Supplements, Chronic Fatigue, And Mitochondrial Dysfunction
There has been in recent years a growing concern about a elusive condition that has been termed as the Chronic Fatigue Syndrome. Described as such, due to the multi-facet nature of this malady and no definitive cause, many other underlying medical conditions are ruled out before a firm diagnose of chronic fatigue is made. This disorder is described as an unrelenting, continuous episode of exhaustion.
Some symptoms of chronic fatigue are:
•chronic joint or muscle pain
•poor sleep patterns
•anxiety and depression
•exhaustion after minimal efforts
Two other common symptoms of chronic fatigue are:
1. Fatigue lasting at least six months, usually rapid in its onset, fatigue that last twenty-four hours or longer after exercising.
2. Sore throat and painful lymph nodes in the neck. While no cure exists for this disease, the etiologic nature or progression of it, there are boundless theories.
Mitochondria and Cellular Energy Energy is a very complex biochemical process and involves many chains of events. Conversion of food molecules into the high energy compound ATP (adenosine triphosphate) occurs in the super minute cells known as the mitochondria.
These specialized cellular organelles are composed of their own lipid membranes, enzymes and genetic information.
These cells metabolism and convert sugars and fats into energy, which are stored in the formidable energy molecule ATP cited above. This cycle of events known as the krebs cycle is an array of organized reactions that release energy from food. This process of oxidation and energy production is one of the most important moment to moment functions of every cell. Wei and Lee have found that excessive oxidation and damage to lipid membranes are major causes of mitochondrial dysfunction.
Impairments deep within the cellular levels, have a profound affect on physical and muscular energy levels. Evidence continues to mount concerning the effectiveness of a number of natural nutritional supplements that have shown remarkable results in supporting mitochondria function, thus reducing the negative symptoms associated with chronic fatigue.
Four such supplements are alpha-lipoic acid, CoQ10, L-carnitine and nicotinamide adenine denine dinucleotide (NADA).
Acid Alpha lipoic acid has been researched since the early 1950s and was recognized as an antioxidant in 1988. Extensively studied by Dr. Lester Packer of the University of California, alpha-lipoic acid is considered a metabolic or all-body antioxidant. This is due to the fact that lipoic acid not only reduces oxidative stress as an antioxidant, it actually charges other antioxidants, thus restoring their power, as confirmed in research by Dr. Packer. Additionally alpha-lipoic acid is needed to produce energy, playing a crucial role in mitochondria function, protecting the genetic material DNA.
Co-enzyme Q10 also known as ubiquinone (found everywhere), provides energy for the body’s cell growth and maintenance. Folkers found that 95% of all cellular energy is modulated by CoQ10, in research conducted at the University of Texas. Folkers, winner of the Priestly Medal, and co-workers confirmed that CoQ10 molecules move between the bioenergy enzyme, directing the transportation of energy from one enzyme to another to create ATP. Additionally, CoQ10 in cells is concentrated within the mitochondria. CoQ10 is vital to cellular respiration (the krebs cycle) and controls how well protons are pumped across the mitochondria membrane, which modulate the energy necessary to sustain life. CoQ10 also acts as a powerful antioxidant that protects the body from free radical and oxidative stress.9 Imagawa and co-workers found CoQ10 to be highly effective in preserving mental functions, (along with iron and B6) as well as controlling immunity10, and appears to increase the heart’s tolerance to a lack of oxygen.
This amino acid gained its notariaty as a ergogenic substance by individuals engaged in weight training to build muscle. It’s specific action is that of breaking down fats into fatty acids, which are transported into the cell’s mitochondria to be burned as fuel. Dificiencies of carnitine are associated with low energy levels and muscular weakness. Hagen and co-workers have postulated that cellular energy production itself produces free radicals that can destroy cell structures, including the mitochondria, thus reducing the body’s natural antioxidant ability to quench free radicals. Being an endogenous antioxidant (naturally present in the body) L-carnitine has the ability to maintain mitochondrial function by reversing age-associated mitochondrial decay. Additionally L-carnitine in clinical trials has shown dramatic results in improving various neurological disorders, as well as slowing down the progression of alzheimer’s disease in young patients.
