Capsaicin found to inhibit the growth of fat cells; cancer fears appear unfounded
by Craig Weatherby
During the 1990’s a Japanese-Canadian research team demonstrated that chili powder tends to reduce the amount of calories consumed at a meal, when it is consumed in relatively hefty doses (Yoshioka M et al 1991, 1995, 1998, 2001, 2004).
Last August, we reviewed the evidence that spicy foods like chilies, black pepper, and ginger may accelerate calorie burning (See “Food Allies in the Weight War: Spices, Tea, and Fish”).
Hot spices work their magic in part by prompting the metabolic process known as thermogenesis (“creation of heat”), by which we turn the energy in food into body heat, instead of storing it as body fat (adipose tissue).
The compound that makes chili peppers hot is capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide): a potent anti-inflammatory substance that does four helpful things:
- Stimulates thermogenesis.
- Suppresses appetite.
- Raises the metabolic rate and stimulates release of adrenaline, thus increasing the body’s propensity to burn stored body fat and sugars (glycogen).
- Inhibits rises in blood sugar for a full 30 minutes after it is consumed. This curbs the tendency toward an over-release of insulin, which would lead to low blood sugar and a craving for carbohydrates.
Now, researchers from Taiwan have shown that the capsaicin in fresh chilies and chili powders (e.g., cayenne pepper) helps forestall the buildup of hard-to-lose body fat.
Chilies’ hot factor halts growth of fat cells
Studies have demonstrated that development of obesity can be discouraged by preventing immature fat cells (adipocytes) from developing into mature cells.
Other investigations show that capsaicin can reduce the proportion of fat tissue in the body and lower fat levels in the blood.
Laast month, researchers at Taiwan’s National Chung Hsing University published the results of their attempt to discover why capsaicin helps shift body composition from fat to lean (Hsu CL, Yen GC 2007).
Drs. Gow-Chin Yen and Chin-Lin Hsu extracted nascent fat cells called “pre-adipocytes” from mice and exposed them to various capsaicin solutions, which ranged in strength from 0 to 250 micromoles.
Significantly, the dilutions tested included ones approximating the concentration of capsaicin found in the stomach fluid of a 130-pound person eating a typical Indian or Thai diet (8-25 micromoles).
After letting the nascent fat cells soak in the capsaicin solution for 24 to 72 hours, the Taiwanese team found that this prevented them from developing into adipocytes (fat cells).
And because the effectiveness of the solution rose along with its capsaicin concentration and cell-exposure duration, this confirmed that capsaicin was responsible for deterring the development of fat cells.
Drs. Yen and Hsu also discovered how capsaicin worked its magic:
- Capsaicin suppressed key cellular factors—PPAR-gamma, C/EBPalpha, and leptin—involved in the formation of fat cells and body fat (adipogenesis).
- Capsaicin caused the burgeoning fat cells to commit “suicide” (apoptosis).
Interestingly, one of these mechanisms—inhibition of PPAR-gamma—is the means by which omega-3s and thiazolidinedione-class drugs (e.g., rosiglitazone and pioglitazone) help control blood sugar in type 2 diabetes and discourage growth of adreno-cortical tumors.
As we noted above, capsaicin inhibits rises in blood sugar for a full 30 minutes after it is consumed.
Can chilies promote cancer?
Some of the media reports of this study mentioned that high intake of hot chilies has been linked with increased risk of stomach cancers in Mexico and South India.
Researchers at Yale University have published a series of lab reports, whose results indicate that capsaicin cold be a double-edged sword: one that may promote or curb different cancers under varying laboratory circumstances (Surh YJ and Lee SS 1995, 1996, 1998; Surh YJ 2002).
But studies in mice or cell cultures suggest that capsaicin inhibits the growth of skin cancer, gastric cancer, and leukemia (Kang JY et al 1992; Zhang J et al 2003; Park KK et al 1998).
And as mentioned above, capsaicin possesses PPAR-inhibiting powers that may retad adreno-cortical and related tumors.
Our non-scientific review of the available epidemiological studies indicates that the majority of evidence points toward capsaicin being an anti-cancer agent, with any risk being associated with very high intake (i.e., 10 to 20 jalapeño peppers per day).
In fact, studies in Malaysia indicate that the risk of gastric cancer—the kind associated with chili intake in Mexican and South Indian investigations—falls as chili intake rises.
