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Welcome to my compendium website on the cancer treatment with capsaicin health benefits. Capsaicin is the active ingredient in chili peppers, the substance that gives chili and cayenne its heat.

Research on the use of capsaicin for cancer patients has focused on several areas:
  • its ability to decrease pain
  • its potential to be carcinogenic
  • any chemoprotective capacity
  • any antimicrobial and detoxification properties

Important words used on this site include:  Capsaicin, Health, Red Chili Peppers, Cayenne, Tumor,  Carinogenic, Chemoprotective, Antimicrobial, Detoxification, Dosage, Precautions, Hot, Trigger,  Jalapenos, Tongue, Extract, Androgen, Proteins, Genes, Prostate Cancer, Superfood, Headache, Arthritis, Relief, Antiinflamatory, Gastric, Apoptosis, Mitochondrial Respiration,  Oxygen, Chemotherapy, Molecules, Intestinal Epithelial Cells, Research,  Cycle, Carcinogens, Chemical, Chillies, Spicy, Kill,


You can find this site again  by typing in the  Google search engine  the unique word " 1niciaspaC "  which is  OR " Capsaicin1 " backwards.

 

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If after you scan to the bottom of this  website and still can't find the information you are looking for try another Google search here.
Contact information for this Website:
 Brian Nelson,
Webpage Marketing Consultant 
 31 Gessner Rd. Houston, TX  77024
 01/10/2007 07:40 PM -0600
713-467-3025  Fax 713-467-3192  Click: E-mail me

You are at: http://www.IamFightingCancer.com/CancerTreatment/Capsaicin-Health-Benefits.html    ud 01/10/2007 07:40 PM -0600  Bookmark this page now!
 
Misspelled words used to find this page 1 of 6. capsiasiegn, capsaisin, capsaicin, capsaicen, capsiasin, capsiacen, capsaiceign, capsaicn, capsaisen, capsiaceign, capsaiin, capsiasen, capsaiseign, capsacin, capsaican, capsiaseign, capsicin, capsiacan, capsaiciegn, capaicin, capsaisan, capsiaciegn, casaicin, capsiasan, capsaisiegn, cpsaicin, capsiacin, capsisiegn, capsiin, capsicen, capscin, capsisen, capicin, capsican, casicin, capsisan, cpsicin, capsisin, capsiceign, capsiseign, capsiciegn, capsicn, capsa1c1n, capsaicim, capsaicni, capsaiicn, capsaciin, capasicin, caspaicin, cpasaicin, acpsaicin, capsaici, apsaicin, health, heath, halth, helth, heelth, hearth, harth, herth, heerth, hialth, hiarth, hath, heth, heeth, hiath, hiart, healt, heart, halt, hart, helt, hert, heelt, heert, hialt, hea1th, healht, heatlh, helath, haelth, ehalth, healh, ealth, red, read, led, erd, erred, eld, rde, chili, chyli, chyri, chilly, chile, chiri, ch111, ch1l1, chiil, chlii, cihli, hcili, pepper, peppur, pepur, peper, peppor, pepor, peppel, pepel, pepers, peppors, pepors, peppels, pepels, peppers, pepurs, pppers, pepprs, peppes, peppurs, p3p3rs, peppesr, peppres, pepeprs, ppepers, epppers, cayenne, caynne, caenne, cyenne, ceighenne, ceighene, cayene, cay3n3, cay3m3, cayenen, caynene, caeynne, cyaenne, acyenne. tumor, tumur, temur, chumor, chumol, chumur, temor, tumol, temol, tunor, tumro, tuomr, tmuor, utmor, car1nogen1c, carinogenic, carimogenic, carinogenci, carinogeinc, carinogneic, carinoegnic, caringoenic, cariongenic, carniogenic, cairnogenic, crainogenic, acrinogenic, carinogeni, carinogenc, carinogeic, carinognic, carinoenic, caringenic, cariogenic, carnogenic, cainogenic, crinogenic, arinogenic, chenoprotect1ve, chenoprotective, chemoprotectiev, chemoprotectvie, chemoprotecitve, chemoprotetcive, chemoprotcetive, chemoproetctive, chemoprtoective, chemoportective, chemorpotective, chemporotective, cheomprotective, chmeoprotective, cehmoprotective, hcemoprotective, chemoprotectiv, chemoprotectie, chemoprotectve, chemoprotecive, chemoprotetive, chemoprotctive, chemoproective, chemoprtective, chemopotective, chemorotective, chemprotective, cheoprotective, chmoprotective, cemoprotective, hemoprotective, chemoprotective, antimicrobial

Definition

Capsaicin is the active ingredient in chili peppers, the substance that gives chili and cayenne its heat.

Purpose

Research on the use of capsaicin for cancer patients has focused on several areas:

  • its ability to decrease pain
  • its potential to be carcinogenic
  • any chemoprotective capacity
  • any antimicrobial and detoxification properties

Description

Folk accounts of capsaicin's medicinal properties in the form of cayenne have included aiding digestion, promoting the sweating process to create cooling (for reducing a fever), fighting infections, and stimulating the function of the kidneys, lungs, stomach, and heart. Research on capsaicin's ability to decrease pain has been in the areas of chronic pain, arthritic pain, migraine pain, and neuropathic cancer pain. It appears to interfere with chemicals that facilitate pain messages to the brain. Capsaicin has a hyperemic effect, which means that it increases blood flow similar to when an area is inflamed. When applied to the skin in cream form, the area becomes red, warm, and may become slightly swollen. Many individuals experience a localized burning sensation when a cream containing capsaicin is applied to the skin. However, with repeated use, the burning sensation usually disappears, and pain relief is noted. The burning or stinging sensation may last a few weeks for some. Capsaicin appears to work through a mechanism that initially causes a hypersensitivity to pain, and then ends in pain relief.

Several clinical studies performed on the effectiveness of various formulations of capsaicin have demonstrated that a majority of patients experience a reduction in pain and few or minor side effects. Capsaicin has been reported to have an effect against H. pylori, and also some antimicrobial properties. It appears to protect the lining of the digestive tract from harm due to aspirin use. Capsaicin has also showed an inhibitory effect on skin carcinogenesis in mice and a suppression of proliferation of human cancer cells.

Early studies on capsaicin raised the concern that capsaicin could be carcinogenic. However, further studies reported that capsaicin was not carcinogenic, and in fact might have chemoprotective properties. Studies investigating its potential to promote tumor development indicate it does not have this ability.

Recommended dosage

The Physician's Desk Reference (PDR) for Herbal Medicines indicates the availability of the following dosages of cayenne:

  • Capsules: 400, 445, 450, 455, and 500 mg strengths
  • Cream containing 0.25% and 0.75% capsaicin
  • Liquid alcohol-based extract

The average daily dose in capsule form for cayenne (capsicum annum) is 30 to 120 mg. Individuals wishing to use capsaicin should do so under the guidance of a practitioner knowledgeable about its properties, to ensure proper monitoring for any adverse reactions.

