*Dietary Reference Intake not established.
Non-medicinal ingredients: : Microcrystalline cellulose. Capsule; hypromellose, sorbitol, silicon dioxide, water.
AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, soy, eggs, fish or shellfish.
Suggested Use
Take one capsule twice daily with food or as directed by a qualified health practitioner.
Main Applications
• Pain
• Inflammation
• Chronic degenerative joint arthritis
• Neuroprotection
Pregnancy / Nursing
Do not take.
Cautions
Do not take if you are taking blood thinners like warfarin or are pregnant or nursing.
| Pain is a protective mechanism; it lets us know that tissue damage is occurring or about to occur. Pain is perceived through nociceptors, which are naked nerve endings specific to the feeling of pain. There are three categories of pain receptors: mechanical, thermal and polymodal. Thermal receptors respond to high or low temperatures, mechanical receptors respond to pressure and polymodal receptors respond to several stimuli. The intensity of pain is influenced by our emotional and behavioral perception, a characteristic that is unique to pain and not seen with other sensations. This occurs because the brain has a way to suppress painful sensations. This analgesic system is based on the presence and activation of several receptors. Once molecules attach to analgesic receptors, the sensation of pain diminishes. The process is known as antinociception. |
| Allgesic contains decursinol, an extract from Angelica Gigas, a plant also known as Korean angelica. Decursinol was shown to reduce the sensation of pain in various animal models known to correspond with painful sensations in humans. Decursinol inhibits the pain associated with inflammation, increases the pain threshold, reduces the reflex action associated with pain and lessens the pain associated with inflammatory messengers. Supplementation with decursinol reduces pain because of the effect the herb has on the central nervous system. Decursinol influences noradrenergic, serotonergic, adenosine and histamine receptors, which are all important for the sensation of pain.
Inflammation is a response to injury; it is therefore not surprising that inflammation and pain are closely connected. Inflammation is driven by immune cells, which release pro-inflammatory cellular messengers such as nitric oxide, COX-2 and matrix-degrading enzymes, IL-1, IL-6, TNF-a, and TGF-ß. Macrophages are intrinsically linked to inflammation. In chronic inflammatory conditions such as rheumatoid arthritis, specific enzymes are released by macrophages and lead to the destruction of the surrounding tissues. In arthritis, this process inflicts serious damage to cartilaginous structures. This leads to weak and inflamed joints. In a study that assessed the usefulness of 14 plants and plant extracts with regards to inflammation, it was found that Angelica Gigantis Radix is the most potent at inhibiting the pro-inflammatory activity of macrophages. Further purification of the plant extract led to the identification of decursin as the agent responsible for the observed effect. In addition, treatment with decursinol did not affect substance P levels. Substance P is an important factor in the tolerance and withdrawal symptoms associated with some analgesics. Therefore, long-term use of decursinol is not associated with an increased tolerance, a significant benefit over other analgesics.
A clinical study using decursinol for pain management in patients suffering from chronic degenerative joint arthritis showed an impressive pain reduction in 67.5% of patients after treatment with decursinol for a period of two weeks. No significant changes in blood pressure, pulse rate, respiration rate, electrocardiogram and blood oxygen saturation were observed in the patients given the herbal extract.
Other studies demonstrated that decursinol is a powerful neuroprotective agent. Decursinol possesses acetylcholinesterase inhibitory activity. Several acetylcholinesterase inhibitors are approved for the treatment of Alzheimer's disease and appear to prevent the programmed cellular death of neurons through the reduction of glutamate toxicity. Acetylcholinesterase inhibitors also improve cognitive function by preventing the breakdown of acetylcholine, a neurotransmitter found in unusually low levels in Alzheimer's disease. In an animal model for Alzheimer's disease, decursinol prevented the memory loss associated with senile plaque formation.
Through its influence on nerve cells, decursinol offers relief for those who are in constant agony because their pain pathways are over stimulated. In addition, decursinol normalizes inflammatory pathways and exhibits powerful anti-inflammatory activity, one of the root causes of pain.
References:
Choi SS, Han KJ, Lee HK, Han EJ, Suh HW. Antinociceptive profiles of crude extract from roots of Angelica gigas NAKAI in various pain models. Biol Pharm Bull. 2003 Sep;26(9):1283-8.
Choi SS, Han KJ, Lee JK, Lee HK, Han EJ, Kim DH, Suh HW. Antinociceptive mechanisms of orally administered decursinol in the mouse. Life Sci. 2003 Jun 13;73(4):471-85.
Kim JH, Jeong JH, Jeon ST, Kim H, Ock J, Suk K, Kim SI, Song KS, Lee WH. Decursin inhibits induction of inflammatory mediators by blocking nuclear factor-kappaB activation in macrophages. Mol Pharmacol. 2006 Jun;69(6):1783-90.
Ohshiro T, Namatame I, Lee EW, Kawagishi H, Tomoda H. Molecular target of decursins in the inhibition of lipid droplet accumulation in macrophages. Biol Pharm Bull. 2006 May;29(5):981-4.
|
|
