Many, if not most ailments of the body cause pain. Pain is a protective mechanism for the body; it occurs when tissues are being damaged and it causes the individual to react and remove the pain stimulus. The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin and also certain internal tissues such as the arterial walls and the joint surfaces. Of the three types of stimuli that excite pain (mechanical, thermal and chemical), the chemical substances are especially important in stimulating the slow, suffering type of pain that occurs following tissue injury. Some of the chemicals that excite the pain receptors are bradykinin, seretonin, histamine, potassium ions, proteolytic enzymes and prostaglandins. In addition prostaglandins enhance the sensitivity of the pain endings.
In contrast to most other sensory receptors in the body, the pain receptors adapt very little or sometimes not at all. In fact, under some conditions excitement of the pain receptors becomes progressively greater as the pain stimuli continue. This increase in the pain sensitivity of the pain receptors is called hyperalgesia. One can readily understand the importance of this failure of pain receptors to adapt for it allows them to keep the individual apprised of a damaging stimulus that causes the pain as long as it persists.
All pain whether chronic or acute, physical or emotional is recognized, interpreted and acted upon by the brain. Sensory neurons located throughout the body react to physical stimuli (pressure, heat, trauma, cold etc.), as well as chemical stimuli (histamine, prostagladins or similar chemical messengers excreted by the body in response to pain and/or inflammation). In response the sensory neuron transmits (“fires”) a message to the brain where the information is rapidly translated and a reactive response formulated.
Pain has two personalities, central pain and pain caused by inflammation. Inflammation is a defensive reaction to injury and arises from the resultant cell damage. Agencies and means of provoking the response include mechanical trauma (injury), radiation (i.e. UV or sunburn), direct chemical damage (caustic chemicals), biochemical damage (metabolic inhibitors), invading organisms (bacteria) and antigen – antibody reactions (allergies). The classical signs of inflammatory reaction are almost invariably listed in the following order; warmth (calor), reddening (rubor), pain (dolor), swelling (tumor) and loss of function (functio laesa).
As a rule of thumb the treatment of acute pain does not present as complex a situation as chronic pain the reason being that acute pain is often clear and the origin easily established. On the other hand the etiology of chronic pain is less clear and might be near impossible to establish. Medication for pain is practically found in every medicine chest and it is commonly taken without regard for their possible side effects.
A natural way to fight pain is to increase the endorphins (the body’s natural painkiller) in the brain. Endorphins are part of the body’s natural painkiller network; they are potent painkillers that can also alter mood. Endorphins block the pain impulse by interfering with pain messages traveling through the nervous system to the brain. Unfortunately the endorphins cannot be synthesized outside of the body and taken as pain medication the effects might be potentially dangerous, costly, or impractical. Fortunately endorphins do not have to be taken in order to benefit from their pain killing effects. Instead individuals can use substances that protect or boost the natural endorphins of the body allowing their levels to rise to higher, more potent concentrations.
Secondly, if one considers pain management strategies, eradication of the underlying cause of the pain seems essential. If inflammation is the direct cause of pain, whether from an injury or a degenerative disease such as rheumatoid arthritis, it seems logical that the inflammation should be addressed functionally through immobilization and by antagonizing the chemical messengers (such as histamine and prostaglandins) that are responsible for the inflammatory response and subsequent pain.
DL-phenylalanine is an essential amino acid that is able to cross the blood brain barrier. Because of it’s ability to cross the blood brain barrier DL-phenylalanine can have a direct effect on brain chemistry. Because of it’s central nervous system actions, DL-phenylalanine reduces pain by blocking the breakdown of endorphins (natural painkillers) in the body.2
White Willow Bark is the original source of salacin – the modern day aspirin. Down through the ages, well before the discovery of salacin, White Willow Bark was used to combat pain of many different sorts including rheumatism, headaches, fever, arthritis, gout and it was used to combat fever and inflammation. The mechanism of action for White Willow Bark is similar to the group of drugs named the Non Steroidal Anti-inflammatories (NSAID’s) which function through the inhibition of the enzymes responsible for the synthesis of prostaglandins. Used in the bark form, other decomposition forms of salacin result in enhanced analgesic, antipyretic and anti-inflammatory properties.3
Pine Bark and Grape Seed extracts contain the flavonoids, oligometric proanthocyanadins (OPC’s) which, in addition to antioxidant protection against heart disease and cancer, also give protection against inflammation and alleviation of the symptoms of inflammation. OPC’s appear to inhibit the chemical mediators of the inflammatory response in a similar fashion as the NSAID’s, thus, through the inhibition of the enzymes responsible for the synthesis of prostaglandin. They decrease tissue inflammation as a result of their inhibition of the enzymes lipoxygenase and cyclooxygenase thus preventing the synthesis of the body’s chemical pain and inflammatory mediators prostaglandins, kinins, histamine, leukotrines and seretonin. Additionally, they decrease allergic reactivity by inhibiting mast cell and basophile degranulation and inhibition of histidine decarboxylase thereby depleting histamine.4
The OPC’s have also been shown to be highly effective free radical scavengers causing a cessation of free radical chain reactions as well as repair of free radical-induced tissue damage. The proanthocyanadin bioflavanoids potentiate and regenerate the antioxidant, antithrombotic, anti-inflammatory and antineoplastic effects of vitamin C and vitamin E. They repair and maintain collagen and elastin fibre structure resulting in the strengthening of the vasculature. As a result an individual will experience reduced capillary fragility, increased venous sufficiency, a resolution of vague swellings, a diminished risk of phlebitis, expedient healing of chronic dermatoses and protection from skin injury from the sun.5
References:
1. Berkow R MD. Editor-in-Chief, et all. The Merck Manual of Diagnosis and Therapy. Published by Merck Research Laboratories, 1992; p.1407 – 1420.
2. Bud K. Use of DL-phenylalanine, an enkephalinase inhibitor, in the treatment of intractable pain. Adv. Pain Res. Ther. 1983; 5: 305 – 308.
3. Bowman WC, Rand MJ. Textbook of pharmacology – 2ND Edition. Blackwell Scientific Publications; p. 16.17 – 16.18.
4. Facino RM, et all. Free radicals scavenging action and anti-enzyme activities of Proanthocyanadins from Vitis vinifera. Arzneim Forsch, 1994; 44: 592 – 601.
5. Schwitters B, Masquelier J. OPC’s in practice: Bioflavanols and their applications. Rome: Alfa Omega, 1993.
6. Brady LR, Tyler VE, Robbers JE. Harpagophytum procumbens. In: Pharmacognosy, 8TH Edition. Philladelphia: Lea & Febiger, 1981, 480.
7. Yoshimoto T, et all. Flavonoids: Potent inhibitors of Arachidonate 5-Lipoxygenase. Biochem. Biophys. Res. Comm. 1983; 116:
OPCXtra – Isotonic OPC