Precautions

Capsaicin's fiery nature requires some precautions to be used when handling it in its natural form or when applying it topically as a cream. Thorough hand washing after contact with it is necessary, as it can cause an intense burning or stinging sensations. Avoid any contact with mucous membranes, such as eyes or mouth, or any open wounds, until hands have been washed. Bottles storing capsaicin or cayenne should be well sealed and kept out of the light. It should not be refrigerated.

The National Cancer Institute (NCI) cautions that it is not known whether capsaicin used by a breast feeding mother will pass into the breast milk. Individuals who have had an allergic reaction to hot peppers should speak to their health care provider before using capsaicin. Some individuals may experience a prolonged burning sensation with topical capsaicin. However, the NCI states that reducing the number of doses per day will not result in decreasing the sensation, and may prolong the time period over which the sensation is experienced. In addition, a reduction in the number of doses may also reduce the degree of pain relief. Patients taking capsaicin should not double-up on a dose if a dose is missed.

Side effects

Research on capsaicin is still in the early stages, but the following has been reported:

  • hypersensitivity reaction such as anaphylaxis and rhinoconjunctivitis
  • abnormal blood clotting ability
  • an increase in bowel function, leading to diarrhea
  • blister formation on the skin
  • contact dermatitis
  • increase in cough with extended exposure to chili peppers
  • long-term use of high dosages can lead to kidney and liver damage, chronic gastritis, and neurotoxic effects

Interactions

If aspirin and capsicum annum extract (in the form of 100 mg of capsaicin) are taken at the same time, decreased bioavailability of aspirin may occur. This treatment may interfere with MAO inhibitors and antihypertensive therapy. As with any medication, patients should notify their physician of any prescription, over-the-counter, or herbal remedies they are taking prior to receiving treatment
Misspelled words used to find this page 2 of 6 ainthymicrobial, anthymicrobyal, aintimicrobial, antimicobial, anthymiclobail, anthymicrobyar, aintimicrobiar, antimirobial, ianthymicrobyal, aintimicrobyal, antimcrobial, anthymiclobial, antimiclobair, antiicrobial, anthymiclobiar, aintimiclobial, antmicrobial, ianthymiclobial, anthymicrobial, animicrobial, antimicrobil, anthymiclobyal, anthymicrobiar, atimicrobial, antimicrobal, anthymicrobail, ianthymicrobial, antimicrobair, antimicroial, anthymicrobair, ianthymicrobiar, andimicrobair, antimicrbial, andimiclobial, iantimiclobail, antimiclobyar, andimiclobail, antimiclobyal, antimicrobail, andimicrobiar, iandimiclobial, iantimiclobyal, iantimicrobial, iandimicrobiar, andimiclobyal, andimicrobial, iantimicrobail, andimicrobyar, antimicrobiar, andimicrobail, antimicrobyal, andimiclobiar, iantimicrobiar, iandimicrobial, iantimicrobyal, antimicrobyar, iandimicrobail, antimiclobial, iantimicrobyar, andimicrobyal, antimiclobail, antimiclobiar, iandimicrobyal, iantimiclobial, iantimiclobiar, ant1m1crob1a1, ant1m1crob1al, amtimicrobial, antimicrobila, antimicroibal, antimicrboial, antimicorbial, antimircobial, antimcirobial, antiimcrobial, antmiicrobial, anitmicrobial, atnimicrobial, natimicrobial, antimicrobia, ntimicrobial, detoxyficatiom, detoxifiction, detoxification, detoxyficachon, ditoxificatiom, detoxificaion, dtoxification, ditoxyficachon, ditoxyfication, detoxificatin, deoxification, detoxificachun, ditoxyficaton, detoxificatiom, detxification, ditoxificachun, ditoxyficashun, detoxyfication, detoification, detoxyficachun, ditoxyficashon, ditoxification, detoxyficaton, detoxfication, ditoxyficachun, ditoxyficasion, ditoxificaton, detoxyficashun, detoxiication, ditoxyficatiom, ditoxificashun, detoxyficashon, detoxifcation, detoxificachon, ditoxificashon, detoxyficasion, detoxifiation, ditoxificachon, ditoxificasion, detoxificaton, detoxificashun, detoxificashon, detoxificasion, detox1f1cat1on, detoxificatino, detoxificatoin, detoxificaiton, detoxifictaion, detoxifiaction, detoxifciation, detoxiifcation, detoxfiication, detoixfication, detxoification, deotxification, dteoxification, edtoxification, detoxificatio, etoxification, dosage, doesage, dousage, osage, oesage, ousage, dosaeg, dosgae, doasge, dsoage, odsage, dosag, dosae, dosge, doage, dsage, plecautiom, precaution, pecaution, prcaution, preaution, precution, precation, precauion, precautin, precautiom, plecausion, precauton, precaushun, precaushon, plecaution, plecauton, plecaushun,

Pepper component hot enough to trigger suicide in prostate cancer cells

 

Capsaicin, the stuff that turns up the heat in jalapeños, not only causes the tongue to burn, it also drives prostate cancer cells to kill themselves, according to studies published in the March 15 issue of Cancer Research.

According to a team of researchers from the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center, in collaboration with colleagues from UCLA, the pepper component caused human prostate cancer cells to undergo programmed cell death or apoptosis.

Capsaicin induced approximately 80 percent of prostate cancer cells growing in mice to follow the molecular pathways leading to apoptosis. Prostate cancer tumors treated with capsaicin were about one-fifth the size of tumors in non-treated mice.

"Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture," said Sören Lehmann, M.D., Ph.D., visiting scientist at the Cedars-Sinai Medical Center and the UCLA School of Medicine. "It also dramatically slowed the development of prostate tumors formed by those human cell lines grown in mouse models."

Lehmann estimated that the dose of pepper extract fed orally to the mice was equivalent to giving 400 milligrams of capsaicin three times a week to a 200 pound man, roughly equivalent to between three and eight fresh habañera peppers – depending on the pepper's capsaicin content. Habañeras are the highest rated pepper for capsaicin content according to the Scoville heat index. Habañero peppers, which are native to the Yucatan, typically contain up to 300,000 Scoville units. The more popular Jalapeño variety from Oaxaca, Mexico, and the southwest United States, contains 2,500 to 5,000 Scoville units.

As described in their study, the scientists observed that capsaicin inhibited the activity of NF-kappa Beta, a molecular mechanism that participates in the pathways leading to apoptosis in many cell types.

Apoptosis is a normal cellular event in many tissues that maintains a balance between newer replacement cells and aged or worn cells. In contrast, cancer cells seek to be immortal and often dodge apoptosis by mutating or deregulating the genes that participate in programmed cell death.