- Hsu CL, Yen GC. Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells. J Agric Food Chem. 2007 Mar 7;55(5):1730-6. Epub 2007 Feb 13.
- Kang JY, Alexander B, Barker F, Man WK, Williamson RC. The effect of chilli ingestion on gastrointestinal mucosal proliferation and azoxymethane-induced cancer in the rat. J Gastroenterol Hepatol. 1992 Mar-Apr;7(2):194-8.
- Lopez-Carrillo L, Hernandez Avila M, Dubrow R. Chili pepper consumption and gastric cancer in Mexico: a case-control study. Am J Epidemiol. 1994 Feb 1;139(3):263-71.
- Lopez-Carrillo L, Lopez-Cervantes M, Robles-Diaz G, Ramirez-Espitia A, Mohar-Betancourt A, Meneses-Garcia A, Lopez-Vidal Y, Blair A. Capsaicin consumption, Helicobacter pylori positivity and gastric cancer in Mexico. Int J Cancer. 2003 Aug 20;106(2):277-82.
- Macho A, Lucena C, Sancho R, Daddario N, Minassi A, Munoz E, Appendino G. Non-pungent capsaicinoids from sweet pepper synthesis and evaluation of the chemopreventive and anticancer potential. Eur J Nutr. 2003 Jan;42(1):2-9.
- Mathew A, Gangadharan P, Varghese C, Nair MK. Diet and stomach cancer: a case-control study in South India. Eur J Cancer Prev. 2000 Apr;9(2):89-97
- Morre DJ, Morre DM. Synergistic Capsicum-tea mixtures with anticancer activity. J Pharm Pharmacol. 2003 Jul;55(7):987-94.
- Park KK, Chun KS, Yook JI, Surh YJ. Lack of tumor promoting activity of capsaicin, a principal pungent ingredient of red pepper, in mouse skin carcinogenesis. Anticancer Res. 1998 Nov-Dec;18(6A):4201-5.
- Surh YJ, Lee E, Lee JM. Chemoprotective properties of some pungent ingredients present in red pepper and ginger. Mutat Res. 1998 Jun 18;402(1-2):259-67. Review.
- Surh YJ, Lee SS. Capsaicin in hot chili pepper: carcinogen, co-carcinogen or anticarcinogen? Food Chem Toxicol. 1996 Mar;34(3):313-6. Review.
- Surh YJ, Lee SS. Capsaicin, a double-edged sword: toxicity, metabolism, and chemopreventive potential. Life Sci. 1995;56(22):1845-55. Review.
- Surh YJ. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem Toxicol. 2002 Aug;40(8):1091-7. Review.
- Yoshida T, Yoshioka K, Wakabayashi Y, Nishioka H, Kondo M. Effects of capsaicin and isothiocyanate on thermogenesis of interscapular brown adipose tissue in rats. J Nutr Sci Vitaminol (Tokyo). 1988 Dec;34(6):587-94.
- Yoshioka M, Doucet E, Drapeau V, Dionne I, Tremblay A. Combined effects of red pepper and caffeine consumption on 24 h energy balance in subjects given free access to foods. Br J Nutr. 2001 Feb;85(2):203-11.
- Yoshioka M, Imanaga M, Ueyama H, Yamane M, Kubo Y, Boivin A, St-Amand J, Tanaka H, Kiyonaga A. Maximum tolerable dose of red pepper decreases fat intake independently of spicy sensation in the mouth. Br J Nutr. 2004 Jun;91(6):991-5.
- Yoshioka M, Lim K, Kikuzato S, Kiyonaga A, Tanaka H, Shindo M, Suzuki M. Effects of red-pepper diet on the energy metabolism in men. J Nutr Sci Vitaminol (Tokyo). 1995 Dec;41(6):647-56.
- Yoshioka M, St-Pierre S, Drapeau V, Dionne I, Doucet E, Suzuki M, Tremblay A. Effects of red pepper on appetite and energy intake. Br J Nutr. 1999 Aug;82(2):115-23.
- Yoshioka M, St-Pierre S, Suzuki M, Tremblay A. Effects of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women. Br J Nutr. 1998 Dec;80(6):503-10.
- Zhang J, Nagasaki M, Tanaka Y, Morikawa S. Capsaicin inhibits growth of adult T-cell leukemia cells. Leuk Res. 2003 Mar;27(3):275-83.