Hot Peppers Cancer Controversy

Hot Peppers

Fun Facts:

Believed to have originated in Bolivia, archaeological evidence suggests that people have been cultivating chili peppers for more than 6,000 years. (i.186)

Christopher Columbus was at least partially responsible for spreading hot peppers around the world. He brought the chili peppers he found Arawak Indians cultivating back with him to Spain, referring to them as pepper, an unrelated spice. But it was the Portuguese traders who really heated up interest in hot peppers when they brought back Pernambuco chili peppers from Brazil to their trading posts in Africa. (i.186)

People from different parts of the world enjoy using hot peppers (Capsicum frutescens, Capsicum annuum, and Capsicum chinense) to spice up their meals. Also referred to as chili peppers, they are particularly common in Creole and Cajun cooking as well as cuisines from Mexico, Peru, China, and parts of Italy and Asia. Although scientific evidence is inconclusive, some studies suggest that hot peppers may also spice up health because they have powerful healing properties that could help prevent or treat cancer. However, other researchers caution that hot peppers may actually be carcinogenic. (i.183-186)

Types of hot peppers include: (i.183184)

Indians from both North and South America have been using hot peppers for centuries (including the ancient Mayans) as both food and medicine. They have also been traditionally used in other natural herbal medicinal systems (including Ayurveda and Traditional Chinese Medicine) to treat a variety of diseases, including poor appetite, arthritis, circulatory complications, and digestive problems. (i.183185186)

Current Use of Capsaicin

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The main active ingredient in hot peppers is capsaicin, which is responsible for their hotness, or burning sensation on the tongue when eating. This compound is concentrated around developing seeds and across fruit walls. It's easy to determine if a pepper is high in capsaicin — the hotter it is, the higher its capsaicin content level. (i.183185187)

Capsaicin by itself is approved by the U.S. Food and Drug Administration (FDA) as a topical pain reliever. Studies suggest that capsaicin may help prevent ulcers and has cardiovascular benefits as well as good pain-relieving properties — including when used in a topical cream for post-mastectomy pain in breast cancer patients. Candy containing capsaicin may also offer temporary pain relief for mouth sores caused by chemotherapy or radiation cancer treatments. (i.183185)

Cayenne Pepper's Cancer-Fighting Nutrient Content

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In addition to capsaicin, hot peppers such as cayenne have other beneficial vitamins, minerals, as well as fiber. They also have beneficial plant compounds called polyphenols that may help prevent or slow down the growth of cancer. (i.187)

Cayenne pepper contains vitamin A, vitamin B6, vitamin C, vitamin E, vitamin K and also manganese. It also has several pro-vitamin A carotenoids. Among them is beta-carotene, which is a powerful antioxidant that stabilizes free radicals, which may help in preventing colon and other cancers. In addition, cayenne also contains the xanthophyll carotenoids lutein and zeaxanthin, and is one of the few vegetables with particularly high concentrations of the latter. Studies show that antioxidant xanthophylls can protect against DNA mutation and other free radical damage. They can also induce cancer cell death and inhibit metastasis by blocking the production of new blood vessels to feed tumor cells. Experts recommend consuming a variety of carotenoids in order to maximize their anti-cancer potential. (i.139187)

Hot Peppers — Cancer Fighter or Carcinogen?

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Animal studies suggest that dietary capsaicin may protect against carcinogenic effects of some known toxins, thereby preventing cancer from developing. DNA and mitochondrial damage from toxic substances and excess free radicals (caused by carcinogens, UV radiation, etc.) helps transform normal cells into malignant cancer cells. Research shows that capsaicin's antioxidant and detoxifying properties can help protect DNA in multiple ways: (i.188)