"When we noticed that capsaicin affected NF-kappa Beta, that was an indication that we might expect some of the apoptotic proteins to be affected," said the study's senior author, Phillip Koeffler, M.D., director of Hematology and Oncology, Cedars-Sinai Medical Center, and professor at UCLA.

The pepper extract also curbed the growth of prostate cancer cells through regulation of androgen receptors, the steroid activated proteins that control expression of specific growth relating genes.

In prostate cancer cells whose growth is dependent on testosterone, the predominant male sex steroid, capsaicin reduced cell proliferation in a dose-dependent manner. Increased concentrations of capsaicin caused more prostate cancer cells to freeze in a non-proliferative state, called G0/G1.

Prostate cancer cells that are androgen independent reacted to capsaicin in a similar manner. Capsaicin reduced the amount of androgen receptor that the tumor cells produced, but did not interfere with normal movement of androgen receptor into the nucleus of the cancer cells where the steroid receptor acts to regulate androgen target genes such as prostate specific antigen (PSA). Capsaicin also interfered with the action of androgen receptors even in cells that were modified to produce excess numbers of androgen receptors.

The hot pepper component also reduced cancer cell production of PSA, a protein that often is produced in high quantities by prostate tumors and can signal the presence of prostate cancer in men. PSA content in the blood of men is used as a diagnostic prostate cancer screening measure. PSA is regulated by androgens, and capsaicin limited androgen-induced increases of PSA in the cancer cell lines.

More men in the United States develop prostate cancer than any other type of malignancy. Every year, more than 232,000 new cases of prostate cancer are diagnosed in the U.S., and more than 680,000 develop the disease worldwide. Approximately 30,000 men die from prostate cancer in the U.S. each year, which is about 13 percent of all new cases. Worldwide, there are 221,000 deaths – approximately 31 per cent – among men with prostate cancer.

Lehman conducted the studies in Koeffler's laboratory in collaboration with UCLA cancer researchers Akio Mori, James O'Kelly, Takishi Kumagai, Julian Desmond, Milena Pervan, and William McBride. Mosahiro Kizaki, a former post-doctoral fellow in Koeffler's laboratory who initiated the capsaicin studies, is currently at the Keio University School of Medicine, Tokyo, Japan.

Superfood No. 7: Hot Peppers

Capsaicin's Health Benefits
 
Headache help: Substance P is the key transmitter of pain to the brain. In fact, Substance P is the body's main mechanism for producing swelling and pain throughout the trigeminal nerve, which runs through the head, temple, and sinus cavity. When the nerve fibers come in contact with Substance P, they react by swelling—an effect that yields headaches and sinus symptoms. Clinical studies have shown that capsaicin, a compound in hot peppers, is extremely effective for relieving and preventing cluster headaches, migraine headaches, and sinus headaches.
Arthritis relief: People suffering from arthritis pain typically have elevated levels of Substance P in their blood and in the synovial fluid that bathes their joints. Research has shown that eating foods that contain capsaicin or applying a topical cream that contains capsaicin can suppress Substance P production.
Capsaiscin as spicy sinus soother: Capsaicin also possesses powerful antibacterial properties, and is very effective in fighting and preventing chronic sinus infections (sinusitis). This purely natural chemical will also clear out congested nasal passages like nothing else, and is helpful in treating sinus-related allergy symptoms. Small daily doses of capsaicin have even been shown to prevent chronic nasal congestion.
Capsaicin as anti-inflammatory: In recent years, researchers discovered that capsaicin is a potent anti-inflammatory, and have even pinpointed how it works to fight chronic, sub-clinical inflammation. The nuclei of human cells contain chemicals called nuclear transcription factors (NTFs), two of which—activator protein 1 (AP-1) and NF-kappa B—are especially important targets when it comes to prevention of cancer and premature aging of skin. Each of these NTFs can be "activated" by ultraviolet light and free radicals: a result that produces a pro-inflammatory chain reaction that promotes premature aging and a wide variety of degenerative diseases. As it turns out, nature offers several effective NTF-activation blockers, including the capsaicin in chilies, and the yellow pigment curcumin in turmeric.
Gastric relief: A recent study on gastric disorders at Duke University showed capsaicin may actually lead to a cure for certain intestinal diseases. The Duke team found that a specific nerve cell receptor appears to be necessary to initiate the development of inflammatory bowel disease (IBD), a general term given to a variety of chronic disorders in which the intestine becomes inflamed—resulting in recurring abdominal cramps, pain and diarrhea. The cause of IBD is unknown, and it is believed that up to 2 million Americans suffer from this disorder.
Capsaicin versus cancer: 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. It is widely regarded by medical experts that this low cancer rate may be tied to the large amounts of capsaicin in their diets, since nearly every main dish in their normal diet contains some form of capsaicin-based food, particularly hot cayenne and jalapeño peppers. Of course we must also take into consideration the fact these cultures also consume fiber-rich beans on a daily basis.
Capsaicin as fat burner: Capsaicin is an active ingredient in many of the most popular "fat burning" supplements on the market. A thermogenic agent, capsaicin helps to increase overall metabolic activity, thus helping the body burn calories and fat. Since the FDA banned the herb ephedra, supplement manufacturers have been searching for new thermogenic ingredients and many have added chilies to the mix. While capsaicin replaces some of ephedra's metabolic effects, it doesn't have that herb's negative, stimulant effects on heart rate. In fact, capsaicin is an actively "heart healthy" supplement.
Misspelled words used to find this page 3 of 6 plecaushon, precausion, plecausions, precautons, precaushuns, precaushons, plecautions, plecautons, plecaushuns, plecaushons, precausions, precautions, precautioms, plecautioms, pecautions, prcautions, preautions, precutions, precations, precauions, precautins, precautios, precaut1ons, precautiosn, precautinos, precautoins, precauitons, precatuions, precuations, preacutions, prceautions, percautions, rpecautions, recautions, hot, hto, oht, trigger, trgger, triggr, triggir, trigir, tliggir, tligir, triggar, trigar, tliggar, tligar, trigel, tligger, tliger, tliggel, tligel, triger, triggel, rigar, rigger, liggar, ligar, riggir, rigir, liggir, ligir, rigor, riggar, riger, ligger, liger, riggel, rigel, liggel, ligel, tiggel, tiggar, tiggir, tiger, tigel, tigar, tigir, tigger, tr1g3r, tr1ger, trigre, triggre, trigegr, trgiger, tirgger, rtigger,jalapeno, jalapeo, jlapeno, jaapeno, jalpeno, jalaeno, jalapno, jarapeno, jalapano, jarapano, ja1apenos, jalapenos, jalapemos, jalapenso, jalapeons, jalapneos, jalaepnos, jalpaenos, jaalpenos, jlaapenos, ajlapenos, jalapens, jalapeos, jalapnos, jalaenos, jalpenos, jaapenos, jlapenos, alapenos, tongue, tung, togue, tonge, tomgue, tongeu, tonuge, tognue, tnogue, otngue, tongu, tonue, tngue, ongue, extract, etract, exract, extact, extrct, extrat, extlact, extratc, extrcat, extarct, exrtact, etxract, xetract, extrac, xtract, androgiegn, adrogen, androgen, andlogiegn, anderogen, anderogiegn, anderogan, androgin, andlogin, androgn, anderogin, androen, androgeign, andrgen, andlogeign, andogen, anderogeign, anrogen, androgan, andlogen, andlogan, amdrogen, androgne, androegn, andrgoen, andorgen, anrdogen, adnrogen, nadrogen, androge, ndrogen, protein, prtein, proein, protin, proten, potein, proteigne, plotiegne, ploteeign, perteiegn, ploteigne, pertiegne, perteeign, porteiegn, perteigne, protine, portiegne, porteeign, plotine, porteigne, pertine, proteiegn, portine, protiegne, proteeign, ploteiegn, protean, plotean, pertean, portean, proteen, ploteen, perteen, porteen, protien, plotein, plotien, pertein, pertien, portein, portien, pertiens, porteins, portiens, protiens, ploteins, plotiens, perteins, proteins, poteins, prteins, proeins, protins, protens, proteis, prote1ns, proteims, proteisn, protenis, proetins, prtoeins, rpoteins, roteins, ganes, genes, gemes, gense, geens, gnees, egnes, prostate, postate, prstate, protate, prosate, prostte, prostae, porustaght, porestate, plostaght, porustate, perstaght, proestaght, porstaght, proustaght, proestate, ploestaght, proustate, ploustaght, ploestate, perestaght, ploustate, perustaght, perestate, porestaght, perustate, prostaght, plostate, perstate, porstate, porstat, prostat, porestat, proestat, porustat, proustat, postat, plostat, prstat, ploestat, protat, ploustat, prosat, perstat, prostt, perestat, perustat, prostaet, prosttae, prosatte, protsate, prsotate, rpostate, rostate,cancer, censer, cancel, cencel, cansel, censel, cacer, cencer, canser, caner, canel, cainl, cainr, ceiner, ceinel, cance, cence, canse, cense, canc, cenc, cancre, camcer, canecr, cacner, cnacer, acncer, cancr, cncer, ancer, sup3rfod, superfodo, superfood, superofod, supefrood, suprefood, sueprfood, spuerfood, usperfood, superfod,headache, hadacze, hedacze, heedacze, heaache, headche, headahe, headace, headacze, hiadache, hiadacze, hadache, hedache, heedache, headaceh, headahce, headcahe, heaadche, hedaache, haedache, ehadache, headach, eadache,arthritis, althritis, arthriis, arthitis, arthrtis, arhritis, arthrits,
Chili pepper  

