by VRP Staff
Pain is clearly one of the most common health problems of our time. However, both clinical practice and research indicate that pain is something that can be conquered.
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Anyone who has experienced a painful injury is all too familiar with its consequences, especially the accompanying unpleasant sensation and loss of mobility. Pain is not a disease, but a symptom of an underlying imbalance. It is defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." Simply stated, pain is a warning mechanism.
Pain is the most frequent reason for physician consultations in the United States, and results in half of all Americans to seek medical care annually. Chronic pain is the third most common healthcare problem and impacts productivity, mobility, and quality of life. More than one-third of the estimated 75 to 85 million persons in the United States who report chronic pain are partially or totally disabled.
Arthritis, a common cause of chronic pain and activity limitation, also is characterized by localized pain and swelling. Approximately 46.9 million adults in the U.S. have been diagnosed with arthritis. The prevalence of arthritis is increasing, and it is estimated that by the year 2030, 67 million adult Americans will be afflicted with this condition.
The most common chronic pain condition is back and neck pain. According to the National Pain Foundation, approximately 85% of Americans will experience back pain by age 50, and more than 26 million Americans between the ages of 20 and 64 experience frequent back pain.
People differ remarkably in their ability to tolerate pain. Tolerance levels can vary depending on several factors including mood, personality, and circumstance. Despite its subjective nature, most pain is associated with tissue damage and has a physiological basis.
Pain is categorized as acute or chronic. Acute pain begins suddenly and is short in duration, while chronic pain can last for weeks to years. Chronic pain typically lasts for at least one month longer than expected based on the illness or injury, recurs on and off for months or years, or is associated with a chronic disease or injury that does not heal. Chronic pain may result in depression, loss of interest in activities, sleep problems, decreased energy, decreased appetite, weight loss, and decreased sex drive. Chronic pain can make the nervous system more sensitive to pain by repeatedly stimulating the nerve fibers and cells that detect, send, and receive pain signals. Repeated stimulation can cause changes in the structure of nerve fibers or make them more active resulting in increased pain transmission to the spinal cord and brain.
The Physiology of Pain
Pain receptors are located almost everywhere in the body, especially the skin, surfaces of the joints, the lining around the bone, and walls of the arteries. Pain from various sources stimulates these receptors, and this stimulus is transferred via specialized nerves to the spinal cord and up to the brain. The brain then processes the pain stimulus and sends an impulse down the spinal cord that commands the body to respond.
Pain receptors (nociceptors) are nerve fibers with endings that can be excited by three types of stimuli: mechanical, thermal, and chemical. Mechanical receptors respond to pressure or stretching. Thermal receptors respond to extreme heat or cold. Chemical receptors react to various stimuli from both internal and external sources including chemical mediators from trauma or inflammation. For example, specific prostaglandins are pro-inflammatory mediators that are locally released with painful stimuli and inflammation and cause increased sensitivity of the pain receptors. Other chemical substances produced by the body that excite pain receptors include bradykinin, serotonin, and histamine. Thus, controlling inflammatory mediators can directly impact pain perception.
Pain signals can also be selectively inhibited in the spinal cord. This analgesic (pain-relieving) response is controlled by neurochemicals called endorphins, which are opioid peptides such as enkephalins that are produced by the body. These substances block reception of stimuli by binding to receptors. Enhancing this natural pain-reducing pathway also can modulate the perception of pain.
Natural Support for Pain
Pain is clearly one of the most common health problems of our time. However, both clinical practice and research indicate that pain is something that can be conquered. One of the most effective natural approaches involves the amino acid DL-phenylalanine, the botanicals turmeric and boswellia serrata, and the proteolytic enzyme nattokinase. Unlike other substances such as glucosamine sulfate, which acts to correct tissue damage after it has occurred, these synergistic substances work specifically to inhibit pain.
L-phenylalanine is an essential amino acid metabolized into tyrosine, which is the precursor used for the synthesis of the neurotransmitters norepinephrine, epinephrine, and dopamine. DL-Phenylalanine is a 50-50 mixture of L-phenylalanine and its mirror image molecule D-phenylalanine. DL-Phenylalanine is among a number of compounds that have been shown to inhibit the break down of enkephalins, which are the body's natural opioid pain reducers. DL-Phenylalanine, one of these enkephalinase inhibitors, has been used successfully for the management of chronic pain in humans. DL-Phenylalanine also exhibits anti-inflammatory properties. It is proposed that the enkephalinase inhibitors may be effective in a number of human "endorphin deficiency diseases" such as depression and arthritis. DL-Phenylalanine may also alleviate other conditions associated with decreased endorphin levels such as opiate withdrawal symptoms. Animal models indicate that phenylalanine supplementation can increase the pain threshold. It is hypothesized that this analgesia is induced by DL-Phenylalanine blocking enkephalin degradation by the enzyme carboxypeptidase A.