Nicotinadmide Adenine Dinucleotide
Nicotinadmide adenine dinucleotide, commonly abbreviated as NADA is a compound found in all cells. NADA is responsible for the generation and transmission of energy within cells. Found abundantly within the mitochondria of the cell, NADA is also referred to as coenzyme1 and is the coenzyme form of the B-vitamin niacin. NADA is intimately involved with human bioenergetic pathways, especially in the brain and nervous system. Research by Birkmayer has confirmed that NADA supplementation can increase the production of dopamine, L-dopa and norepinephrine, which translates into improved vitality,mental clarity, alterness, energy production and age related cognitive decline.
1. Slater, L.C., “The mechanism of the conversion of energy of biological oxidation,” Eur. Journal of Biology,” 1987,: 166-489.
2. Spector, A.A., Yorek, M.A., “Membrane lipid composition and cellular function,” Journal of Lipid Research, 1985, 26:10105.
3. Wei, Y.H., Lee, H.C., “Oxidative stress, mitochondrial DNA mutation and impairment of antioxidant enzymes in aging,” Experiemental Biol. Med. 2002: 671-682.
4. Becker, W., Energy and The Living Cell: An Introduction to Bioenergetics, Lippincott Publishers, Philadelphia, PA, 1977.
5. Krebs, E.C., Beavo, J.A., Phosphorylation-dephosphorylation of enzymes, Annual Rev. Biochemistry, 1979, 48:923.
6. Packer, L. et. al., “Alpha-lipoic acid as a biological antioxidant,” Free Radical Biol. Med., 1995:19:227-250.
7. Folkers, K., et. al., Biolmedical and clinical aspects of coenzyme Q10, (Vol. I), E Science Publishers, 1977.
8. Weber, C., Jakobsen, T. S., Mortensen, S.A. et. al., “Antioxidative effect of dietary coenzyme Q10 in human blood plasma,” International Journal of Vit. Nutr. Res., 1994; 64:311-315.
9. Imagawa, M., Naruse, S., Tsuji, S., et. al., “Coenzyme Q10, iron and vitamin B6 in genectically confirmed alzheimer’s disease,” Lancet, 1992; 340:671.
10. Folkers, K., Shizukuis, S., Takkemura, K., et. al., “Increase levels of IsG in serum of patients treated with coenzyme Q10,” Res. Commun. Pathol., Pahrmacol., 1982; 38:335-338.
11. Tanaka, J., Tominga, R., Yoshitoshi, M., et. a., “Coenzyme Q10: the prophylatic effect on low cardiac output following cardiac valve replacement,” Annals of Thorac Surgery, 1982; 33:145-151.
12. Hagen, T.M. et. al, “Mitochondrial decay in hepatocytes from old rats: embrane potential declines, heterogenicity and oxidants increase,” Proc. Of Natl. Acad. of ScienceI, USA, 1997; 94; 3064-3069.
13. Hagen, T.M., Wehr, C., Ames, B.N., “Mitochondrial decay in aging: Reversal through supplementation of acetyl-L-carnitine and N-tert-butyl-a-phenyl-nitrone,” Annals of NY Acad. of Science, 1998, 854:214-223.
14. Forloni, G., et. al., “Neuroprotective activity of acetyl-L-carnitine: studies in vitro,” Journal of Neuroscience Res., 1994, 37:92:96. 15. Brooks, J., O., et. al., “Acety-L-carnitine slows decline in younger patients with alzheimer’s disease: A reanalysis of a double-bline placebo-controlled study using the trilinear approach,” Int. Jour. Of Psychogeriatry, 1998, 10: 193-203. 16. Birkmayer, G. D., NADA, The Energizing Coenzyme, Menuco, Co: New York, 1996.
Dr. George Redmon
Impairments deep within the cellular levels, have a profound affect on physical and muscular energy levels.