In the countries where diets are traditionally high in capsaicin (the chili pepper substance, the fruits contain 0.1-1.5% capsaicin), the cancer death rates for men and women are significantly lower than they are in countries with less chili pepper consumption (World Health Organization statistics). When capsaicin was administered to rats receiving carcinogenic agents, the incidence of certain tumors was decreased over controls. Capsaicin has been found to preferentially inhibit the growth of cancer cells in laboratory studies. Experiments have shown that capsaicin seems to be able to detoxify a wide range of chemical carcinogens which, if left free to roam the body, could set up mutations that lead to cancers. It also induces apoptosis in various immortalized or malignant cell lines.
Researchers tested the capsaicin on human skin cancer cells to analyze how the cells reacted. They found that the majority of the skin cancer cells exposed to the substances died. The researchers say these substances seem to kill cells by damaging the cell membranes and limiting the amount of oxygen that reaches the cancer cells.
Study authors Numsen Hail Jr. and Reuben Lotan, PhD, of the University of Texas M.D. Anderson Cancer Center in Houston say if more studies confirm these findings, the compounds may eventually be used in skin patches or creams that could treat or prevent skin cancers.
A different human study found that people who ate the most cayenne actually had lower rates of stomach cancer.
A chili pepper tincture can be used in the amount of 0.3–1 ml TID. An infusion can be made by pouring a cup of boiling water onto 1/2–1 tsp of cayenne powder and let set for 10 minutes. A teaspoon of this infusion can be mixed with water and drunk three to four times daily. 

Capsaicin induces apoptosis by inhibiting mitochondrial respiration
Last Updated: 2002-09-09 11:17:23 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Scientists have discovered that capsaicin, the pungent constituent of hot chili peppers, and a more potent structurally related vanilloid found in the plant Euphorbia called resiniferatoxin, induce apoptosis of tumor cells by inhibiting mitochondrial respiration, in effect starving them of oxygen.

"Capsaicin can prevent cancer development in animal models and cause cancer cell death in cultured tumor cells," Dr. Reuben Lotan of the University of Texas M. D. Anderson Cancer Center in Houston told Reuters Health. "But the mechanism underpinning this effect has not been elucidated. Our study addressed the mechanism by which capsaicin induces cancer cell death."

In the September 4th issue of the Journal of the National Cancer Institute, Dr. Lotan and Dr. Numsen Hail, Jr., report that when they exposed human cutaneous squamous cell carcinoma (SCC) cells to capsaicin or resiniferatoxin for 12 hours, the majority of cells died.

The apoptotic effects appeared to be triggered by inhibition of mitochondrial respiration as evidenced by an increase in the permeability of the inner mitochondrial membrane. Exposure to either capsaicin or resiniferatoxin led to a "rapid increase in hydroperoxide generation and a decrease in oxygen consumption," the team reports.

This shows that "capsaicin and resiniferatoxin act at the level of oxygen consumption (respiration) in mitochondria and this causes cells to die," Dr. Lotan told Reuters Health.

When they exposed respiration-deficient clones of human SCC cells to capsaicin or resiniferatoxin, the cells released less hydroperoxide compared with control cells and were resistant to mitochondrial permeability and the induction of apoptosis.

The demonstrated apoptogenic and antiproliferative effects of these two compounds "warrant further studies in animal models and, if positive, also in clinical trials to assess the potential application of capsaicin or resiniferatoxin against skin cancer," Dr. Lotan said.

In a JNCI editorial, Dr. Young-Joon Surh of Seoul National University in South Korea congratulates the scientists for their elegant series of experiments demonstrating that the "oxidative stress that is stimulated by vanilloid treatment of SCC cells is primarily of mitochondrial origin and contributes to the death of these cells by apoptosis."

Dr. Surh also urges further study, particularly to see if the increased oxidative stress brought on by vanilloids may have harmful effects on nonmalignant cells. "If this is the case, the vanilloids would be metabolic poisons rather than valuable candidates for use in preventive therapy for skin cancer or other cutaneous disorders," the researcher cautions
Program: Cell cycle regulatory molecules as targets for chemotherapy; Alterations in transcription factors in cancer
Progression from a normal cell to cancer involves the acquisition of multiple changes. These changes, which can be genetic or epigenetic, ultimately give rise to alterations in gene expression that affect the levels and/or activities of factors involved in regulation of cell growth and survival. Thus, a major contribution to the development of rational strategies for treatment and prevention of cancer will come from characterization of proteins whose expression or activity is changed during tumorigenesis and identification of drugs that can exploit these cancer specific changes. This approach has the advantage that that it not only sheds light on the mechanisms of action of such drugs, but it also identifies molecular targets that can be used to track drug actions in animal models and eventual clinical trials.

