| But "radicalized" antioxidants can do long-term harm if they aren't properly dealt with. The most well studied example of this phenomenon is tocopherol-mediated peroxidation, or TMP, in which vitamin E family members block an incoming free radical from attacking a particle of LDL ("bad") cholesterol, but the "radicalized" antioxidant then initiates a slower, more insidious pattern of lipid peroxidation. Several studies suggest that TMP may play a devastating role in the long-term development of atherosclerosis.
The potential for slow-acting pathology from "radicalized" antioxidants can be prevented through taking advantage of the unique synergistic interactions of an elite antioxidant strike force: the Networking Antioxidants.
When taken together, these specific, biologically essential nutrients form a dynamic team of synergistic "co antioxidants." Networking antioxidants can "recycle" one another from their "radicalized" forms back into their active, antioxidant forms. By this process of mutual regeneration, networking antioxidants enhance and extend one another's capacities, fueled by the fires of life in the body's cellular "power plants" (mitochondria). There are exactly five networking antioxidants: R (+)-lipoic acid, the vitamin E complex (including the four tocopherols and four tocotrienols), vitamin C, coenzyme Q10, and glutathione (GSH).
The cycle is ultimately kept going thanks to role played by R (+)-lipoic acid in the body's energy-production cycle. As food energy is converted into cellular energy by your cellular "power plants" (the mitochondria), supplemental R (+)-lipoic acid is "charged up" into its more potent antioxidant form, dihydrolipoic acid (DHLA). It is DHLA, rather than R (+)-lipoic acid itself, that "recycles" other networking antioxidants. And so, because the "charging-up" of R (+)-lipoic acid to DHLA piggybacks on the ongoing process of energy production, the mitochondria fuel a renewing cycle of co-regeneration amongst the networking antioxidants.
The "bird's eye view" of the antioxidant network recycling process looks like this. First, the original free radical attacker is neutralized by a networking antioxidant. Unfortunately, the result is that the networking antioxidant is degraded into its free radical form. To save the body from disaster, the networking antioxidant is rejuvenated by a co antioxidant from the antioxidant network team. A game of electron donating "hot potato" ensues, which ultimately results in rejuvenation by DHLA of the networking antioxidant free radical. And at this point, the "hot potato" game is halted when DHLA is restored through R (+)-lipoic acid's cycling through the mitochondrial energy-production process.
For the Antioxidant network to work optimally, it's critical to ensure that your lipoic acid supplement is in the form of R (+)-lipoic acid. Supplements labeled "alpha-lipoic acid" or simply "lipoic acid" contain up to 50% S (-)-lipoic acid, an unnatural molecule that hinders the ability of mitochondria to "charge up" R (+)-lipoic acid into DHLA. As a result, the S (-)-lipoic acid in conventional "lipoic acid" supplements actually interferes with the recycling activity of the Networking antioxidants.
The networking antioxidants have a genuine synergy with one another. The effects of each networking antioxidant support greater functionality of the antioxidant network as a whole. No other antioxidants participate in the interlocking cycles of the antioxidant network. In fact, the ability of other antioxidants to play a protective role in the body depends on having a functional Antioxidant network - but not vice-versa.
However, a few antioxidants do play a supporting role to networking antioxidants, without fully participating in the antioxidant network recycling system. The best understood of these Network "boosters" are bioflavonoids and the mineral selenium. Among bioflavonoids, carnosic acid - which is found in the herb rosemary - is especially interesting because of its ability to repeatedly rearrange itself into a "cascade" of new antioxidant "booster" forms before being exhausted. Selenium supports the network by maintaining the body's supply of two key enzymes: glutathione peroxidase (GSH-Px) and thioredoxin reductase (TrxR). Only very low doses of selenium are needed to maximize the levels and activity of these enzymes.
You'll want to ensure that you're taking the complete team of networking antioxidants, plus carnosic acid, resveratrol, and Se-methylselenocysteine, as proven "boosters" of the Network itself.
The days of throwaway "kitchen sink" antioxidant mishmashes are over. The recycling system of the Antioxidant Network is the path to cellular sustainability.
References
i. Packer L, Weber SU, Rimbach G. "Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling." J Nutr. 2001 Feb; 131(2): 369S-73S.
ii. Upston JM, Terentis AC, Stocker R. "Tocopherol-mediated peroxidation of lipoproteins: implications for vitamin E as a potential antiatherogenic supplement." FASEB J. 1999 Jun; 13(9): 977-94.
iii. Sen CK, Packer L. "Thiol homeostasis and supplements in physical exercise." Am J Clin Nutr. 2000 Aug; 72(2 Suppl): 653S-69S.
iv. Biewenga GP, Haenen GR, Bast A. "The pharmacology of the antioxidant lipoic acid." Gen Pharmacol. 1997 Sep; 29(3): 315-31.
v. Packer L, Kraemer K, Rimbach G. "Molecular aspects of lipoic acid in the prevention of diabetes complications." Nutrition. 2001 Oct; 17(10): 888-95.
vi. Nordberg J, Arner ES. "Reactive oxygen species, antioxidants, and the mammalian thioredoxin system." Free Radic Biol Med. 2001 Dec 1; 31(11): 1287-312.
|
