(Adult): Take 1 capsule four times daily with food, or as directed by a qualified health care practitioner.
Your Premium All-In-One Antioxidant Formula
Antioxidants are nutrients found in all types of fruits and vegetables, plants, nuts and seeds. They help to protect the body from the damage caused by free radicals or oxidants - the toxic molecules that play a role in the development of diseases from cataracts to heart disease, from arthritis to abnormal cell development.
Antioxidants neutralize free radicals before they can damage cells. They do this by stabilizing the free radical, but in the process, they themselves become unstable mild free radicals and must be “recycled” back to their original form.
Antioxidant Synergy is based on the interactions between specific antioxidants in the body known as the “networking antioxidants”. This “antioxidant network” includes R-lipoic acid, vitamin E, vitamin C, coenzyme Q10 and N-acetyl-cysteine, with added support from selenium, resveratrol and rosemary extract. The networking antioxidants have a cumulative effect when working together. In fact, the ability of other antioxidants to play a protective role in the body depends on first having a functional antioxidant network. Networking antioxidants "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 to have a better preventative effect on chronic diseases and aging.
AOR’s Antioxidant Synergy offers the most powerful combination of antioxidants to reduce inflammation and cellular damage that contribute to aging, infertility, heart disease and many other chronic health conditions.
Antioxidant Synergy provides a research-backed combination of synergistic antioxidants for the maintenance of good health.
|Amount Per Serving Amount: 4 Capsules|
|200 mg R(α) lipoic acid (sodium salt)*|
Vitamin E Complex
|420 mg Vitamin C (magnesium ascorbate, ascorbyl palmitate)|
|30 mg Coenzyme Q10|
|50 mg N-Acetyl-L-Cysteine (NAC)|
|50 mcg Selenium (Selenomethionine)|
|5 mg trans-Resveratrol|
|*Contains 20 mg sodium per serving. †Tocopherols: <61 mg alpha, >4 mg beta, >204 mg gamma, >44 mg delta. ‡Tocotrienols: >14 mg alpha, 2 mg beta, >25 mg gamma, >7 mg delta.|
|Non-medicinal ingredients: rosemary extract (5 mg), silicon dioxide, sodium alginate, gum Arabic, maltodextrin, pea starch, sorbitan stearate, dicalcium phosphate, palm oil, hydroxypropyl cellulose. Capsule: hypromellose.|
AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, nuts, peanuts, sesame seeds, sulphites, mustard, dairy, eggs, fish, shellfish or any animal byproduct.
(Adult): Take 1 capsule four times daily with food, or as directed by a qualified health care practitioner.
Do not use if you are pregnant or breastfeeding. Consult a health care practitioner prior to use if you have diabetes, cystinuria, heart disease or cancer, or if you are taking blood pressure medication, blood thinners, nitroglycerin or antibiotics. Consult a health care practitioner for use beyond 6 weeks. If you experience sweating, paleness, chills, headaches, dizziness and/or confusion, discontinue use and consult a health care practitioner as these may be symptoms of serious low blood sugar.
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.
Problems with Antioxidants
Did you know that once many antioxidants have quenched a free radical, they actually become mild free radicals themselves? Do not be concerned! This is a natural and quite important part of the oxidation-reduction signaling process. However, when some antioxidants are consumed in excess, they can actually cause more damage than good! 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. So then yet other antioxidants are required to quench this process. But some antioxidants are more effective in certain locations in the body than others, meaning that you need to take the right antioxidants to halt this vicious cycle of antioxidants turning pro-oxidant! How can this vicious cycle be stopped?
The One & Only Antioxidant Network
The vicious cycle of oxidation 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, working within and around the mitochondria where most of the oxidation occurs. 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 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.
How Does the Network Function?
First, the original free radical is neutralized by a networking antioxidant. Unfortunately, the result is that the networking antioxidant is degraded into its free radical form. That antioxidant is rejuvenated by another co-antioxidant from the network team. A game of electron donating “hot potato” ensues, which ultimately results in rejuvenation of the last networking antioxidant free radical by dihydrolipoic acid (DHLA, the charged form of R-lipoic acid). And at this point, the “hot potato” game is halted when R-lipoic acid is cycled through the mitochondrial energy-production process.
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. Resveratrol, found in grapes and wine, is a gene-activator in the mitochondria that helps reduce free-radical production in the first place.
The antioxidant network showing the interaction between vitamin E, ubiquiol, vitamin C, glutathione and R-lipoic acid redox cycles. (Packer L, Kraemer K, Rimbach G. “Molecular aspects of lipoic acid in the prevention of diabetes complications.” Nutrition. 2001 Oct; 17(10): 888-95.)