Recent advances have led to the recognition of the pathway in which cyclin/cyclin-dependent kinase complexes phosphorylate and inactivate the retinoblastoma protein as a critical regulator of cell growth. This pathway is a promising target for cancer therapy since it is disrupted in most, if not all, cancers. Of the members of this pathway, cyclin D1 is of particular interest since a) it regulates cell growth and progression through G1 phase of the cell cycle by multiple mechanisms, b) it is a critical sensor of the cellular growth environment, and c) overexpression of cyclin D1 is one of the most common abnormalities in cancer. Studies in this laboratory have determined that treatment of colon and prostate cancer cells with vanilloids (capsaicin and resiniferatoxin) leads to a dramatic downregulation of cyclin D1 which is accompanied by growth arrest, indicating that these naturally occurring substances may be useful in cancer treatment and/or prevention.

Due to their central role in regulation of gene expression, growth-related transcription factors are also of particular interest as targets for cancer therapy. The krüpel-like factor family of transcription factors has been implicated in both positive and negative growth regulation in multiple systems, and work from this laboratory has identified changes in expression of one member of this family (intestinal krüpel-like factor) as an early event in colon cancer progression (see below).

Progress
Effect of vanilloids on cell cycle regulatory molecules, cell growth and cell survival. Capsaicin (the major pungent ingredient of chili pepper, Capsicum annuum) and resiniferatoxin (derived from Euphorbia resinifera) are vanilloids that stimulate and subsequently desensitize primary afferent neurons through their binding to the vanilloid receptors. Due to these properties, vanilloids are undergoing clinical trails for pain management and treatment of diseases with neurological components such as psoriasis and overactive bladder. Recent studies have also determined that vanilloids can affect cell growth and survival in a vanilloid receptor-independent manner and it has been suggested that these effects may be specific to cancer cells. In keeping with an anticancer role, animal studies have indicated that oral capsaicin can protect against carcinogen-induced cancers, including those of the lung, liver, and intestine, and epidemiological data pointing to a possible protective effect in urological cancers have been reported. That these apparent anticancer effects of vanilloids may be exploited clinically is supported by the current characterization and acceptance of vanilloids in conventional medicine, together with the long-standing and widespread use of chili as a food additive and the use of extracts of chili and Euphorbia in alternative medicine.

Although several mechanisms for vanilloid receptor-independent action of capsaicin and resiniferatoxin have been proposed (e.g. inhibition of a tumor-specific, ubiquinol (NADH) oxidase, inhibition of protein synthesis through competition with tyrosine, disruption of mitochondrial membrane potential, oxidative stress and effects on calcium flux), the relative importance of these mechanisms in various cell types remains to be determined. Thus, rational design of vanilloid-based cancer treatments will require detailed analysis of their modes of action in vitro and in vivo. Based on data from animal and epidemiological studies, we are examining the effects of vanilloids on intestinal epithelial and prostate cancer cells. It is hoped that characterization of their actions in these models will allow optimization of vanilloids for cancer therapy/prevention and identification of molecular markers of drug action for use in in vivo/clinical studies.

Intestinal Epithelial Cells. Studies in IEC-18 intestinal crypt cells and colon cancer cell lines indicate that resiniferatoxin and capsaicin can inhibit the growth of both normal and transformed intestinal epithelial cells and that this growth inhibition is accompanied by a rapid downregulation of cyclin D1. Resiniferatoxin is at least 20-fold more potent than capsaicin and analysis of the actions of these two compounds, together with differences in their relative potencies in different cell types, indicates that resiniferatoxin may act through a novel mechanism. Thus, in addition to contributing to the potential development of vanilloids for colon cancer therapy and prevention, elucidation of the mechanisms of action of these compounds may identify novel target(s) for cancer treatment.

Prostate Cancer Cells. Analysis of the effects of vanilloids on prostate cancer cells indicates that these cells are highly sensitive to both capsaicin and resiniferatoxin. The observed growth inhibition is accompanied by rapid (<4 h) downregulation of cyclin D1 protein and mRNA and delayed (12-24 h) induction of the cyclin dependent-kinase inhibitor, p21WAF1/CIP1. Longer treatments (24-48 h) lead to a significant amount of cell killing. Comparison of androgen-dependent and -independent prostate cancer cell lines indicates that androgen-independent cells are equally, or more, sensitive to vanilloids. Thus, vanilloids offer promise for treatment of androgen-independent prostate cancer, for which no effective treatment currently exists. Levels of capsaicin that lead to growth arrest and cell killing are similar to those reported to be transferred to the blood following application of capsaicin-containing creams to the skin. This finding, together with the fact that capsaicin and resiniferatoxin are undergoing clinical trails for other urological disorders, further supports the potential of vanilloids for chemoprevention and chemotherapy of prostate cancer.

Role of krüppel-like transcription factors in intestinal tumorigenesis. The Sp1/krüppel-like factor (KLF) family of transcription factors has been implicated in growth regulation in many systems. Members of this family have a highly conserved DNA binding domain near their C-terminus which contains three krüppel-type zinc fingers, together with a non-conserved N-terminal transcriptionally active domain(s). In keeping with the lack of conservation in their N-terminal domains, these factors have diverse effects on transcription, being repressive or activating. Interestingly, individual family members can repress or activate transcription, dependent on the promoter and cell type being examined. Due to their highly conserved DNA binding domains, KLFs bind DNA with overlapping sequence specificity. These properties, together with the fact that cells express multiple family members, indicate that these factors may form a network through which transcription of individual genes can be fine-tuned. Reports have indicated that krüppel-like factors may play a role in tumor progression in the intestine.

The intestinal epithelium shows reciprocal expression of two krüppel-like factors. Gut krüppel-like factor (GKLF, KLF4) is expressed in the non-growing epithelial cells of the intestinal villi and surface mucosa, but not in the growing cells of the crypts, indicating that it has a role in growth arrest, differentiation and/or mature function in this tissue. In keeping with this role, GKLF is downregulated in intestinal adenomas and tumors, relative to normal mucosa. Furthermore, overexpression of GKLF in colon cancer cells, leads to growth inhibition and cell death. In contrast, intestinal krüppel-like factor (IKLF, KLF5) is expressed in the growing cells of the crypts but is downregulated on the villus and surface mucosa, arguing that this factor may have a growth-promoting role in the intestinal epithelium. This idea is supported by studies in fibroblasts in which IKLF overexpression led to increased cell growth. In order to elucidate potential roles of IKLF in intestinal tumorigenesis, we have utilized laser-capture microdissection (LCM) and reverse-transcription-polymerase chain reaction (RT-PCR) analysis to examine the expression of IKLF in normal intestinal epithelial cells and in adenomas derived form APCmin mice and human familial adenomatous polyposis (FAP) patients.

