Capsaicin 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 herbivores.
Pure capsaicin is a hydrophobic, colorless,
odorless, crystalline to waxy compound.
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 adhesive 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.
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 the vanilloid receptor subtype 1 (VR1). First cloned in 1997, VR1 is an ion 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 super family of TRP ion
channels, and as such is now referred to as
TRPV1. 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.
Acute health effects
Capsaicin is a highly irritant material
requiring proper protective goggles,
respirators, and proper hazmat handling
procedures. It is hazardous in cases of skin
contact (irritant, sensitizer), of eye
contact (irritant), of ingestion, of
inhalation (lung irritant, lung sensitizer).
Severe over-exposure can result in death.
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. For extreme reactions, milk-soaked rags can be placed on the skin to neutralize the acids as the milk absorbs.
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