Thiol redox cycles play central roles in the antioxidant defense network. Both glutathione and lipoate redox cycles can be driven by cellular-reducing equivalents to generate their respective reduced forms (GSH and DHLA). The ability of lipoate to increase cell GSH is mediated by the reduction of cystine to the GSH precursor cysteine by dihydrolipoate. LA, lipoate; GSSG, oxidized glutathione; vit, vitamin. (Sen CK & Packer L. “Thiol homeostasis and supplements in physical exercise.” Am J Clin Nutr. 2000 Aug; 72(2 Suppl): 653S-69S.)
Some antioxidants have gained phenomenal reputations and hold a lot of market traction, such as Vitamins C & E and CoQ10. Others like resveratrol have benefited from “fountain-of-youth” hype. While these are noteworthy antioxidants, it may be more beneficial to take a scientifically-proven combination of antioxidants rather than dosing with large amounts of any single one.
AOR’s Antioxidant Synergy provides a scientifically-backed combination of antioxidants, not just a mish-mash of the most popular ones on the market. Get the most out of your antioxidant regime with Antioxidant Synergy!
Biewenga GP, Haenen GR, Bast A. “The pharmacology of the antioxidant lipoic acid.” Gen Pharmacol. 1997 Sep; 29(3): 315-31.
Nordberg J, Arner ES. “Reactive oxygen species, antioxidants, and the mammalian thioredoxin system.” Free Radic Biol Med. 2001 Dec 1; 31(11): 1287-312.
Packer L, Kraemer K, Rimbach G. “Molecular aspects of lipoic acid in the prevention of diabetes complications.” Nutrition. 2001 Oct; 17(10): 888-95.
Packer L, Weber SU, Rimbach G. “Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling.” J Nutr. 2001 Feb; 131(2): 369S-73S.
Sen CK, Packer L. “Thiol homeostasis and supplements in physical exercise.” Am J Clin Nutr. 2000 Aug; 72(2 Suppl): 653S-69S.
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.
Resveratrol improves insulin resistance of catch-up growth by increasing mitochondrial complexes and antioxidant function in skeletal muscle.
Metabolism. 2012 Jul;61(7):954-65.
Zheng J, Chen LL, Zhang HH, Hu X, Kong W, Hu D.
Caloric restriction followed by refeeding, a phenomenon known as catch-up growth (CUG), affects mitochondrial function and results in systemic insulin resistance (IR). We investigated the potential of resveratrol (RES) in CUG to prevent IR by increasing activity of the mitochondrial respiratory chain and antioxidant enzymes in skeletal muscle. Rats (8 weeks of age) were divided into 3 groups: normal chow, CUG, and CUG with RES intervention. Skeletal muscle and systemic IR were measured in each group after 4 and 8 weeks. Mitochondrial biogenesis and function, oxidative stress levels, and antioxidant enzyme activity in skeletal muscle were assessed. Catch-up growth-induced IR resulted in significant reductions in both average glucose infusion rate(60-120) at euglycemia and skeletal muscle glucose uptake. Mitochondrial citrate synthase activity was lower; and the activity of complexes I to IV in the intermyofibrillar and subsarcolemmal (SS) mitochondria were reduced by 20% to 40%, with the decrease being more pronounced in the SS fraction. Reactive oxygen species levels were significantly higher in intermyofibrillar and SS mitochondria, whereas activities of antioxidant enzymes were decreased. Oral administration of RES, however, increased silent information regulator 1 activity and improved mitochondrial number and insulin sensitivity. Resveratrol treatment decreased levels of reactive oxygen species and restored activities of antioxidant enzymes. This study demonstrates that RES protects insulin sensitivity of skeletal muscle by improving activities of mitochondrial complexes and antioxidant defense status in CUG rats. Thus, RES has therapeutic potential for preventing CUG-related metabolic disorders.
Heart disease and single-vitamin supplementation.
Am J Clin Nutr 85(suppl): 293S-9S.
Maret G Traber (2007).
Heart disease is the number one cause of death in the United States and has long been recognized to be multifactorial. A growing body of evidence suggests that not only free radical–mediated reactions but also inflammatory responses play major roles in atherogenesis. Vitamin E has both antioxidant and anti-inflammatory properties and is the most widely studied vitamin in clinical trials and thus will be the primary example used in this review. Clinical trials of vitamin E efficacy, in hindsight, have been overly optimistic in their expectation that a vitamin could reverse poor dietary habits and a sedentary lifestyle as well as provide benefit beyond that of pharmaceutical agents in treating heart disease. However, it is also apparent that most Americans do not consume dietary amounts adequate to meet established vitamin E requirements. In response to oxidative stressors, vitamin E can decrease biomarkers of lipid peroxidation, is itself killed, and requires optimal vitamin C status to function most effectively. Thus, adequate vitamin E intakes are clearly needed, but what is adequate for what function has yet to be defined. It is noteworthy that in most trials, biomarkers were not used nor were oxidative stress and lipid peroxidation markers used or plasma vitamin E concentrations measured.