These studies indicate that IKLF mRNA is downregulated in adenomas relative to normal mucosa. Furthermore, preliminary analysis comparing gene expression between adenomas and growing cells of intestinal crypts, has revealed that, while there is a marked down-regulation of IKLF expression, there was little difference in the levels of GKLF mRNA between these populations of growing cells. This latter finding indicates that the downregulation of GKLF observed when comparing tumors with normal mucosa may reflect a failure of cancer cells to undergo normal growth arrest/differentiation in the upper crypts. Thus, while GKLF expression is clearly detrimental to colon cancer cells, it may affect cell survival rather than having a direct role in aberrant growth regulation. The finding that IKLF is downregulated in adenomas compared with both total normal mucosa and growing crypt cells indicates that loss of this factor is an early event in intestinal tumorigenesis. Thus, IKLF may have a tumor suppressive role in the intestine.

Students:
General Research Interest

  • Cell cycle control in cancer
  • Transcriptional alterations in cancer
  • High-throughput screening for drugs affecting specific molecular targets

Research Background and Interest

The efforts of the laboratory are aimed at understanding the implications of changes in cell cycle molecules and transcription factors for cancer progression and therapy.

Cell cycle control. Current efforts are aimed at understanding mechanisms underlying altered expression of cyclin D1 and p21waf1/cip1 in prostate and colon cancer. Overexpression of cyclin D1 is one of the most common alterations in cancer and p21 has been implicated in altered growth and apoptosis in tumor cells. Thus, an understanding of the regulation of these proteins is likely to present a novel target for therapeutic intervention.

Transcriptional regulation. Particular emphasis is placed on the Sp1 and krüppel-like family of transcription factors. This family contains over 20 members many of which have been implicated in cancer progression in multiple systems. Current studies include the roles of this family in colon cancer progression and in transforming growth factor beta resistance.

High-throughput screening. Strategies are being developed to allow for high-throughput screening of chemical libraries for drugs that affect the expression of specific molecular targets.
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Capsaicin pepper, cancer and ethnicity.

Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah 84111-5120, USA. varcher@dfpm.utah.edu

The 'hot' sensation produced by exposure to pepper is apparently due to two natural carcinogens: capsaicin in chili type peppers and safrole in black/white pepper. There are four cookeries in the United States that are noted for their high pepper content: Mexican-American, Cajun, white Creole, and black Creole. Each is largely confined to a single ethnic-cultural group which is concentrated in some counties. By use of county population and mortality data, significantly higher rates for stomach and liver cancer were found in counties inhabited by these four ethnic-cultural groups than in matched control counties. This involved both sexes. The cancer increase was dependent on the concentration of these groups in a county. These results strengthen and extend an earlier case-control study which found odds ratios above 5 for the stomach cancer association with capsaicin pepper.

It is further evidence that capsaicin is a human carcinogen.

Experimental Therapeutics, Molecular Targets, and Chemical Biology

Capsaicin, a Component of Red Peppers, Inhibits the Growth of Androgen-Independent, p53 Mutant Prostate Cancer Cells

Akio Mori1, Sören Lehmann1, James O'Kelly1, Takashi Kumagai1, Julian C. Desmond1, Milena Pervan2, William H. McBride2, Masahiro Kizaki3 and H. Phillip Koeffler1

1 Division of Hematology/Oncology, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine; 2 Department of Radiation Oncology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California; and 3 Division of Hematology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan

Requests for reprints: Sören Lehmann, Cedars-Sinai Medical Center/University of California at Los Angeles School of Medicine, 8700 Beverly Boulevard, Los Angeles, CA 90048. Phone: 310-423-7758; Fax: 310-423-0225; E-mail: LehmannS@cshs.org .

 

Capsaicin is the major pungent ingredient in red peppers. Here, we report that it has a profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines associated with an increase of p53, p21, and Bax. Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR. Promoter assays showed that capsaicin inhibited the ability of dihydrotestosterone to activate the PSA promoter/enhancer even in the presence of exogenous AR in LNCaP cells, suggesting that capsaicin inhibited the transcription of PSA not only via down-regulation of expression of AR, but also by a direct inhibitory effect on PSA transcription. Capsaicin inhibited NF-{kappa} activation by preventing its nuclear migration. In further studies, capsaicin inhibited tumor necrosis factor-{alpha}–stimulated degradation of I{kappa}B{alpha} in PC-3 cells, which was associated with the inhibition of proteasome activity. Taken together, capsaicin inhibits proteasome activity which suppressed the degradation of I{kappa}B{alpha}, preventing the activation of NF-{kappa}B. Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts as measured by size [75 ± 35 versus 336 ± 123 mm3 (±SD); P = 0.017] and weight [203 ± 41 versus 373 ± 52 mg (±SD); P = 0.0006; capsaicin-treated versus vehicle-treated mice, respectively]. In summary, our data suggests that capsaicin, or a related analogue, may have a role in the management of prostate cancer. (Cancer Res 2006; 66(6): 3222-9)

Experimental Therapeutics, Molecular Targets, and Chemical Biology

Capsaicin, a Component of Red Peppers, Inhibits the Growth of Androgen-Independent, p53 Mutant Prostate Cancer Cells

Capsaicin is the major pungent ingredient in red peppers. Here, we report that it has a profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines associated with an increase of p53, p21, and Bax. Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR. Promoter assays showed that capsaicin inhibited the ability of dihydrotestosterone to activate the PSA promoter/enhancer even in the presence of exogenous AR in LNCaP cells, suggesting that capsaicin inhibited the transcription of PSA not only via down-regulation of expression of AR, but also by a direct inhibitory effect on PSA transcription. Capsaicin inhibited NF-{kappa} activation by preventing its nuclear migration. In further studies, capsaicin inhibited tumor necrosis factor-{alpha}–stimulated degradation of I{kappa}B{alpha} in PC-3 cells, which was associated with the inhibition of proteasome activity. Taken together, capsaicin inhibits proteasome activity which suppressed the degradation of I{kappa}B{alpha}, preventing the activation of NF-{kappa}B. Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts as measured by size [75 ± 35 versus 336 ± 123 mm3 (±SD); P = 0.017] and weight [203 ± 41 versus 373 ± 52 mg (±SD); P = 0.0006; capsaicin-treated versus vehicle-treated mice, respectively]. In summary, our data suggests that capsaicin, or a related analogue, may have a role in the management of prostate cancer. (Cancer Res 2006; 66(6): 3222-9)
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Hot Pepper Ingredient Kills Prostate Cancer Cells

Capsaicin, the pungent alkaloid in jalapeños and other chile peppers that makes them hot, not only puckers the mouth and burns the tongue but also drives prostate cancer cells to kill themselves off, according to studies published in the March 15 issue of Cancer Research.