Vanilloid Cell Membrane Receptors

Recent research indicates that activating or suppressing TRP proteins (depending on cancer type) may be another mechanism that may explain capsaicin's antitumor activity. These cell membrane receptor proteins are found in skin, muscle, immune system, liver, and neurons (nerve cells), and abnormally increased or decreased levels can either promote or block cancer cell growth and metastasis. For example, increased expression of two different TRP proteins (TRPV6 and TRPM8) are found in prostate cancer, while low levels of others (TRPM1 and TRPV1) are associated with metastasis in melanoma skin cancer and progression of brain, bladder, cervical, and liver cancers. Capsaicin has been shown to increase the expression of TRPV1, which has been shown to trigger the following antitumor effects: (i.189)

Evidence of Antitumor and Carcinogenic Effects

Lab and animal research indicates that capsaicin and other hot pepper polyphenols may be able to block tumor growth and/or metastasis in various cancers. However, population studies show that greater consumption of chili peppers is associated with noticeably higher rates of gallbladder cancer in Chilean women. Recent investigations suggest that chronic low-level exposure to aflatoxin contamination in the hot peppers may actually be to blame, since capsaicin, the most prevalent bioactive component of chili peppers, appears to be non-mutagenic in lab studies. But even lab results on the carcinogenic and mutagenic potential of hot peppers and capsaicin are conflicting. (i.137188190)

Below is a summary of study results demonstrating the benefits of hot pepper constituents (particularly capsaicin, the most tested) and, when applicable, the carcinogenic effects which caution against the use of them for various types of cancer.

Bladder Cancer

The effects of capsaicin on bladder cancer have been tested in lab and animal experiments:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

Inhibited bladder tumor growth in animal studies. Injections of capsaicin into grafted human bladder cancer tumors significantly blocked them from growing. (i.189)

May improve chemotherapy treatment. Lab studies suggest that it may also enhance the effectiveness of certain chemotherapy treatments for bladder cancer. Both of these effects appear to be at least partially due to stimulating TPV1 membrane proteins in cancer cells. (i.189)

May stimulate tumor-promoting factors while inhibiting those that suppress tumors. In lab tests on bladder cancer cells that lack TRPV1 receptors, capsaicin downregulated tumor suppressor gene activity while stimulating production of tumor growth factors. It also upregulated activity of genes that produce proteins which promote invasion and metastasis (in TRPV1-deficient cancer cells). (i.189191)

Breast Cancer

The effects of capsaicin on breast cancer have been tested in lab and animal experiments:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

May stimulate enzymes that promote cancer cell death. Capsaicin killed cancer cells by stimulating production of enzymes that triggered cancer cell death in lab experiments on breast epithelial cells.  (i.188)

Low doses of capsaicin inhibit metastases. While high doses of capsaicin led to breast cancer metastasis, in the same animal study low doses (25 mg/kg of body weight) had the opposite effect. It activated the sensory neurons and markedly decreased the number of lung metastases (compared to the control group not treated with capsaicin). (i.192)

High doses of capsaicin can deactivate nerve cells and led to breast cancer metastasis. In an animal study that is often mentioned as evidence of capsaicin's carcinogenic potential, injections of neurotoxic doses of capsaicin (125 mg/kg of body weight) appeared to inactivate sensory neurons in the heart and lungs. When the mice were injected with breast cancer cells 1-3 weeks after capsaicin injection, there was significant metastasis of breast cancer tumors to the heart and lungs. It should be noted that this extremely high dose equates to over 23 times higher than the upper limit of that considered safe for human consumption, and 12.5 times the dosage successfully used in animal studies on small cell lung cancer. (i.192-198)

The metastatic effect is reversible. As the nerve cells regenerated, the number and size of metastatic nodules decreased to the same as the control group which was not injected with capsaicin. (i.192)

Deactivating nerve cells with toxic doses of capsaicin may create a more aggressive breast cancer cell type. The primary breast cancer tumors in the above-mentioned study showed lower levels of certain types of proteins which other studies indicate may make the breast cancer cells more invasive and resistant to cell death. This led the researchers to speculate capsaicin had triggered a more aggressive genetic variant of the breast cancer cells originally injected. However, the researchers did not explain the apparently contradictory reversal of metastatic effect over time as the neurons regenerated. (i.192196199)

