The Supporting Nutrients

We include important nutrients that help the “4-Pillar” nutrients in our Mitochondria Energy Blend, Mito-Life, be even more effective. They include:

R-Alpha Lipoic Acid (RLA or R-ALA)

Mitochondria ATP energy production also produces a lot of antioxidants. ALA is becoming increasingly recognized as a ‘mitochondrial antioxidant.’  Now a more potent form of ALA (R-lipoic acid R-ALA) is available to health consumers. Research shows that (R)-lipoic acid is a more biologically active form of ALA that offers greater antioxidant benefits at lower doses. The R-enantiomer (R-ALA) mainly has anti-inflammatory activity, being stronger by a factor of 10!¹

Five Reasons – (in adding R-ALA to our formula):

1. 1. Its ability in the mitochondria is 10x stronger (see above) especially in protecting the inner mitochondrial membrane.
   2. Makes ACL more effective. Treatment with a combination of RLA and ALC significantly improved mitochondrial function and increased mitochondrial biogenesis (some support for PQQ) related transcription factors while the treatments with only LA or ALC alone showed little effect.²
   3. Helping create more mitochondria. RLA is the most stable and bioavailable form of lipoic acid. It reduces oxidative stress and repairs oxidative damage. In doing so, it helps prevent and even reverses mitochondrial decay, in effect helping create new mitochondria in the brain.³
   4. Recycling – It helps the body recycle vitamin C, A, and most important to us, CoQ10 (a 4-Pillar nutrient) in the mitochondria.
   5. The only form used – Only the ‘R’ form is used by the mitochondria and increases ATP systhesis.⁴

Acetyl-L-Carnitine (ALC)

ALC works together with CoQ10 in mitochondrial activity. It unites with fatty acids and helps carry them into the mitochondria so they can be used for energy and to the individual cells.^5-6

ALC exhibits a protective effect on mitochondrial through different mechanisms:

1. 1. By preventing the production of oxidants essential for the transport of acyl groups through the mitochondrial membrane, and their complete oxidation. (An increase of acyl groups into the cell inhibits the transfer of ATP produced in the mitochondria.)
   2. ALC up-regulates complex bc1 gene expression increasing the mitochondrial antioxidant defenses; facilitating either the repair of less damaged mitochondria or the degradation of the most damaged ones.⁷
   3. By enhancing the mitochondrial DNA transcription and stability of mRNA and protecting membrane integrity against lipid peroxidation and membrane breakdown.⁸

Researchers are even now saying it shows promise in the treatment of aging and (brain function) neurodegenerative pathologies likely due to effects of ALC through modulation of gene expression.⁹

For all these considerations, ALC has been considered a “mitochondrial nutrient” that helps reverse aging-related mitochondrial dysfunction.¹⁰ – (I’ll take anything I can get.)

We mentioned in the 4-Pillars article that we use NAD+ precursors instead of NAD+ directly. It is a safety issue choosing to let the body determine its NAD needs.

These are the nutrients the body needs to do so.

Niacin (Nicotinic Acid) – is the fastest, able to elevate NAD+ to peak liver levels in only 15 minutes.
L-Tryptophan – is the preferable long term base for NAD+ production in the liver, resulting in the highest hepatic NAD+ concentrations.
Nicotinamide – is slower acting than niacin, taking 8 hours to reach peak NAD+ levels in the liver.¹¹  However, it adds a wonderful slow continuous release of NAD+ booster to help the niacin levels stay high.
Resveratrol – Resveratrol has become a popular dietary supplement because of its ability to activate sirtuin proteins in our cells.¹² Even better, the activation of NMNAT1 by resveratrol also increased NAD+ levels by up to 5 fold.¹³

These support nutrients help bring the most effective, balanced and safe building of natural body energy.

Resources:

1. Ulrich H, Weischer CH, et al. Pharmaceutical composition containing R-alpha-Lipoic Acid or S-alpha-Lipoic Acid as active ingredient. US Patent 5,728,735,1998.
2. Shen W, Liu K, Tian C, Yang L, Li X, et al. R-alpha-Lipoic acid and acetyl-L: -carnitine complementarily promote mitochondrial biogenesis in murine 3T3-L1 adipocytes. Diabetologia. 2008;51:165–174. [PubMed]
3. http://www.lifeextension.com/magazine/2011/8/Lipoic-Acid-Reverses-Mitochondrial-Decay/Page-01 -or- http://www.lef.org/magazine/mag2011/aug2011_Lipoic-Acid-Reverses-Mitochondrial-Decay_01.
4. Tory Hagen, Russell Ingersoll, et al. (R)–Lipoic Acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate. FASEB 13:411-418, 1999.
5. http://lpi.oregonstate.edu/infocenter/othernuts/carnitine/
6. Weili Shen, 1 Jiejie Hao, 1 , 2 Chuan Tian, et al. A Combination of Nutriments Improves Mitochondrial Biogenesis and Function in Skeletal Muscle of Type 2 Diabetic Goto–Kakizaki Rat. PLoS One. 2008; 3(6): e2328.
7. G Traina, G Federighi, M Brunelli, R Scuri. Cytoprotective effect of acetyl-L-carnitine evidenced by analysis of gene expression in the rat brain. Mol Neurobiol 39(2), 101-106 (2009).

8. MA Virmani, V Caso, A Spadoni, S Rossi, F Russo, F Gaetani: The action of acetylL-carnitine on the neurotoxicity evoked by amyloid fragments and peroxide on primary rat cortical neurones. Ann N Y Acad Sci 939, 162-178 (2001).
9. Giovanna Traina. The neurobiology of acetyl-L-carnitine. Frontiers in Bioscience, Landmark, 21, 1314-1329, June 1, 2016.
10. EJ Lesnefsky: Reversal of mitochondrial defects before ischemia protects the aged heart. FASEB J 20, 1543-1545 (2006).

11. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. (Trammell, 2016a).
12. Higashida K, Kim SH, Jung SR, et al. Effects of resveratrol and SIRT1 on PGC-1alpha activity and mitochondrial biogenesis: a reevaluation. PLoS Biol. 2013;11(7):e1001603.
13. Ross S. Grant, Resveratrol Increases Intracellular NAD+ Levels Through Up regulation of The NAD+ Synthetic Enzyme Nicotinamide Mononucleotide Adenylyltransferase. U. of New South Wales, Pharmacology, 05 May 2010.