Physics defines “energy” the ability to do work. This energy is needed to drive bodily functions such as muscle contraction, the beating of the heart, conduction of messages among neurons and the migration of white blood cells to a site of injury in the immunological response.

Mitochondria are located in the cell membrane and are the cellular powerhouses that generate adenosine triphosphate (ATP), the energy source that powers cellular activities. ATP is produced in cells by from (the oxidation of ) carbohydrates, proteins and fats. ATP is also the energy source produced during photosynthesis in plants. Mitochondria also participate in signaling, cell differentiation, cell death as well as control of the cell cycle and cell growth.

The mitochondrial content of tissues can undergo adaptive increases or decreases in responses to changes in energy demand and substrate supply. The cells of the brain, skeletal muscle, heart muscle, and the eye have the highest energy demands and contain the highest number of mitochondria (approximately 10,000 per cell) while the skin which does not require as much energy contain only a few hundred mitochondria.

The mitochondrial production of ATP results in the creation of free radicals. Free radicals can damage other tissues by stealing electrons. This is referred to as oxidative stress or oxidative damage. Free radicals can also damage mitochondrial DNA (leading to genetic mutations) and a depletion of telomeres which help in cell repair. Free radicals can also oxidize proteins such as LDL which promote atherosclerotic plaque.

At low levels, these free radicals (reactive oxygen and nitrogen species) are signaling molecules. If the free radical load is too great (either because there are too few free mitochondria or because the mitochondria are not working properly) some free radicals escape and will do damage particularly to the mitochondria. Damaged mitochondria results in energy depletion, accumulation of toxic substances within the cell and cell death. When the mitochondria are not overburdened, there is less free radical creation during ATP production.

Mitochondrial health is an important factor for health and aging. The disruption of mitochondrial function has been implicated in many disease including atherosclerosis, ischemic heart disease, cancer, diabetes and neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and ALS. With aging and cumulative free radical attack, mitochondrial health deteriorates.


Poor mitochondria function can result from nutritional deficiencies and environmental toxins. Hence, the approach to improve mitochondrial health will include life style changes such as diet, supplements, exercise and avoiding exposure to environmental toxins).


Exercise especially endurance training increases mitochondrial function, sparks neurogenesis (the creation of new brain cells.) It increases the muscle density of mitochondria in muscles and al other tissues. 1,2 Exercise also increases neurogenesis, and neuronal stem cells, increases the size of the hippocampus (one of the early targets of Alzheimer’s Disease), and improves memory and cognition.


Mitochondrial health depends on a diet that stabilizes blood sugar, and normalizes fatty acids. Fresh vegetables, healthy fat such as olive oil, avocado oil, coconut oil and products, nuts, seeds, and grass fed and free range animals.

Turning away from sugar burning to fat and ketone burning can help mitochondrial health. Mitochondria burn fatty acids cleaner than they burn carbohydrates. Generating ATP via fats/ ketone produces fewer free radicals because it is more efficient and sustains mitochondrial health.

Minimizing methionine consumption can reduce mitochondrial oxygen radical production. 3

High levels of methionine is found in eggs, sesame seeds, brazil nuts, fish, meats, and cereal grains. Most fruits, vegetables and legumes are low in methionine.

Caloric restriction not only increases energy output (mitochondrial biogenesis), but it reduces oxidative stress, inflammatory factors, and decreases apoptotic factors (factors leading to cell destruction). It also is neuro-protective, improves memory and helps regulate gene expression. While some researchers found that caloric restriction increased mitochondrial function, Hancock et al. found that a 30 % caloric restriction did not increase mitochondrial biogenesis. 4

Telomere dysfunction induces metabolic and mitochondrial compromise. 5 Life style choices results in shortened telomeres. Telomeres shorten with age, birth from older parents, stress, environmental toxins such as toluene, benzene, and poly aromatic hydrocarbons. Telomeres can be improved with antioxidants, exercise, decreased poly unsaturated fatty acids, and control of blood sugar, blood pressure, homocysteine, and c reactive protein levels. Avoiding excess iron levels is also essential to mitochondrial health. 6


There are many supplements including minerals, amino acids, and antioxidants that boost mitochondrial function

Acetyl L carnitine improves mitochondrial function. It transports fatty acids to the mitochondrial membrane so it can be converted to ATP. Acetyl L carnitine also protects brain cells and has been postulated to protect brain cells from the toxic effects of the aggregated amyloid beta plaques (which are found in Alzheimer’s Disease). It helps neutralize free radicals.

Carnosine is an antioxidant and free radical scavenger. It prevents age related damage known as glycation (contributing to wrinkles and the corneal opacity of cataracts)

Lipoic acid decreases oxidative stress and improves mitochondrial function and protects brain cells . It is a potent antioxidant. It regenerates levels of vitamin C, vitamin E and boosts the antioxidant, glutathione. it also helps in diabetic neuropathy, glycemic control and to protect brain cells.

Glutathione supports mitochondria function and supports ketogenic burning so less energy is diverted to cleaning up free radicals. Supplementation with glutathione difficult because glutathione is poorly absorbed

Co Q 10 is a powerful antioxidant, cofactor in cellular energy and is vital in the production of ATP. It plays a unique role as an electron carrier in the electron transport chain in the inner mitochondrial membrane and in the production of ATP.. It prevents the breakdown and loss of ATP metabolites. It has cardioprotective, neuroprotective properties and is a calcium channel blocker and cell membrane stabilizer

Vitamin K2 is a mitochondrial electron carrier resulting in more efficient ATP production. 7

Autophagy, (cell destruction) at controlled levels can help regulate mitochondrial function. Nicotinamide enhances mitochondria quality possibly by regulating the levels of autophagy. 8- 10


1. Reynolds G. How exercise can strengthens the brain. Well, September 28, 2011.

2. Steiner JL et al. Exercise training increases mitochondrial biogenesis in the brain. J Appl Physiol. 2011 Oct;111(4):1066-71.

3. Caro P et al. Forty percent methionine restriction decreases mitochondrial oxygen radical production and leak at complex during forward electron flow and lowers oxidative damage to proteins and mitochondrial DNA in rat kidney and brain mitochondria. Rejuvenation Res. 2009 Dec;12(6):421-34.

4. Hancock CR, et al. Does caloric restriction induce mitochondrial biogenesis? A reevaluation. FASEB J. 2011 Feb;25(2):785-91.

5. Sabin E et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature. 2011 Feb 17;470(7334):359-65.

6. Chitambar CR. cellular iron metabolism: mitochondria in the spotlight Blood March 1, 2005 vol 105 no 5:1844-1845

7. Vos M et al. Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. Science. 2012 Jun 8:336(6086): 1306-10.

8. Kang HT& Hwang ES. Nicotinamide enhances mitochondria quality though autophagy activation in human cells. Aging Cell. 2009 Aug;8(4): 426-38.

9. Lee, J et al. autophagy, mitochondria and oxidative stress: cross-talk and redox signaling. Biochem J. 2012 January 15;441(Pt 2): 523-540.

10. Jang S et al nicotinamide-induced mitophagy: an event mediated by high NAD+/NADH ratio and SIRT 1 activation The J of Biol Chem April 9, 2012