Glioma Brain Cancer

The effects of capsaicin on brain cancer have been tested in multiple lab experiments:

Evidence of Anticancer Effects

May stimulate free radicals and antitumor receptor proteins. In lab experiments, capsaicin acted as a pro-oxidant instead of an antioxidant by stimulating production of several kinds of free radicals that led to the death of glioma brain cancer cells. Recent studies suggest that capsaicin also induces glioma cell death by increasing vanilloid receptor activity. (i.188)

Could help boost effectiveness of conventional cancer treatments. Results of recently published lab studies suggest that capsaicin may help overcome cancer cell resistance to TRAIL immunotherapy. Glioma cancer cells are aggressive, highly invasive, and often resistant to treatment, even though they possess the receptors targeted by the chemotherapy. Capsaicin (in nontoxic doses) upregulated a membrane death-receptor protein that sensitizes the cancer cell to TRAIL, and also suppressed expression of survivin, a protein that blocks cancer cell death. The combination treatment significantly increased glioma cancer cell death. (i.194)

Colon and Bowel Cancer

The effects of capsaicin and other polyphenols in hot peppers on colon and bowel cancer have been tested in multiple lab experiments:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

Non-pungent hot pepper prevention of risk factors for colon cancer. Nor-dihydrocapsiate, a non-spicy vanilloid substance from hot peppers, was shown in one animal study to significantly inhibit inflammatory damage in the colon that could lead to cancer. (i.188)

Low doses of capsaicin could inhibit tumor growth as well as chemotherapy. Results of randomized animal studies published in 2010 showed that capsaicin inhibited colon tumor growth (developed from colo205 human colon cancer cell line). Interestingly, lower doses (1 mg/kg of body weight) inhibited tumor growth more than both 5-fluorouracil chemotherapy and 3 mg/kg capsaicin doses. (i.195)

Low doses of capsaicin upregulates an enzyme that can promote colon cancer growth. In lab and animal studies, low doses of capsaicin increased expression of an enzyme that promotes cancer growth and metastasis in a human colon cancer cell line (HCT116). (i.196)

Some animals given capsaicin developed bowel tumors. In an animal study from the 1980s, results indicated that capsaicin caused a type of bowel cancer. However, other food safety experts note that there was no concurrent control group of animals in the study, and that the occurrence of tumors was not dose related. Interestingly. none of the mice who received the highest dosages of pure capsaicin developed tumors. (i.197198)

Esophageal Epidermoid Carcinoma Cancer

The effects of capsaicin on cancer in the esophagus have been tested in lab experiments:

Evidence of Anticancer Effects

Downregulation of proteins that control the growth cycle of cancer cells by capsaicin in lab studies slowed tumor growth, while interrupting mitochondrial functioning and generation of free radicals helped kill esophageal cancer cells. (i.188)

Leukemia

The effects of capsaicin on cancer of the blood have been tested in lab and animal experiments:

Evidence of Anticancer Effects

In lab studies, capsaicin stopped cancer cells from replicating by inhibiting cell cycle proteins. It also killed leukemia cells by stimulating production of proteins that engage in tumor suppressor activity, and inhibited growth of leukemia cells in animal studies on immune-deficient and diabetic mice. (i.188)

Liver Cancer

Capsaicin may promote the carcinogenic effects of toxins in the liver:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

Capsaicin killed liver cancer cells by activating genes that trigger apoptosis-type cellular death (in lab experiments). (i.188)

Capsaicin promoted the development of liver tumors in mice. The tumors were initiated by a known carcinogen, not by capsaicin alone. (i.198)

Small Cell Lung Cancer

Capsaicin has been tested and shown to be effective against lung cancer both in lab and animal studies:

Evidence of Anticancer Effects

Both lab and animal studies have demonstrated that capsaicin can potently inhibit multiple types of small cell lung cancers by inducing cell cycle arrest, inhibiting growth factors and development of tumor-feeding new blood vessels, and stimulating tumor suppressors. (i.194)

Melanoma

The effects of capsaicin on melanoma have been tested both in the lab and in animals:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

Capsaicin can block melanoma growth and metastasis at low doses. Studies show that capsaicin inhibited growth of an aggressive line of melanoma skin cancer cells in several ways: (i.188200)

  • Downregulated Bcl-2 proteins that help cancer cells survive mechanisms the body has to get rid of damaged or unhealthy cells before they can replicate abnormal, cancerous copies of themselves.
  • Inhibited the inflammatory cytokine protein IL-8 from activating transcription factor proteins that promote cancer growth.