According to a team of researchers from the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center, in collaboration with colleagues from UCLA, the pepper component caused human prostate cancer cells to undergo programmed cell death or apoptosis.

Capsaicin induced approximately 80 percent of prostate cancer cells growing in mice to follow the molecular pathways leading to apoptosis. Prostate cancer tumors treated with capsaicin were about one-fifth the size of tumors in non-treated mice.

"Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture," said Sören Lehmann, M.D., Ph.D., visiting scientist at the Cedars-Sinai Medical Center and the UCLA School of Medicine. "It also dramatically slowed the development of prostate tumors formed by those human cell lines grown in mouse models."

Lehmann estimated that the dose of pepper extract fed orally to the mice was equivalent to giving 400 milligrams of capsaicin three times a week to a 200 pound man, roughly equivalent to between three and eight fresh habañera peppers – depending on the pepper’s capsaicin content. Habañeras are the highest rated pepper for capsaicin content according to the Scoville heat index. Habañera peppers, which are native to the Yucatan, typically contain up to 300,000 Scoville units.

The more popular Jalapeño variety from Oaxaca, Mexico, and the southwest United States, contains 2,500 to 5,000 Scoville units. As described in their study, the scientists observed that capsaicin inhibited the activity of NF-kappa Beta, a molecular mechanism that participates in the pathways leading to apoptosis in many cell types.

Apoptosis is a normal cellular event in many tissues that maintains a balance between newer replacement cells and aged or worn cells. In contrast, cancer cells seek to be immortal and often dodge apoptosis by mutating or deregulating the genes that participate in programmed cell death.

"When we noticed that capsaicin affected NF-kappa Beta, that was an indication that we might expect some of the apoptotic proteins to be affected," said the study’s senior author, Phillip Koeffler, M.D., director of Hematology and Oncology, Cedars-Sinai Medical Center, and professor at UCLA.

The pepper extract also curbed the growth of prostate cancer cells through regulation of androgen receptors, the steroid activated proteins that control expression of specific growth relating genes.

In prostate cancer cells whose growth is dependent on testosterone, the predominant male sex steroid, capsaicin reduced cell proliferation in a dose-dependent manner. Increased concentrations of capsaicin caused more prostate cancer cells to freeze in a non-proliferative state, called G0/G1.

Prostate cancer cells that are androgen independent reacted to capsaicin in a similar manner. Capsaicin reduced the amount of androgen receptor that the tumor cells produced, but did not interfere with normal movement of androgen receptor into the nucleus of the cancer cells where the steroid receptor acts to regulate androgen target genes such as prostate specific antigen (PSA). Capsaicin also interfered with the action of androgen receptors even in cells that were modified to produce excess numbers of androgen receptors.

The hot pepper component also reduced cancer cell production of PSA, a protein that often is produced in high quantities by prostate tumors and can signal the presence of prostate cancer in men. PSA content in the blood of men is used as a diagnostic prostate cancer screening measure. PSA is regulated by androgens, and capsaicin limited androgen-induced increases of PSA in the cancer cell lines.

More men in the United States develop prostate cancer than any other type of malignancy. Every year, more than 232,000 new cases of prostate cancer are diagnosed in the U.S., and more than 680,000 develop the disease worldwide. Approximately 30,000 men die from prostate cancer in the U.S. each year, which is about 13 percent of all new cases. Worldwide, there are 221,000 deaths – approximately 31 per cent – among men with prostate cancer.

Q & A about Chile Pepper
 

What part of the chile pepper is "hottest" and highest in capsaicin? According the Chile Pepper Institute at New Mexico State University and the Chemo Society :

Contrary to popular belief, the highest concentration of Capsaicin and source of most the heat (pungency) is in peppers' membranes (the fibrous placenta), not the seeds. The placental tissue holds the seeds, and seeds do absorb some capsiacins from the placental tissues during processing. Seeds in fresh pods absorb hardly any. 

Have you tried our recipe for Vegetarian Fajitas?

Are Hot Peppers Bad for You?

Some cancer specialists say that while research on capsaicin might lead to a new anti-cancer drug, patients must not try to cure themselves by eating hot chilis, "as these have been linked to high rates of stomach cancers in India and Mexico." How strong is this association? Read more in our blog and add your comments or recipes.

Also see this Texas Veterans Administration Medical Center Spicy food and the stomach... JAMA 1988 :
" ... to examine the effect of spices directly on the gastric mucosa; approximately 30 g of fresh jalapeno peppers was ground in a food processor and then placed directly into the stomach. Endoscopy after 24 hours revealed no visible mucosal damage. The ingestion of highly spiced meals by normal individuals is not associated with endoscopically demonstrable gastroduodenal mucosal damage." 

Habanero Red peppers are among the hottest of all. Organic Habanero red plants and other varieties available from Cross Country Nurseries Chile Plants

  

Chillies turn up the heat on tumors 

The same component of jalapeño peppers that makes them burn the tongue also appears to kill prostate cancer cells. Prostate tumors in mice treated with the compound, called capsaicin, shrank to one-fifth the size of those in non-treated mice, found a new study.

To explore capsaicin’s effect, Phillip Koeffler of the Cedars-Sinai Medical Center in Los Angeles, US, and colleagues exposed human prostate cancer cells in a laboratory dish to the natural compound. They found that capsaicin dramatically slowed the proliferation of the cells in the dish.

And this effect increased as the dose of the chilli compound was raised. Three per cent of prostate cancer cells committed “suicide” – programmed cell death – at low concentrations, rising to up to 75% of tumour cells dying at a higher dose.

Koeffler says this is the first experimental evidence supporting the notion that capsaicin stops the growth of prostate cancer cells.

Human cancer

He believes that capsaicin jump starts a pathway that triggers cell death. Molecular tests suggest that it achieves this by causing a cascade of events inside the cell that inhibits the release of a protein complex called NF-kappa B, which subsequently causes the cell to self-destruct. This is crucial since cancer is characterized by the uncontrolled growth of cells.

The team also found that capsaicin suppressed the growth of human prostate cancer cells by about 80%. These cells were grafted into mice with suppressed immune systems.

But Koeffler says that men concerned about prostate cancer should not interpret these findings as a reason to up their consumption of hot peppers. He stresses that the compound has not been shown to prevent prostate cancer but instead simply slows its growth. And he adds that he hopes to see human trials in the next two years assessing capsaicin’s effect on prostate cancer.

Take a chilli pill

After prostate cancer is surgically removed, it tends to reappear in about a quarter of patients, the researchers note. For this reason, they say that capsaicin may be most effective in slowing cancer’s return instead of stopping it from first developing.

