined Carbohydrates: Particularly avoid high fructose corn syrup, as it depletes adenosine triphosphate (ATP), the primary energy carrier in cells. High fructose corn syrup also increases uric acid levels, which can contribute to diabetes and obesity. Be cautious of sweeteners labeled as fructose, invert sugar, honey, evaporated cane juice, sugar, and sucrose, as they are chemically similar to high fructose corn syrup. Even in moderation, these sweeteners can lead to cardiovascular disease, cancer, liver failure, tooth decay,19 metabolic syndrome,20 and memory problems.21
Caloric Restriction: Reducing calorie intake by 20-40% from normal levels is a promising strategy to extend both median and maximal lifespan.22 Caloric restriction may help prevent or delay diseases such as cancer, cardiovascular diseases, neurodegenerative disorders, diabetes, and autoimmune diseases. Additionally, it can protect against age-related mitochondrial dysfunction and reduce mitochondrial DNA (mtDNA) damage.
Vision Diet Recommendations
We Recommend the Mediterranean Diet and the Alkalizing Diet:
- Pure Water: Sip throughout the day.
- Fresh Vegetables and Fruits: Aim for 1/2 cup cooked or 1 cup raw with every meal, prioritizing vegetables over fruits and including dark leafy greens.
- Olive Oil: Use first cold-pressed extra-virgin olive oil stored in a dark bottle.
- Whole Grains, Legumes, and Starches: Incorporate daily, with potatoes limited to once or twice a week.
- Nuts and Seeds: Consume a few each day, or if more than a few, limit to twice a week.
- Seafood: Limit to 2–3 times per week, favoring wild-caught options.
Dairy: Limit to once a day. - Poultry and Eggs: Limit to 2–3 times per week.
- Natural Sweets: Opt for cobblers and pies sweetened with fruit.
- Go Organic: Be mindful of what you are putting into your body.
Avoid Harmful Ingredients that Negatively Impact Your Health
- Limit Sweets: Especially white or refined sugar. Avoid artificial sweeteners like aspartame.
- Limit Alcohol: To one glass of red wine daily; alcohol can reduce protective glutathione levels by interfering with liver function.
- Reduce Caffeine: Limit coffee and tea to one cup a day.
- Read Labels: When buying processed foods, avoid artificial sweeteners, flavorings, colorings, MSG, and fat blockers like Olestra.
- Cut Down on Fast Foods: Reduce or eliminate deep-fried foods.
Exercise and Mitochondrial Aging
Exercise, whether on its own or combined with caloric restriction, can be an effective strategy to delay mitochondrial aging and age-related decline. It enhances oxidative capacity and protein quality control, and research has shown that it promotes mitochondrial biogenesis in aging men.23 24 This approach may have significant implications not only for reducing fatigue but also for addressing central nervous system diseases and age-related dementia, which are often linked to mitochondrial dysfunction.
New Eyedrops
Dryness Homeopathic Eyedrops – Natural, homeopathic eyedrops for relief of chronic dry eye and eye irritation symptoms.
RED Homeopathic Eyedrops – Helps reduce redness and irritation caused by allergies, dryness, and is used to help reduce related inflammation and swelling.
Digital Eye Strain Homeopathic Eyedrops – Helps reduce eye stress related symptoms that can result from daily use of digital devices and other types of near work.
Suggested Supplements
Advanced Eye & Vision Support Formula (whole food) 60 vcaps
Dr. Grossman’s Meso Plus Retinal Support and Computer Eye Strain Formula with Astaxanthin 90 vcaps
Dr. Grossman’s Advanced Eye and Dr. G’s Whole Food Superfood Multi1 20 Vcap Combo – 2 months supply
Nitric Oxide Supplement – help promoted increased oxygen through the body and eyes.
