Capsaicin for Pain Relief
Capsaicin for Pain Relief
Capsaicin for Pain Relief: All-Natural BullRyder Body Balm™ Active Ingredient
Benefits: Capsaicin provides temporary relief of minor aches and pains of muscles and joints associated with arthritis, simple backache, strains and sprains. As an ingredient in BullRyder Body Balm™, Capsaicin relieves the pain of peripheral neuropathy such as post-herpetic neuralgia caused by shingles. Recently, capsaicin has even been tested for the prevention of pain post surgery.
Capsaicin /kæp-se-ɪ.sɪn/ (8-methyl-N-vanillyl-6-nonenamide), one of the components in BullRyder Body Balm™, is the active component of chili peppers, which are plants belonging to the genus Capsicum. It is an irritant for mammals, including humans, and produces a sensation of burning in any tissue with which it comes into contact. Capsaicin and several related compounds are called capsaicinoids and are produced as a secondary metabolite by chili peppers, probably as deterrents against certain herbivores and fungi. Pure capsaicin is a hydrophobic, colorless, odorless, and crystalline to waxy compound.
Note: Capsaicin is but one component in our amazing all-natural BullRyder Body Balm™. Each of the active ingredients in our unique blend has exceptional pain relieving qualities alone but, in combination, the pain relieving qualities of each works synergistically with the others to produce an extraordinary pain relief salve whose unique formula was developed by Dr. Joie Power. The ten active ingredients in our all-natural BullRyder Body Balm™ include Essential Oils of: Balsam Poplar, Sweet Birch, Cajuput, Eucalyptus Globulus, Silver Fir, Helichrysum, Lavender and Plai plus St. John’s Wort Oil and Capsaicin.
History: The molecule was first isolated in 1816 in crystalline form by P. A. Bucholz and again 30 years later by L.T. Thresh, who gave it the name “capsaicin”. In 1878, the Hungarian doctor Endre Hogyes (calling it capsicol) isolated it and proved that it not only caused the burning feeling when in contact with mucous membranes but also increased secretion of gastric juice. The structure of capsaicin was partly elucidated by E. K. Nelson in 1919. Capsaicin was first synthesized in 1930 by E. Spath and F. S. Darling. In 1961, similar substances were isolated from chili peppers by the Japanese chemists S. Kosuge and Y. Inagaki, who named them capsaicinoids.
Capsaicinoids: Capsaicin is the main capsaicinoid in chili peppers, followed by dihydrocapsaicin. These two compounds are also about twice as potent to the taste and nerves as the minor capsaicinoidsa; nordihydrocapsaicin, homodihydrocapsaicin, and homocapsaicin. Dilute solutions of pure capsaicinoids produced different types of pungency; however, these differences were not noted using more concentrated solutions.
Capsaicin is believed to be synthesized in the interlocular septa of chili peppers by addition of a branched-chain fatty acid to vanillylamine. Biosynthesis depends on the gene AT3, which resides at the pun1 locus, and which encodes a putative acyltransferase.
Besides the six natural capsaicinoids, one synthetic member of the capsaicinoid family exists. Vanillylamide of n-nonanoic acid (VNA) is used as a reference substance for determining the relative pungency of capsaicinoids.
Natural function: Capsaicin is present in large quantities in the placental tissue (which holds the seeds), the internal membranes and, to a lesser extent, the other fleshy parts of the fruits of plants in the genus Capsicum. Contrary to popular belief, the seeds themselves do not produce any capsaicin, although the highest concentration of capsaicin can be found in the white pith around the seeds.
The seeds of Capsicum plants are predominantly dispersed by birds, as birds lack the receptor to detect capsaicin (i.e., because they cannot sense capsaicin, it is not an irritant to birds). Chili pepper seeds consumed by birds pass through the digestive tract unharmed, whereas those consumed by mammals do not germinate at all. The presence of capsaicin in the fruits therefore protects them from being consumed by mammals, which have molars that can kill seeds.
In 2006 it was discovered that tarantula venom activates the same pathway of pain as is activated by capsaicin, the first demonstrated case of such a shared pathway in both plant and animal anti-mammal defense.