Preliminary studies of chronic pain patients have shown a response rate to DL-Phenylalanine from 32-75%. Analysis suggests that it may be mediated in part by up-regulation of the endogenous analgesia system (EAS). Since enkephalins are key neurotransmitters in the EAS, it is reasonable to suggest that promoting enkephalin activity by DL-Phenylalanine should potentiate EAS-mediated analgesia.
* Turmeric (Curcuma longa)
Turmeric (an herbaceous perennial plant related to ginger) is used for numerous inflammatory conditions as it has anti-inflammatory and antioxidant activity. The primary constituent is curcumin, which is believed to exert these anti-inflammatory properties. Preliminary studies have shown turmeric may be supportive in several conditions such as inflammatory bowel disease, rheumatoid arthritis, inflammatory eye diseases, chronic pancreatitis, psoriasis, hyperlipidemia, and cancers.
Curcumin has been shown to inhibit important enzymes that mediate inflammatory processes in the body. These enzymes are cyclooxygenase (COX), lipoxygenase (LOX), and inducible nitric oxide synthase (iNOS). Improper up-regulation of COX-2 and iNOS has been associated with the pathology of inflammatory disorders as well as certain types of cancer. A number of studies have been conducted that support curcumin-mediated regulation of the COX and LOX pathways at both the cellular and molecular level.
In one study, the anti-inflammatory properties of turmeric were evaluated using animal models of rheumatoid arthritis. The results showed that turmeric profoundly inhibited joint inflammation and joint destruction in a dose-dependent manner. Turmeric prevented local activation of NFkB, which is involved in regulation of expression of the pro-inflammatory enzymes COX-2 and iNOS. Additionally, inflammatory cell influx, joint levels of pro-inflammatory prostaglandin E2, and local osteoclast (cells that resorb bone) formation were inhibited by turmeric extract treatment.
* Boswellia serrata
Boswellia serrata, also known as Indian frankincense, is widely used as a traditional herb in Ayurvedic medicine for treating inflammatory disease and has reported anti-inflammatory and analgesic activity. The resin, or gum, from the plant contains boswellic acids, which produce much of this plant's anti-inflammatory activity. It is believed that the mechanism of action for the anti-inflammatory activity of the boswellic acids is the ability to inhibit the synthesis of pro-inflammatory leukotrienes and the enzyme 5-lipoxygenase (5-LOX). Several clinical trials have attributed beneficial effects of this herb in treating chronic inflammatory diseases such as rheumatoid arthritis, chronic colitis, ulcerative colitis, Crohn's disease, asthma, and tumor-associated brain edema.
In a randomized, double-blind, placebo-controlled crossover study in 30 patients with osteoarthritis of the knee, Boswellia serrata extract or placebo was given for 8 weeks. All of the patients receiving Boswellia supplementation reported a decrease in knee pain and frequency of swelling, and an increase in knee flexion and walking distance.
Nattokinase is a proteolytic (protein-dissolving) enzyme derived from a Japanese food known as natto, a preparation of soybeans that has undergone fermentation with a bacterium known as Bacillus subtilis natto. Proteolytic enzymes have analgesic effects in addition to their well-recognized anti-inflammatory and anti-edemic properties, indicating they may have a role to play in pain management. Enzyme-derived analgesia is based on inhibition of the inflammatory cascade as well as exerting a direct influence on nociceptors. Enzymes increase speed of healing and pain relief, and decrease inflammation.
Another mechanism by which nattokinase may help control pain is through its actions as a fibrinolytic enzyme, which means it breaks down fibrin deposits by inactivating plasminogen activator inhibitor 1 (PAI-1). Studies show that it has fibrinolytic activity 4-times more potent than plasmin, the body's natural fibrinolytic enzyme. The fibrinolytic system is closely linked to control of inflammation, and plays a role in disease states associated with inflammation.
In animal studies, nattokinase can reduce markedly the thickening of blood vessel walls that normally occurs following an injury to the blood vessel lining (endothelium). In addition, nattokinase leads to dissolution of clots that build inside vessel walls as responses to injuries. Enzyme therapy is used to digest the fibrin and reverse the inflammation, which is the likely mechanism by which nattokinase may help to reduce pain.
Controlling pain is a challenge for many individuals. It is a major symptom in numerous medical conditions, and can significantly interfere with a person's quality of life and general functioning. Natural substances that inhibit inflammation and work directly on the sensitivity of the nervous system may improve the body's natural pain-reducing mechanisms. Therefore, consuming a synergistic blend of DL-phenylalanine, turmeric, boswellia serrata, and nattokinase, which work directly on pain and inflammation, may help individuals regain mobility.
Vitamin Research Products, empowering healthy aging since 1979, recently introduced Back in Action™, a powerful pain management formula containing DL-phenylalanine, turmeric, boswellia serrata, and nattokinase. This unique nutrient blend provides a comprehensive approach to reducing the inflammatory response that contributes to discomfort. For more information, visit www.vrp.com or call 800-877-2447.
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