He adds that one also must take dosages into consideration. A 200-pound (90-kilogram) person would have to eat about 10 fresh habañera peppers – one of the hottest chillies around – per week to consume an amount of capsaicin equivalent to the levels received by Koeffler’s mice.

A habañera typically contains 300,000 Scoville units – a scale used to measure the hotness of chillis – making them positively scorching to the mouth in comparison with the more popular jalapeños, which contain roughly 2500 to 5000 Scoville units. For this reason, he says it is unreasonable to imagine anyone eating fresh peppers to prevent the return of prostate cancer: “You would have to take it in pill form.”
Capsaicin Cancer

Killing cancer with capsaicin

Back in January, I wrote about a new type of therapy called resiniferatoxin where polymodal nociceptors were destroyed by a cousin of capsaicin. Now a new treatment involving resiniferitoxin’s cousin, capsaicin, is showing promise in killing tumor cells.

Capsaicin is what’s found in spicy foods — it’s what gives these food their burn. It’s also remarkably good at dulling pain (it’s the active ingredient in Zostrix, for example), and now it appears that it can also kill prostate cancer cells by increasing the rates of apoptosis. Apoptosis is programmed cell death; for instance skin cells undergo apoptosis to make way for newer cells. Cancer cells, on the other hand, are notorious for proliferating without ever dying, which is the definition of cancer: uncontrolled cellular proliferation.

In any event, a baseline rate of cell death of 3% was established with low concentrations of capsaicin. By increasing the dose, researchers at Cedars-Sinai Medical Center were able to increase the rates of apoptosis to as high as 75%.

He believes that capsaicin jump starts a pathway that triggers cell death. Molecular tests suggest that it achieves this by causing a cascade of events inside the cell that lead to the release of a protein complex called NF-kappa Beta, which subsequently causes the cell to self-destruct. This is crucial since cancer is characterised by the uncontrolled growth of cells.

The team also found that capsaicin suppressed the growth of human prostate cancer cells – grafted into mice with suppressed immune systems – by about 80%.

There is no indication that increased capsaicin intake decreases one’s risk of developing prostate cancer; rather, it only appears to slow its rate of growth. Nonetheless, Phillip Koeffler, head of the research team hopes to see clinical trials within the next two years to determine capsaicin’s actual effect on men with prostate cancer.

It would be interesting to see if resiniferatoxin can kill bone cancer cells via a similar pathway — while it might not save a terminal patient’s life life, it could prolong it.

Capsaicin kills prostate cancer cells

Posted Mar 17th 2006 11:29AM by Keith McDuffee
Filed under: Vegetables

chili peppersGather 'round, men, for the spicy food cook-off. You don't want to miss this one; it could save your life.

Capsaicin, the chemical in hot peppers (particularly cayenne and habenero) that makes them hot, literally stops prostate cancer cells in their tracks. Really. They actually commit suicide (apoptosis), leading to an eighty percent reduction in the size of the tumors compared with the mice spared from the hot stuff.

This is great news, but not really a surprise that the cancer cells commit suicide when exposed to the capsaicin. After all, haven't there been times you've wanted to kill yourself when eating those nuclear-hot buffalo wings or that seven-alarm chili? Makes perfect sense to me.
 

Spicy food could provide compound to fight cancers

By Cahal Milmo

Published: 10 January 2007

 
The compound that makes spicy food hot and generates the heat in muscle strain remedies could be the key to a new generation of cancer drugs which kill tumors with no side effects, a leading scientist has said.

Capsaicin, the active component of chilies, has produced "startling" results in tests to kill a variety of tumour cells including pancreatic cancer, one of the most difficult versions of the disease to treat.

Dr Timothy Bates, who led the research at Nottingham University, said his team have discovered a potential Achilles heel for all cancers because capsaicin targets the "powerhouse", or energy source, of tumour cells. The discovery could lead to the production of drugs to cure a variety of cancers at a fraction of the £410m cost of developing conventional medicines, as capsaicin is already consumed daily by millions of people. Capsaicin is also commonly used as an active ingredient in muscle rub creams and the treatments for psoriasis.

Dr Bates said: "This is incredibly exciting and may explain why people living in countries like Mexico and India, who traditionally eat a diet which is very spicy, tend to have lower incidences of many cancers that are prevalent in the Western world. We appear to have discovered a fundamental weakness with all cancer cells. Capsaicin specifically targets cancerous cells, leading to the possibility that a drug based on it would kill tumours with few or no side effects for the patient."

When released onto cancer cells, capsaicin attacks the mitochondria in the cell, which is responsible for generating ATP, the major energy-producing chemical in the body. Capsaicin specifically binds to the protein within the mitochondria of tumour cells and triggers apoptosis, the process of natural cell death.

Experiments by the Nottingham team found this took place in cancer cells without affecting surrounding healthy cells. The team applied the compound to human lung cancer cells, considered a gold standard test for anti-cancer drugs, and produced a "startling" rate of cell death. A similar rate was recorded on pancreatic cancer cells. The researchers said: "These results are highly significant as pancreatic cancer is one of the most difficult cancers to treat and has a five-year survival rate of less than one per cent."

Dr Bates said the fact that capsaicin, part of a group of food compounds called vanilloids, was a common part of the diet in many countries would dramatically reduce the number of regulatory hurdles that any anti-cancer drug would have to overcome.

It costs around £410m and takes 10 years for a large-scale pharmaceutical company to develop a new compound from scratch. But the Nottingham team, who are also working in conjunction with Chinese scientists to develop active ingredients from herbal remedies, is looking for industrial partners to start clinical trials at a fraction of the cost.

The researchers have also found dramatic results with a common anti-depressant, chlorimipramine, in targeting tumors.

Josephine Querido, cancer information officer at Cancer Research UK, said: "This research does not suggest that eating vast quantities of chili pepper will help prevent or treat cancer. The experiments showed that pepper extracts killed cancer cells grown in the laboratory, but these have not yet been tested to see if they are safe and effective in humans. It will be interesting to see how research on capsaicin progresses."

Hot Peppers Have Chilling Effect on Prostate Cancer Cells
Written by Rita Jenkins|  16 March, 2006  15:37 GMT


capsaicin prostate cancer peppers
'Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture. It also dramatically slowed the development of prostate tumors formed by those human cell lines grown in mouse models.' The substance that makes jalapeños fiery, called capsaicin, also spurs cancer cells to self-destruct, according to research published in Cancer Research.

The pepper component caused human prostate cancer cells to undergo programmed cell death, or apoptosis, according to a team of researchers from the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center and colleagues from UCLA.

More men in the United States develop prostate cancer than any other type of malignancy. Every year, more than 232,000 new cases of prostate cancer are diagnosed in the US, and more than 680,000 develop the disease worldwide. Approximately 30,000 men die from prostate cancer in the US each year, which is about 13 percent of all new cases. Worldwide, there are 221,000 deaths -- approximately 31 percent -- among men with prostate cancer.

'Profound