Lab experiments and animal studies indicate that at low doses capsaicin also inhibits the invasion and migration of aggressive melanoma cells without damaging normal cells. It does so by inhibiting proteins (e.g., VEGF) that promote tumor growth and blocking cancer cell signals that trigger metastatic activity. (i.201202)

Works with chemotherapy to inhibit melanoma. In an animal study using mouse melanoma cells, combined treatment with capsaicin and a chemotherapy agent reduced cancer growth in vivo. More recent research demonstrated that low doses of capsaicin inhibited melanoma growth in vivo by itself. (i.188202)

High concentrations of capsaicin may stimulate VEGF growth factors before blocking cancer growth. Results of earlier lab experiments published in 2002 showed that high concentrations of capsaicin raised VEGF levels in two different melanoma cell lines. Although experts suggest the increases in VEGF levels reported in 2002 indicate capsaicin may have tumor and metastasis-promoting effects, the researchers in a later study imply otherwise. They note that while the high concentration of capsaicin in the 2002 lab tests reportedly raised VEGF levels, it also significantly inhibited melanoma cell growth. (i.188202)

Multiple Myeloma

The effects of capsaicin on multiple myeloma have been tested and shown to be effective both in vitro and in vivo:

Evidence of Anticancer Effects

Capsaicin stopped inflammatory factors from activating oncogenes that produce cancer growth-promoting cell cycle proteins. It also inhibited VEGF, a growth factor that promotes both tumor growth and metastasis, which stopped multiple myeloma cancer cell growth in lab and animal studies. (i.188)

Pancreatic Cancer

Capsaicin has tested positively against pancreatic cancer in both in vitro (lab) and in vivo (animal) experiments:

Evidence of Anticancer Effects

Lab and animal research show that capsaicin can induce pancreatic cancer cell death by disrupting mitochondrial function. In mice, adding capsaicin to their diet resulted in reduced natural antioxidant activity but increased free radical levels — both of which severely damaged the energy-producing mitochondria and resulted in tumor cells. (i.203)

Other animal studies demonstrated that oral administration of low doses of capsaicin resulted in significant reductions in pancreatic tumor volume (42%). (i.204)

Prostate Cancer

Study results are conflicting on capsaicin's effects in prostate cancer:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

Capsaicin may induce cell death in hormone receptive and non-receptive prostate cancers. In 2006, researchers from Cedars-Sinai Medical Center's Samuel Oschin Comprehensive Cancer Institute studying the effects of capsaicin found in lab experiments it forced multiple types of prostate cancer cells to undergo apoptotic cell death in a dose and time-dependent way. (i.205)

Lab studies demonstrate that capsaicin can kill both androgen receptor positive and negative prostate cancer cells by generating free radicals that target and damage cancer cell mitochondria as well as promoting tumor suppressor proteins. (i.205)

Shrinks tumor size. Oral administration of capsaicin also significantly reduced the size of grafted androgen-independent prostate cancer tumors on mice. (i.205)

May stimulate hormone-receptive cancer cells. However, results of lab tests published in 2009 on LNCaP prostate cancer cells showed capsaicin stimulated cancer cell proliferation by promoting production of androgen receptor proteins. (i.200)

Skin Cancer (Non-Melanoma)

Study results are conflicting on the effects of capsaicin and its derivatives on non-melanoma skin cancer:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

May induce cancer cell death. Research suggests that capsaicin, nor-dihydrocapsiate, and capsiate from hot peppers can kill non-melanoma cancer cells by: (i.188)

  • Suppressing mitochondrial function that give cells energy and protect them from damage (a good thing in cancer cells).
  • Generating free radicals to degrade cancer cells.
  • Activating genes that initiate cell death.

