An in vitro test has shown that allicin reacts with blood and oxidizes it: All allicin disappeared within a few minutes after being mixed with blood (1). At the same time, the color of the blood changed from red to black (Figure 1). This finding showed that allicin oxidized the red pigment hemoglobin in the red blood cells to methemoglobin, which irreversibly cannot carry oxygen to the organs/tissues (Figure 2). Cases of anemia have been seen from excessive consumption of some raw garlic preparations containing allicin and its degraded compounds (2,3). Therefore, such preparations should be used in moderation and with caution. Since most nutrients/substances taken orally and absorbed by the intestine must first go through the liver, allicin reactivity in the liver has also been studied (4). Small amounts of allicin could be detected in the effluent (fluids surrounding the cells) only when allicin was injected into the liver tissue at a high concentration, which caused severe liver cell damage. At lower dosages, which did not cause cell injury, allicin could not be detected in the effluent. In another study, allicin disappeared very rapidly when incubated with liver tissue (5).
Furthermore, it has been shown that after ingestion of 25 g of raw garlic containing a significant amount of allicin, neither allicin nor sixteen of its common transformation products were detected in either the serum or urine from 1 to 24 hours after ingestion (6).
These data suggest that allicin taken orally may not be delivered to the organs and tissues, and that it does not appear to be a biologically beneficial compound in garlic.
The Activity Of Allicin Taken Orally Is Very Questionable
Since allicin lacks bioavailability as previously mentioned, if at all, it is beneficial only when applied topically. The other methods of administration, including oral ingestion, will unlikely result in any beneficial effects.
The following recent studies have clearly shown that allicin does not contribute to the major pharmacological effects of garlic.
Allicin in Commercial Garlic Products
The instability of allicin has been confirmed by various studies. One study has shown that allicin decreased to non-detectable amounts after only six days (10) while another study showed that all allicin was lost within a day (20 hours) (11). When eight garlic supplements were purchased at health food stores and allicin content in them was determined using HPLC, the most sensitive method for detecting this compound, none of them were found to contain even a detectable amount of allicin (less than 1 ppm) due to the instability of allicin (1).
Since manufacturers have begun to realize that there is no allicin in any garlic supplement, they have started promoting "allicin potential" as a way to claim that their products can provide allicin to the body. Generally, allicin potential is determined by adding water to garlic products. However, the production of allicin inside the body is very doubtful.
Alliinase, the enzyme that catalyzes the conversion of alliin to allicin, is irreversibly deactivated at pH 3 or below, an acidic environment typically found in the stomach (12). No allicin was produced when pH 2 and pH 3 citrate buffers were added to garlic powder.
Simulated stomach fluids (SGF) and simulated intestinal fluids (SIF) have commonly been used to determine the effects of typical digestion on nutrients or chemicals in question. Compared to the amount of allicin produced by garlic powder upon water contact, only about 4% of that amount of allicin was produced when the garlic powder was incubated in SGF, and about 60% when incubated in SIF. Moreover, the subsequent incubation of garlic powder in SGF and SIF reduced the allicin production to about 1 % of its production in water (1).
These recent findings indicate that only insignificant amounts of allicin can be produced inside the body.
Volume I References
1. Freeman, F. and Kodera, Y. 1995. J. Agric. Food Chem. 43: 2332-2338.
2. Nakagawa, S. Masamoto, K. Sumiyoshi, H. Kunihiro, K. and Fuwa, T. 1980. J. Tox. Sci. 5: 91-112.
3. Imada, O. 1990. Nutrition International Co., P.O. Box 50632, Irvine, CA 92619-0632, p. 47.
4. Egen-Schwind C., Eckard R, and Kemper F.H. Planta Medica, 58: 301-305, 1992.
5. Egen-Schwind C., Eckard R., Jekat F.W, and Wirterhoff H. Planta Medica, 58: 8-13, 1992.
6. Lawson L,D., Ransom D.K. and Hughes B,G. Thrombosis Research, 65: 141-156, 1992.
7. Caporaso N, Smah S,M. and Eng R.H,K. Antimicrobial Agents and Chemotherapy, 23: 700-702, 1983.
8. Gebhardt R. Arzneim,-Forsch,/Drug Res., 41 : 800-804, 1992.
9. Sendl A., Elbl G., Steinke B. at al. Planta Medica, 58: 1-7, 1992.
10. Yu T-H, and Wu, C-M. Journal of Food Science 54(4): 977-981, 1989.
11. Brodnitz, M.H. Pascale, J.V., and Derslice, L.V. J. Agr. Food. Chem. 19(2):273-275, 1971.
12. Abramovitz, D. et al. Coron Artery Dis, 10(7):515-519, 1999.
13. Lawson, L.D. and Hughes, B.G. Planta Med. 58: 345-350. 1992.