A quantitative approach to the free radical interaction between alpha-tocopherol and the coantioxidants eugenol, resveratrol or ascorbate.
In Vivo. 2006 Jan-Feb;20(1):61-7.
Kadoma Y, Ishihara M, Fujisawa S.
The regeneration of alpha-tocopherol (vitamin E; VE) by coantioxidants such as phenolics and ascorbate has been studied in homogeneous hydrocarbon solution and in biological systems. However, VE phenoxyl radicals (VE*) may be sufficiently reactive to cooxidize phenolic compounds and ascorbates. The coantioxidant behavior of some relevant phenols such as eugenol (EUG), isoeugenol (IsoEUG), 2,6-di-tert-butyl-4-methoxyphenol (DTBMP), trans-resveratrol (RES) and L-ascorbyl-2,6-dibutyrate (ASDB; an ascorbate derivative) with the antioxidant VE at a molar ratio of 1:1 was investigated by the induction period (IP) method in the kinetics of polymerization of methyl methacrylate (MMA) initiated by the thermal decomposition of 2,2′-azobis(isobutyronitrile) (AIBN; a source of alkyl radicals, R*) or benzoyl peroxide (BPO; a source of peroxy radicals, PhCOO*) under nearly anaerobic conditions. Synergism, implying regeneration of VE by the coantioxidant, was observed with only two of these combinations, VE/EUG with PhCOO* and VE/DTBMP with R*. For other mixtures of VE with a phenolic coantioxidant, VE was able to cooxidize the phenolic. Regeneration can only be observed if the bond dissociation energy (BDE) of the coantioxidant is lower than, or at least close to, that of VE. The driving force for regeneration of VE by EUG may be removal of the semiquinone radical of EUG by VE, leading to the formation of VE and EUG-quinonemethide, even though the BDE value of EUG is greater by 5.8 kcal/mol than that of VE. Further evidence for this mechanism of regeneration is provided by the value of approximately 2 for the stoichiometric factor (n) of EUG induced by PhCOO*, but not by R*, again implying the formation of EUG-quinonemethide. The regeneration of VE by DTBMP in the R* system may result from their much smaller difference in BDE (0.1-1.3 kcal/mol). Since VE is rapidly oxidized by PhCOO*, regeneration of VE by DTBMP was not found in this system. The observed IP for the VE/ASDB mixture in the R* system was much lower than that for VE alone, whereas the IP for VE/ASDB in the PhCOO* system was similar to that of VE. In the R* system, VE* was sufficiently reactive to cooxidize ASDB and, in addition, the prooxidation of VE may be promoted by the catalytic action of the ascorbate derivative. The present system, under nearly anaerobic conditions, is relatively biomimetic, since oxygen in living cells is sparse. Such studies could help to explain the mechanism of regeneration of VE by coantioxidants such as phenolic compounds and vitamin C in vivo.
Reactive oxygen species, antioxidants, and the mammalian thioredoxin system.
Free Radic Biol Med 2001 Dec 1; 31(11): 1287-312.
Nordberg J, Arner ES.
Reactive oxygen species (ROS) are known mediators of intracellular signaling cascades. Excessive production of ROS may, however, lead to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis. A balance between oxidant and antioxidant intracellular systems is hence vital for cell function, regulation, and adaptation to diverse growth conditions. Thioredoxin reductase (TrxR) in conjunction with thioredoxin (Trx) is a ubiquitous oxidoreductase system with antioxidant and redox regulatory roles. In mammals, extracellular forms of Trx also have cytokine-like effects. Mammalian TrxR has a highly reactive active site selenocysteine residue resulting in a profound reductive capacity, reducing several substrates in addition to Trx. Due to the reactivity of TrxR, the enzyme is inhibited by many clinically used electrophilic compounds including nitrosoureas, aurothioglucose, platinum compounds, and retinoic acid derivatives. The properties of TrxR in combination with the functions of Trx position this system at the core of cellular thiol redox control and antioxidant defense. In this review, we focus on the reactions of the Trx system with ROS molecules and different cellular antioxidant enzymes. We summarize the TrxR-catalyzed regeneration of several antioxidant compounds, including ascorbic acid (vitamin C), selenium-containing substances, lipoic acid, and ubiquinone (Q10). We also discuss the general cellular effects of TrxR inhibition. Dinitrohalobenzenes constitute a unique class of immunostimulatory TrxR inhibitors and we consider the immunomodulatory effects of dinitrohalobenzene compounds in view of their reactions with the Trx system.