Safe by itself. Topical application of capsaicin or trans-capsaicin failed to induce skin tumors in animal studies. (i.188200)

Can promote skin cancer caused by other toxins. In a recently published study, animals treated with capsaicin and TPA (a known carcinogen), capsaicin alone, or TPA by itself. Capsaicin significantly promoted both the development and size of skin tumors when combined with TPA (compared to the group treated only with TPA). It did so by stimulating expression of a growth factor protein often found at higher levels in skin cancer. However, capsaicin by itself did not induce any skin tumors (while TPA did). (i.200)

Stomach Cancer

Study results are unclear on whether or not eating hot pepper increases the risk of gastric cancer, as are those reflecting capsaicin's effects:

Evidence of Anticancer Effects Evidence of Carcinogenic Effects

May be able to enhance chemotherapy treatment results. Studies show capsaicin triggers gastric cancer cell death by upregulating tumor suppressor and cell-death proteins. Although capsaicin and chemotherapy drugs can work individually to kill gastric cancer cells individually, lab studies showed that combining capsaicin with either etoposide or Adriamycin® killed dramatically more cancer cells. (i.206)

In some populations it is associated with lower risks of GI cancer. Rates of gastrointestinal cancer Thailand, where capsaicin is used regularly in their spicy cuisine, are lower than the rest of Asia. (i.198)

Can promote the cancer-causing activities of a toxin known to be carcinogenic. Although some researchers mention that animal studies showed that capsaicin promoted stomach cancer, this was in gastric cancer initiated by a known carcinogen, not by capsaicin alone. (i.193200)

Consumption of chili peppers has been associated with higher rates of stomach cancer in some countries. Several case-control population studies found an association between higher rates of stomach cancer in people who reported eating chili peppers. Risk also appeared to increase with greater intake: consuming hot peppers was linked to over 5 times the risk and heavy consumption with 17 times the risk of developing stomach cancer than those who didn't eat chili peppers. (i.200)

Other Precautions

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Medical experts report stomach irritation and pain when ingesting capsaicin supplements or foods, leading some experts to advise people with heartburn and ulcers to not use it. And although clinical trials suggest eating hot peppers such as cayenne can actually help improve symptoms from peptic ulcers caused by aspirin, for some people it can aggravate heartburn. (i.52183185)

Be aware that: (i.183185)

Adding Hot Peppers to Your Diet

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The wide variety of spices and other dried herbs in local spice stores makes them ideal for getting the best hot pepper. You are more likely to get fresher ones there than in the supermarkets. The organically grown varieties are preferable. Avoid direct sunlight when storing hot peppers. Seal them tightly in a glass jar or freeze for storage. (i.187207)

Cayenne pepper may be used as a spice in cooked dishes or as a table spice when ground. Try adding to hot cocoa for some spicy Mexican flavor. (i.187)

Growing Hot Peppers

Hot peppers require loose soil that is well-drained with pH values of between 5.5 to 6.5 and average moisture content. Start seeding indoors six to eight weeks before planting outside if in cooler climates as they require a long growing season in warm temperatures. (i.207)

Panax ginseng(i.272)
Especially in the Hunan and Szechuan regions. (i.185)
Mayans used hot peppers to treat infected wounds, earaches, and intestinal problems. (i.186)
This is the equivalent to 10.1 mg/kg of human body weight, or about 608 mg for a person weighing a little over 130 lbs. (i.195)
10 mg/kg body weight of mice. (i.194)
Tumor-associated NADH oxidase (tNOX/ENOX2). (i.199)
Specifically, adenocarcinoma of the duodenum. (i.193)
Specifically, benzene hexachloride. (i.193)
A particularly aggressive cancer with a 5-year survival rate of under 5%. (i.194)
2.5 mg/kg of body weight. (i.204)
Specifically, methyl-acetoxy methyl nitrosamine. (i.193)