NMN Wonderfeel Capsul 60 vegcaps
Mitochondria Support
PQQ Caps with BioPQQ® 20 mg 30 vegcaps – helps support mitochondrial function and overall energyUBQH 100mg 60 softgels (easily absorbed form of CoQ10) – helps support mitochondrial function and overall energy
Mitochondrial Cofactors 90 vegcaps (A78270)
Packages
Brain and Memory Support Package 1
AMD Package 1 (3-month supply)
Mitochondria Eye Brain Support Package
Recommended Books
Natural Eye Care: Your Guide to Healthy Vision and Healing
Natural Parkinson’s Support: Your Guide to Preventing and Managing Parkinson’s
- Swerdlow RH, Burns JM, Khan SM. (2014). The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives. Biochim Biophys Acta. Aug; 1842(8):1219-31. ↩
- Murray J, Tsui WH, Li Y, McHugh P, Williams S, et al. (2014). FDG and Amyloid PET in Cognitively Normal Individuals at Risk for Late-Onset Alzheimer’s Disease. Adv J Mol Imaging. Apr; 4(2):15-26. ↩
- 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. ↩
- Reddy PH. (2008). Mitochondrial medicine for aging and neurodegenerative diseases. Neuromolecular Med. 10(4):291-315. ↩
- Calkins MJ, Manczak M, Reddy PH. (2012). Mitochondria-Targeted Antioxidant SS31 Prevents Amyloid Beta-Induced Mitochondrial Abnormalities and Synaptic Degeneration in Alzheimer’s Disease. Pharmaceuticals (Basel). 5(10):1103-19. ↩
- Reddy PH, Tripathi R, Troung Q, Tirumala K, Reddy TP, et al. (2012). Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer’s disease: implications to mitochondria-targeted antioxidant therapeutics. Biochim Biophys Acta. May; 1822(5):639-49. ↩
- Pavlides C, Nivon LG, McEwen BS. Effects of chronic stress on hippocampal long-term potentiation. Hippocampus. 2002;12:245–257. ↩
- Biswal, M.R., Ahmed, C.M., Ildefonso, C.J., Han, P., Li, H., et al. (2015). Systemic treatment with a 5HT1a agonist induces anti-oxidant protection and preserves the retina from mitochondrial oxidative stress. Exp Eye Res, Nov;140:94-105. ↩
- Han, Y., Chen, J.Z. (2013). Oxidative stress induces mitochondrial DNA damage and cytotoxicity through independent mechanisms in human cancer cells. Biomed Res Int, 2013:825065. ↩
- Jou SH, Chiu NY, Liu CS. Mitochondrial dysfunction and psychiatric disorders. Chang Gung Med J. 2009;32:370–379. ↩
- McIntosh LJ, Sapolsky RM. Glucocorticoids may enhance oxygen radical-mediated neurotoxicity. Neurotoxicology. 1996;17:873–882. ↩
- Arts MJ, Grun C, de Jong RL, Voss HP, Bast A, Mueller MJ, Haenen GR. Oxidative degradation of lipids during mashing. J Agric Food Chem. 2007;55:7010–7014 ↩
- Lavie L. Oxidative stress–a unifying paradigm in obstructive sleep apnea and comorbidities. Prog Cardiovasc Dis. 2009;51:303–312. ↩
- Schmelzer C. and Doring F. Micronutrient special issue: Coenzyme Q(10) requirements for DNA damage prevention. Mutat Res 733: 61–68, 2012 ↩
- Liu J., Ames B. N. (2005) Nutr. Neurosci. 8, 67–89 ↩
- Carter C. S., Hofer T., Seo A. Y., Leeuwenburgh C. (2007) Appl. Physiol. Nutr. Metab. 32, 954–966 ↩
- Zimmer L, Delpal S, Guilloteau D, Aioun J, Durand G, Chalon S. Chronic n-3 polyunsaturated fatty acid deficiency alters dopamine vesicle density in the rat frontal cortex. Neurosci Lett. 2000;284:25–28. ↩
- Brunner J, Parhofer KG, Schwandt P, Bronisch T. Cholesterol, essential fatty acids, and suicide. Pharmacopsychiatry. 2002;35:1–5. ↩
- Hyman, M. (2011). 5 Reasons High Fructose Corn Syrup Will Kill You. Retrieved from http://drhyman.com/blog/2011/05/13/5-reasons-high-fructose-corn-syrup-will-kill-you/. ↩
- Legeza, B., Marcolongo, P., Gamberucci, A., Varga, V., Banhegyi, G. (2017). Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome. Nutrients, Apr. 26;9(5). ↩
- Noble, E.E., Hsu, T.M., Liang, J., Kanoski, S.E. (2017). Early-life sugar consumption has long-term negative effects on memory function in male rats. Nutr Neurosci, Sept 25:1-11. ↩
- Peterson CM, Johannsen DL, Ravussin E. (2012). Skeletal muscle mitochondria and aging: a review. J Aging Res. 2012:194821. ↩
- Menshikova EV, Ritov VB, Fairfull L, Ferrell RE, Kelley DE, et al. (2006). Effects of exercise on mitochondrial content and function in aging human skeletal muscle. J Gerontol A Biol Sci Med Sci. Jun; 61(6):534-40. ↩
- Viña J, Gomez-Cabrera MC, Borras C, Froio T, Sanchis-Gomar F, et al. (2009). Mitochondrial biogenesis in exercise and in ageing. Adv Drug Deliv Rev. Nov 30; 61(14):1369-74. ↩