Latin name: Allium sativum
Pharmacopoeial name; Allii sativi bulbus
Other names: garlic clove
Ancient medical texts prescribed garlic for a number of applications including improving performance, reducing infections, and protection against toxins. These medicinal properties, coupled with its savory characteristics, have made garlic a true cultural icon in many parts of the world.
The whole bulbs of garlic contain alliin, γ-glutamyl-S-allylcysteine, S-methylcysteine sulphoxide, S-trans-1-propenylcysteine sulphoxide, S-2-carboxypropylglutathione and S-allylcysteine (1,2). But the chemical composition of the preparations obtained by extraction of garlic fractions depends on the extraction conditions: temperature, time and solvent’s polarity. The content of organosulphur compounds in garlic bulbs also changes during cultivation and storage. Its biological activities depend on many factors, including country of origin and various processing methods of garlic to isolate new organosulphur compounds and to decompose organosulphur compounds. A wide variety of organosulphur compounds have been attributed to the medicinal properties and health benefits of garlic.
Among the several functional compounds of garlic, alliin is the most abundant organosulphur compound in whole garlic. It is a derivative of the amino acid cysteine. Processing of garlic (cutting or chewing) generates a vacuolar enzyme (allinase), which acts upon alliin to give rise to allicin and other alkyl alkane-thiosulfinates (3). Commercial garlic preparations are often standardized on the content of sulphur-containing constituents, particularly to alliin, or on the allicin yield. Allicin and related thiosulfinates are decomposed to yield various organosulphur compounds including Diallyl trisulphide (DATS). It is considered that 1 mg alliin is equivalent to 0.45 mg allicin (5). Diallyl sulphide (DAS) is also easily transformed from allicin. Ajoene is another degradation product of allicin. Incubation temperature is a very important factor for ajoene formation. S-allyl cysteine (SAC), a major transformed product from γ- glutamyl-S-allyl-L-cysteine, is the water-soluble organosulphur compound and its concentration increases through a long-term extraction in an aqueous medium. Diallyl disulphide (DADS) is one of the principal components of the distilled oil of garlic. DADS is also an allergen causing garlic allergy.
Given that so many different manufacturing processes deliver such a wide variety of biologically active metabolites of garlic and that many of these processes depend upon cultural perspectives, clinical assessments are necessarily heterogeneous, since researchers have used different extracts, produced by different techniques and standardised to different components.
Uses of Garlic
Experimental evidence indicates that garlic ingestion lowers blood cholesterol levels and inhibits cholesterol synthesis. Zeng and his colleagues deduced from 26 studies that hypercholesterolemic patients treated with garlic (garlic powder and aged garlic extract) had a statistically significant mean serum TC and TG concentrations lower than that of patients treated with placebo (6).
Several experimental studies have indicated that garlic and its constituents inhibit key enzymes involved in cholesterol and fatty acid synthesis (7-10). These results indicate that compounds containing an allyl-disuphide or allyl-sulfhydryl group are most likely responsible for the inhibition of cholesterol synthesis by garlic.
It has also been shown that the more water-soluble compounds like SAC present in aged garlic extract are less cytotoxic and more efficient in inhibiting cholesterol biosynthesis than the lipid-soluble organosulphur compounds such as DAS (10).
In patients with uncontrolled hypertension, systolic blood pressure was lower in the garlic group who consumed four capsules of aged garlic extract (960 mg containing 2.4 mg SAC) daily for 12 weeks compared with controls over the 12-week treatment period (11).
Garlic appears to reduce blood pressure (BP) through enhancement of nitric oxide (NO) synthesis, and one possible mechanism by which garlic might induce its hypotensive effect could be through the direct and indirect vasodilatory actions of NO. Cumulating evidence indicates that hydrogen sulphide (H2S) also plays a cell signaling role similar to NO. In vivo and in vitro cardiovascular effects of H2S include decreased blood pressure and cardioprotection against ischemic damage (12-14). Garlic-mediated and H2S-mediated vascular smooth muscle relaxation indicate that both were based on NO signaling pathways (15).
As with cholesterol and blood pressure lowering effects, garlic also has a beneficial effect on platelet aggregation in humans. Platelet aggregation and subsequent thrombus formation are significantly reduced by garlic and its constituents. Aqueous garlic extracts inhibited human platelet aggregation (16). The inhibition of platelet aggregation is thought to work via the inhibition of calcium mobilization (17).
Recent studies have demonstrated beneficial effects of one active ingredient-SAC- in Alzheimer disease models (18-20). The therapeutic effects of SAC were also assessed in various models of neurodegenerative diseases including stroke (21), ischemia/reperfusion (22), Alzheimer’s disease (23), and Parkinson’s disease (24). The molecular mechanisms of these effects may include protecting neurons against oxidative/nitrosative (reactive oxygen/nitrogen species) stress, mitochondrial damage, and subsequent cell death.
Recent human studies suggests that garlic offers protection against oxidative stress and antioxidant activities in alcoholic liver disease patients. Preclinical studies have shown that garlic ameliorates alcohol-induced oxidative stress (25), inhibits induction of cytochrome P450 (CYP) (26) and prevents fatty liver and liver cirrhosis. One of the major protective functions of garlic is to decrease the oxidative damage in the liver (27). The antioxidative property of garlic has been ascribed mainly to its four major chemical components, i.e. allinin, SAC, DADS, and allicin (28).
