Nutrition & Anti-Oxidant Accelerator- 60 caps - Conners Clinic
Nutrition & Anti-Oxidant Accelerator- 60 caps - Conners Clinic
Nutrition & Anti-Oxidant Accelerator- 60 caps - Conners Clinic
Nutrition & Anti-Oxidant Accelerator- 60 caps

Nutrition & Anti-Oxidant Accelerator- 60 caps

Vendor
Prof Health Products
Regular price
$56.00
Sale price
$56.00
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This product may be termed as one of the, 'multiples for your genes' as it helps support several pathways.

Ingredients:

  • Zinc
  • Copper
  • Manganese
  • Selenomethionine
  • Apple Polyphenols
  • Bee Pollen
  • Kale
  • Liver
  • Organic Turkey Tail Mushrooms
  • Catalase
  • Superoxide Dismutase
  • Marine Phytoplankton

Potential Benefits:

  • provides food-based ingredients for complete vitamin, mineral, amino acid, and antioxidants
  • provides SOD and Catalase
  • Supports SOD production

Description

Oxidative Stress and Antioxidants Normal metabolism, and exposure to toxins and stress, leaves a residue of free radicals – reactive atoms with one or more unpaired electrons. The reactive nature of free radicals gives rise to potentially harmful interactions with sensitive cellular proteins, lipids and DNA. These interactions, called oxidative stress, occur when free radicals overwhelm the antioxidant defenses, causing an imbalance favoring oxidants. The result is disruption of a delicate cellular redox signaling matrix, and molecular damage known to underly many diseases. Normally, oxidative stress is controlled by small-molecule, low-molecular-weight, nonenzyme antioxi- dants such as vitamins A, C and E, carotenoids, polyphenols, and glutathione, and especially by antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase.

These control mechanisms operate in plants and animals alike, acting to check cell degradation and death, which appears in the case of plants like spoilage or progressive rotting.

Free Radical Theory

For many years, free radicals and oxidative stress were held to be a prime cause of chronic disease and premature aging. This was known, and widely embraced, as the free radical theory of aging.

It was thought that liberal supplementation with antioxidant compounds would quench the reactive free radicals, mitigate oxidative stress, and prevent many diseases, perhaps even slow the aging process. Research in recent years, including the failure of several high-profile antioxidant supplement trials, has forced a revision of the theory. Although the reaction has been excessive and unfair, legitimate questions have been raised regarding the wisdom of supplementing with high doses of isolated antioxidant compounds.

Free radicals have beneficial as well as harmful roles, and not all oxidation caused by free radicals leads to harmful oxidative stress. Although the evidence is overwhelming that uncontrolled oxidative stress is pathogenic, and that consumption of diets rich in antioxidant nutrients and phytochemicals is beneficial, there also exists oxidative "stress" that is physiologic and desirable. Mitochondrial oxidations, for example, are vital for energy production and all cellular functions, and oxidations in white blood cells are vital for destruction of invasive microbes.

The situation was summed eloquently by Levonen and colleagues: "the idea that free radicals are bad and antioxidants are good' is clearly undergoing a critical and high-profile reappraisal.... the oxidative stress hypothesis has reached the limits of its utility and should be replaced with the 'redox biology paradigm' in which antioxidants play the primary role of modulating the complex networks controlling cell signaling and metabolism."

In this view, antioxidants serve as regulators of cellular redox networks – the complex of signaling pathways that control cell function, including free radicals in their beneficial roles – rather than exclusively protecting against the free radical "bad actors".

Embracing the New Paradigm In adopting this new paradigm, it is important still to retain the lessons of the preceeding several decades of research, which showed beyond question that uncontrolled oxidative stress damages fragile lipid and other molecules, promotes inflammation, is generally pathogenic, and speeds the aging process. There remains a massive literature linking oxidative stress with most degener- ative diseases including cancer, atherosclerosis, cognitive impairment and Alzheimer's disease, cataracts, macular degeneration and many others. Whole books are still written on this subject.[5]

The old paradigm had value, but led to foolishly-de- signed trials using very high doses of isolated small-molecule antioxidants, with the expectation that this would cure or mitigate major diseases. These expectations were unwise. Although such supplementation might have been effective in Controlling inappropriate oxidative stress, it may also have depressed essential oxidations such as those required for synthesis of prostaglandins or for mitochondrial energy production.

Whatever the mechanism, the bottom line was that too much of a good thing led to typically null results, and in a very few cases bad results. The new paradigm modifies but does not overthrow the old. There is room for both, and the new paradigm encourages not abandonment of antioxidants, but more mature and wise use of them: in combination, in lower doses, and with an emphasis on activating defensive enzymes rather than direct scavenging of free radicals.