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Eye & Body Mitochondriaal Health

Friday, October 20, 2017


Today we celebrate ever-growing awareness with a green ribbon mitochondria science refresher. Mitochondria are the organelles in energy-dependent cells, including those in ocular, brain, heart, and muscle tissues.

The British Society for Cell Biology suggested in one of their publications that they probably originated billions of years ago when a bacterial cell was engulfed when visiting what was to become a host cell. The bacterial cell was not digested and stayed on in a symbiotic relationship. 

"Mitochondria convert chemical energy from nutrients into energy in a form usable to its host cell. The scientific name for this function is oxidative phosphorylation (the addition of a phosphate group to a protein or other organic molecule), and it happens inside the mitochondria. This function is also known as the Krebs cycle, and it produces a chemical used by enzymes embedded in the mitochondria inner membrane to generate adenosine triphosphate (ATP) energy.

"In return the host cell provides physical protection and a constant supply of nutrients and oxygen.  

"Recent research indicates that in addition to converting energy, mitochondria play a large part in determining if a cell will die by ordinary cell death (necrosis) or programmed cell death (apoptosis). In apoptosis the mitochondrion releases a chemical called cytochrome C, and this triggers programmed cell death.

"Mitochondria are thought to influence, by exercising a veto, which eggs in a women should be released during ovulation and which should be destroyed by programmed cell death. It appears that in this process mitochondria and the nucleus of the host cell are screened for biochemical compatibility. The pairs that are incompatible are shut down by programmed cell death.

"Mitochondria also produce waste products called reactive oxygen species (ROS) that include free radicals that can damage DNA mitochondrial, which becomes the source of mitochondrial disease affecting areas of high-energy demand including the eye, brain, muscles, and central nervous system.

"Mitochondrial DNA is only inherited through the maternal line. Any mitochondrial DNA contributed by the father is actively destroyed by programmed cell death after a sperm fuses with an egg. This interesting situation has provided genetics and anthropologists with a useful analytical and measuring tool."

A review published in Molecular Aspects of Medicine on more than 130 biochemistry, molecular biology and nutrition peer-reviewed journal articles suggests that optimal metabolic function of mitochondria depends on the availability of many essential minerals, vitamins, and other metabolites.

Unfortunately, micronutrient deficiencies are widespread in the US population, and these deficiencies are associated with most degenerative disease processes. The mitochondria micronutrients specifically include:

Zinc: Low zinc intakes are common, as 10 percent of the US population ingest less than 50 percent of the RDA. Zinc deficiency in human cells in culture causes marked release of oxidants resulting in significant oxidative damage to DNA.

Copper: A link between copper and iron metabolism is well established. Extreme copper deficiency increases dietary iron absorption, which is probably a compensatory mechanism to increase mitochondria heme production. Zinc and copper metabolize to super oxide dismutase (SOD).

Manganese: The major component of the mitochondrial antioxidant defense system is manganese-dependent super oxide dismutase (MnSOD). Inadequate manganese levels increase mitochondrial oxidants and subsequent mitochondrial decay. Low levels of manganese can be associated with impaired glucose tolerance, as well as altered carbohydrate and lipid metabolism.

Selenium: Several reports have shown selenium deficiency causes defects in mitochondrial structure, integrity, and electron-transport chain function. Dietary selenium deficiency occurs in areas of the world where selenium is deficient in the soil. An increased risk of cancer and decreased immune system function has been associated with selenium deficiency.

Magnesium: The mitochondria account for nearly one-third of total cellular magnesium. Magnesium is required for mitochondria ATP energy. Moderate magnesium deficiency is common, particularly among African Americans, and is associated with increased risk for hypertension and diabetes.

Calcium: Calcium is sequestered in mitochondria, and it participates in cellular calcium signaling. Calcium is also a required cofactor in several mitochondrial proteins, including dehydrogenates (enzymes that take up hydrogen).

Vitamin B6: Vitamin B6 is converted to pryidoxal-5 phosphate, which is directly involved in mitochondrial heme biosynthesis. Approximately 10 percent of the US population consumes less than half of the B6 RDA. Recent epidemiological studies have indicated an association between B6 deficiency and increased cancer.

Vitamin B12: Vitamin B12 is taken into the mitochondria and plays an important role in amino acid metabolism. A B12 deficiency has been shown to affect 10 to 15 percent of individuals over the age of 60 in the US. Patients with B12 deficiency exhibit megaloblastic anemia and often hyperhomocysteinemia. 


Biotin: Biotin deficiency is suggested to deplete the amino acid glycine from the mitochondrial matrix. Glycine depletion results in iron deficiency.

Pantothenic acid: Also known as vitamin B5, pantothenic acid is the precursor of coenzyme A (CoA), which is necessary for mitochondrial ATP energy production.

Riboflavin: Also known as vitamin B2,  riboflavin supports mitochondrial energy production by stimulating metabolism of fats, carbohydrates, and proteins. It is required for red blood cell formation and respiration, antibody production, growth, and reproduction. It also helps in the prevention of many types of eye disorders, including bloodshot, itching, or burning eyes and abnormal sensitivity to light.

The big three mitochondria housekeepers

Lipoic acid: Lipoic acid is both water and fat soluble and is a vital cofactor for production of enzymes necessary for mitochondrial function. Both lipoic acid and B5 are essential for the normal supply of succinyl-CoA, another precursor for heme biosynthesis.

Acetyl-l-carnitine: ALC is a delivery form for the amino acid l-carnitine. It transports long-chain fatty acids across the mitochondrial membranes into the mitochondria and transports small-chain and medium-chain fatty acids out of the mitochondria in order to maintain normal coenzyme A levels in these organelles. This is particularly important for retina health.

Coenzyme Q10: CoQ10 is a fat-soluble compound primarily synthesized by the body and also consumed in the diet. It is required for mitochondrial ATP synthesis. It also functions as an antioxidant in cell membranes and lipoproteins. Statin drugs deplete CoQ10 levels, therefore CoQ10 supplements should be routinely taken with all statin drugs.

Ellen Troyer with Spencer Thornton, MD, David Amess and the Biosyntrx staff



PEARL

Given the  ever growing amount of published science linking mitochondria function to ocular health, it's a mystery to the Biosyntrx science team why so many ocular-focused supplement designers don't include the nutrients clearly associated with optimal mitochondrial function in their formulations. 











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Bibliography

Clinical references available in the Biosyntrx office.