Food: Because of the burning sensation caused by capsaicin when it comes in contact with mucous membranes, it is commonly used in food products to give them added spice or “heat” (pungency). In high concentrations capsaicin will also cause a burning effect on other sensitive areas of skin. The degree of heat found within a food is often measured on the Scoville scale.
Cooling and mechanical stimulation are the only proven methods to relieve the pain; capsaicin is not water-soluble, so water and most other liquids will only dull the pain by cooling the area, but will not have any lasting effect. The burning sensation will slowly fade away if no actions are taken. Dairy products are one of the most effective forms of relief; casein, a phosphoprotein found in milk, acts as a detergent to dissociate the capsaicin from nerve receptors, allowing it to wash away. (Dustrophsky, 2006).
It is common for people to experience pleasurable and even euphoriant effects from eating capsaicin-flavored foods. Folklore among self-described “pepperheads” attributes this to pain-stimulated release of endorphins, a different mechanism from the local receptor overload that makes capsaicin effective as a topical analgesic. In support of this theory, there is some evidence that the effect can be blocked by naloxone and other compounds that compete for receptor sites with endorphins and opiates.
Medical: Capsaicin is currently used in topical ointments to relieve the pain of peripheral neuropathy such as post-herpetic neuralgia caused by shingles. It may be used in concentrations of between 0.025% and 0.075%. It may be used as a cream for the temporary relief of minor aches and pains of muscles and joints associated with arthritis, simple backache, strains and sprains. The treatment typically involves the application of a topical anesthetic until the area is numb. Then the capsaicin is applied by a therapist wearing rubber gloves and a face mask. The capsaicin remains on the skin until the patient starts to feel the “heat”, at which point it is promptly removed. Capsaicin is also available in large bandages that can be applied to the back.
Recently, capsaicin is being tested for the prevention of pain post surgery. David Julius, a physiology professor at the University of California, San Francisco, recently discovered that capsaicin selectively binds to a protein known as TRPV1 that resides on the membranes of pain and heat sensing neurons. TRPV1 a heat activated calcium channel, with a threshold to open between 37 and 45 Celsius degrees (37 degrees is normal body temperature). When capsaicin binds to TRPV1, it causes the channel to lower its opening threshold, thereby opening it at temperatures less than the body’s temperature, which is why capsaicin is linked to the sensation of heat. Prolonged activation of these neurons by capsaicin depletes presynaptic substance P, one of the body’s neurotransmitters for pain and heat. Neurons that do not contain TRPV1 are unaffected. This causes extended numbness following surgery, and the patient does not feel pain as the capsaicin is applied under anesthesia.
The result appears to be that the chemical mimics a burning sensation; the nerves are overwhelmed by the influx, and are unable to report pain for an extended period of time. With chronic exposure to capsaicin, neurons are depleted of neurotransmitters and it leads to reduction in sensation of pain and blockade of neurogenic inflammation. If capsaicin is removed, the neurons recover.
Capsaicin is being explored as a possible cure for diabetes by researchers in Toronto, Canada; capsaicin was injected into pancreatic sensory nerves of mice with Type 1 diabetes because of a suspected link between the nerves and diabetes.
The American Association for Cancer Research reports studies suggesting capsaicin is able to kill prostate cancer cells by causing them to undergo apoptosis. The studies were performed on tumors formed by human prostate cancer cell cultures grown in mouse models, and showed tumors treated with capsaicin were about one-fifth the size of the untreated tumors. It has long been noted that in Thailand, where much spicy food is consumed, there is very low incidence of gastrointestinal cancers, including colorectal and stomach cancers, compared to the rest of Asia, including Japan and China. Mexico also has low rates of the same cancers compared to the USA. Several recent studies have shown that capsaicin may actually prevent the growth of certain types of cancer. In particular, there have been several clinical studies conducted in Japan and China that showed natural capsaicin directly inhibits the growth of leukemic cells. Although these studies used pure capsaicin directly injected into isolated diseased cells in a laboratory setting, scientists have also concluded that daily consumption of hot peppers (thus capsaicin) may actually prevent certain types of cancer. Throughout South America, intestinal, stomach, and colon cancer rates are very low compared to the United States. Another study carried out at the University of Nottingham suggests capsaicin is able to trigger apoptosis in human lung cancer cells as well.
Capsaicin is also the key ingredient in the experimental drug Adlea, which is in Phase 2 trials as a long-acting analgesic to treat post-surgical and osteoarthritis pain for weeks to months after a single injection to the site of pain.
