Nutrients that are shown to activate mitochondrial biogenesis


Mitochondria are the only cell components (other than the nucleus) to possess their own DNA. This means mitochondria have the ability to replicate and increase their number within a single human cell. Human cells may house anywhere from 2 to 2,500 mitochondria, depending on tissue type, antioxidant status, and other factors.

It is claimed in scientific circles that mitochondrial number and function determine human longevity. Thus the more functional mitochondria you have in your cells, the greater your overall health and durability.

As we age and grow older, the problem is that our mitochondria degrade and become dysfunctional. Age-related destruction of the mitochondria occurs more rapidly than in other cell components, meaning that for most people it is loss of functional mitochondria that ultimately leads to personal extinction.

Up until recently, mitochondrial biogenesis, the creating of new mitochondria within cells, has been problematic and the only recognized natural ways to stimulate mitochondrial biogenesis were:

  • calorie restriction or
  • aerobic exercise

Fortunately, the scientific substantiation and research on mitochondrial biogenesis has indicated that there are certain nutrients to enhance mitochondrial performance and biogenesis. These nutrients have been identified in the scientific literature to activate mitochondrial biogenesis, and are as follows:

  • Acetyl-L-Carnitine
  • Alpha Lipoic Acid
  • Branched Chain Amino Acids
  • Nicotinamide
  • Pyrroloquinoline quinone (PQQ)
  • Pterostilbene (doubly methylated resveratrol)
  • Quercetin
  • Resveratrol
  • Se-Methyl L-Selenocysteine (Selenium)


Lanza IR, Nair KS. Mitochondrial function as a determinant of life span. Pflugers Arch. 2010 Jan;459(2):277-89.

Robb EL, Page MM, Stuart JA. Mitochondria, cellular stress resistance, somatic cell depletion, and life span. Curr Aging Sci. 2009 Mar;2(1):12-27.

Alexeyev MF, LeDoux SP, Wilson GL. Mitochondrial DNA and aging. Clin Sci. 2004;107:355-364.

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