Thiol homeostasis and supplements in physical exercise.
Am J Clin Nutr 2000 Aug; 72(2 Suppl): 653S-69S.
Sen CK, Packer L.
Thiols are a class of organic sulfur derivatives (mercaptans) characterized by the presence of sulfhydryl residues. In biological systems, thiols have numerous functions, including a central role in coordinating the antioxidant defense network. Physical exercise may induce oxidative stress. In humans, a consistent marker of exercise-induced oxidative stress is blood glutathione oxidation.Physical training programs have specific effects on tissue glutathione metabolism that depend on the work program and the type of tissue. Experimental studies show that glutathione metabolism in several tissues sensitively responds to an exhaustive bout of exercise. Study of glutathione-deficient animals clearly indicates the central importance of having adequate tissue glutathione to protect against exercise-induced oxidative stress. Among the various thiol supplements studied, N-acetyl-L-cysteine and alpha-lipoic acid hold the most promise. These agents may have antioxidant effects at the biochemical level but are also known to influence redox-sensitive cell signaling.
Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling.
J Nutr 2001 Feb; 131(2): 369S-73S.
Packer L, Weber SU, Rimbach G.
Vitamin E, the most important lipid-soluble antioxidant, was discovered at the University of California at Berkeley in 1922 in the laboratory of Herbert M. Evans (Science 1922, 55: 650). At least eight vitamin E isoforms with biological activity have been isolated from plant sources. Since its discovery, mainly antioxidant and recently also cell signaling aspects of tocopherols and tocotrienols have been studied. Tocopherols and tocotrienols are part of an interlinking set of antioxidant cycles, which has been termed the antioxidant network. Although the antioxidant activity of tocotrienols is higher than that of tocopherols, tocotrienols have a lower bioavailability after oral ingestion. Tocotrienols penetrate rapidly through skin and efficiently combat oxidative stress induced by UV or ozone. Tocotrienols have beneficial effects in cardiovascular diseases both by inhibiting LDL oxidation and by down-regulating 3-hydroxyl-3-methylglutaryl-coenzyme A (HMG CoA) reductase, a key enzyme of the mevalonate pathway. Important novel antiproliferative and neuroprotective effects of tocotrienols, which may be independent of their antioxidant activity, have also been described.
The pharmacology of the antioxidant lipoic acid.
Gen Pharmacol 1997 Sep; 29(3): 315-31.
Biewenga GP, Haenen GR, Bast A.
1. Lipoic acid is an example of an existing drug whose therapeutic effect has been related to its antioxidant activity.
2. Antioxidant activity is a relative concept: it depends on the kind of oxidative stress and the kind of oxidizable substrate (e.g., DNA, lipid, protein).
3. In vitro, the final antioxidant activity of lipoic acid is determined by its concentration and by its antioxidant properties. Four antioxidant properties of lipoic acid have been studied: its metal chelating capacity, its ability to scavenge reactive oxygen species (ROS), its ability to regenerate endogenous antioxidants and its ability to repair oxidative damage.
4. Dihydrolipoic acid (DHLA), formed by reduction of lipoic acid, has more antioxidant properties than does lipoic acid. Both DHLA and lipoic acid have metal-chelating capacity and scavenge ROS, whereas only DHLA is able to regenerate endogenous antioxidants and to repair oxidative damage.
5. As a metal chelator, lipoic acid was shown to provide antioxidant activity by chelating Fe2 and Cu2 ; DHLA can do so by chelating Cd2 .
6. As scavengers of ROS, lipoic acid and DHLA display antioxidant activity in most experiments, whereas, in particular cases, pro-oxidant activity has been observed. However, lipoic acid can act as an antioxidant against the pro-oxidant activity produced by DHLA.
7. DHLA has the capacity to regenerate the endogenous antioxidants vitamin E, vitamin C and glutathione.
8. DHLA can provide peptide methionine sulfoxide reductase with reducing equivalents. This enhances the repair of oxidatively damaged proteins such as alpha-1 antiprotease.
9. Through the lipoamide dehydrogenase-dependent reduction of lipoic acid, the cell can draw on its NADH pool for antioxidant activity additionally to its NADPH pool, which is usually consumed during oxidative stress.
10. Within drug-related antioxidant pharmacology, lipoic acid is a model compound that enhances understanding of the mode of action of antioxidants in drug therapy.