Mechanism of action: The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called thevanilloid receptor subtype 1 (VR1). First cloned in 1997, VR1 is anion channel-type receptor. VR1, which can also be stimulated with heat and physical abrasion, permits cations to pass through the cell membrane and into the cell when activated. The resulting depolarization of the neuron stimulates it to signal the brain. By binding to the VR1 receptor, the capsaicin molecule produces the same sensation that excessive heat or abrasive damage would cause, explaining why the spiciness of capsaicin is described as a burning sensation.
The VR1 ion channel has subsequently been shown to be a member of the superfamily of TRP ion channels. There are a number of different TRP ion channels that have been shown to be sensitive to different ranges of temperature and probably are responsible for our range of temperature sensation. Thus, capsaicin does not actually cause a chemical burn, or indeed any damage to tissue at all; it causes only the sensation of one.
Painful exposures to capsaicin-containing peppers are among the most common plant-related exposures presented to poison centers. They cause burning or stinging pain to the skin, and if ingested in large amounts by adults or small amounts by children, can produce nausea, vomiting, abdominal pain, and burning diarrhea. Eye exposure produces intense tearing, pain, conjunctivitis, and blepharospasm.
Treatment after exposure: The primary treatment is removal from exposure. Contaminated clothing should be removed and placed in airtight bags to prevent secondary exposure. Capsaicin could be washed off the skin using soap, shampoo, or other detergents, or rubbed off with oily compounds such as vegetable oil, paraffin oil, petroleum jelly (Vaseline), creams, or polyethylene glycol. Plain water as well as home remedies such as vinegar, bleach, sodium metabisulfite, or topical antacid suspensions are ineffective in removing capsaicin.
Burning and pain symptoms can be effectively relieved by cooling, e.g., from ice, cold water, cold bottles, cold surfaces, or a flow of air from wind or a fan. In severe cases, eye burn might be treated symptomatically with topical ophthalmic anesthetics; mucous membrane burn with lidocaine gel. Capsaicin-induced asthma might be treated with nebulized bronchodilators or oral antihistamines or corticosteroids.
Effects of dietary consumption: Ingestion of spicy food or ground jalapeño peppers does not cause mucosal erosions or other abnormalities. Some mucosal microbleeding has been found after eating red and black peppers, but there is no significant difference between aspirin (used as a control) and peppers. Other studies have shown an association between chronic consumption of capsaicin-rich foods and stomach cancer.
• Dray A (1992). “Mechanism of action of capsaicin-like molecules on sensory neurons”. Life Sci. 51 (23): 1759–65.
• Garnanez RJ, McKee LH (2001) “Temporal effectiveness of sugar solutions on mouth burn by capsaicin” IFT Annual Meeting 2001
• Henkin R (1991). “Cooling the burn from hot peppers”. JAMA 266 (19): 2766.
• Nasrawi CW, Pangborn RM (1990). “Temporal effectiveness of mouth-rinsing on capsaicin mouth-burn”. Physiol. Behav. 47 (4): 617–23.
• Tewksbury JJ, Nabhan GP (2001). “Seed dispersal. Directed deterrence by capsaicin in chilies”. Nature 412 (6845): 403–4.
• Kirifides ML, Kurnellas MP, Clark L, Bryant BP (2004). “Calcium responses of chicken trigeminal ganglion neurons to methyl anthranilate and capsaicin”. J. Exp. Biol. 207 (Pt 5): 715–22.
• Tarantula Venom, Chili Peppers Have Same “Bite,” Study Finds http://news.nationalgeographic.com/news/2006/11/061108-tarantula-venom.html
• TRPV1, the only known receptor (a transient receptor potential channel) for capsaicin.
• Piperine, the active piquant chemical in black pepper
• Allylisothiocyanate, the active piquant chemical in mustard, radishes, horseradish, and wasabi
• Allicin, the active piquant flavor chemical in uncooked garlic and onions (see those articles for discussion of other chemicals in them relating to pungency, and eye irritation)
• Naga Jolokia pepper, the world’s most capsaicin-rich fruit
The above article is an excerpt from the full Wikipedia, the free encyclopedia article: http://en.wikipedia.org/wiki/Capsaicin