Several studies suggested anti-allergic properties for garlic extract. Kyo et al reported that in their cell line model, addition of garlic extract reduced histamine release (anti-histamine effect) (29). They showed suppression of IgE-mediated antigen-specific skin reaction and concluded that garlic extract could beneficially balance, or modify the function of mast cells, basophils, and activated T lymphocyte factors, which all play a leading role in allergic cascade reactions and inflammation.
Several studies have also shown that garlic extract is helpful at preventing arthritis. Consumption of alliums (garlic, leeks,
and onions) showed the strongest protective association with hip osteoarthritis (OA) (30). They suggested that diallyl disulphide, a compound found in garlic and other alliums, represses the expression of matrix-degrading proteases in chondrocyte like cells, providing a potential mechanism of action.
One double-blind RCT assessing 146 patients over a 12-week treatment period was identified (31). Common cold infections and symptoms were recorded in a daily diary. Patients in the treatment group had significantly fewer colds than patients in the placebo group who had also a longer duration of symptoms.
Pre-eclampsia and complications
A Cochrane review identified one single-blind study that showed not clear difference between garlic and placebo in the risk of developing gestational hypertension or pre-eclampsia (32).
Therapeutic doses may interfere with existing hypoglycaemic and anticoagulant therapies and may potentiate the effects of antithrombotic medications. There are no experimental or clinical reports of adverse effects during pregnancy, but high doses should be avoided.
Keywords: cholesterol; hypertension; Platelet aggregation; neurological diseases; liver diseases; allergy; arthritis; common cold; pre-eclampsia
There is currently no EMEA monograph for garlic
1. Amagase, H. (2006). J Nutr 136(3 Suppl.), 716S–725S
2. Kimbaris, A.C., Siatis, N. G., Daferera, D. J., Tarantilis, P. A., Pappas, C. S., & Polissiou, M. G. (2006). Ultrason Sonochem 13(1), 54–60.
3. Block, E. (1985). Sci Am 252(3), 114–119.
4. European Scientific Cooperative of Phytotherapy. Monographs on the medicinal uses of plant drugs: fascicules 1 and 2 (1996), F., 4 and 5 (1997), Fascicule 6 (1999). Exeter: European Scientific Cooperative of Phytotherapy.
5. Barnes, J., Anderson, L. A., & Phillipson, D. J. (2007). Herbal Medicines. London: Pharmaceutical Press, 279–289.
6. Zeng, T., Guo, F. F., Zhang, C. L., Song, F. Y., Zhao, X. L., & Xie, K. Q. (2012).. J Sci Food Agric 92(9), 1892–1902
7. Gebhardt, R. (1993). Lipids 28(7), 613–619.
8. Liu, L., & Yeh, Y. Y. (2001). . Lipids 36(4), 395–400.
9. Yeh, Y. Y., & Yeh, S. M. (1994). Lipids 29(3), 189–193.
10. Yeh, Y. Y., & Liu, L. (2001). . J Nutr 131(3s), 989S–993S.
11. Ried, K., Frank, O. R., & Stocks, N. P. (2010). Maturitas 67(2), 144–150.
12. Koenitzer, J. R., Isbell, T. S., Patel, H. D., Benavides, G. A., Dickinson, D. A., Patel, R. P., et al. (2007). Am J Physiol Heart Circ Physiol 292(4), H1953–H1960.
13. Sivarajah, A., McDonald, M. C., & Thiemermann, C. (2006). Shock 26(2), 154–161.
14. Zhao, W., Zhang, J., Lu, Y., & Wang, R. (2001). EMBO J 20(21), 6008–6016.
15. Benavides, G. A., Squadrito, G. L., Mills, et al (2007). Proc Natl Acad Sci U S A 104(46),17977–17982.
16. Pierre, S., Crosbie, L., & Duttaroy, A. K. (2005). Platelets 16(8), 469–473.
17. Qi, R., Liao, F., Inoue, K., Yatomi, Y., Sato, K., & Ozaki, Y. (2000). Biochem Pharmacol 60(10), 1475–1483.
18. Ray, B., Chauhan, N.B., & Lahiri, D. K. (2011a). Curr Med Chem 18(22), 3306–3313.
19. Ray, B., Chauhan, N.B., & Lahiri, D. K. (2011b). J Neurochem 117(3), 388–402
20. Kim, J. M., Chang, N., Kim, W. K., & Chun, H. S. (2006). Biosci Biotechnol Biochem 70(8), 1969–1971.
21. Atif, F., Yousuf, S., & Agrawal, S. K. (2009). Brain Res 1265,128–137.
22. Ashafaq, M., Khan, M. M., Shadab Raza, S., Ahmad, A., Khuwaja, G., Javed, H., et al. (2012). Nutr Res 32(2), 133–143.
23. Javed, H., Khan, M. M., Khan, A., Vaibhav, K., Ahmad, A., Khuwaja, G., et al. (2011). Brain Res 1389, 133–142
24. Garcia, E., Villeda-Hernandez, J., Pedraza-Chaverri, J., Maldonado, P. D., & Santamaria, A. (2010). Phytomedicine 18(1), 65–73.
25. Nencini, C., Franchi, G. G., Cavallo, F., & Micheli, L. (2010). J Med Food 13(2), 329–335.
26. Kishimoto, R., Ueda, M., Yoshinaga, H., Goda, K., & Park, S. S. (1999). J Nutr Sci Vitaminol (Tokyo) 45(3), 275–286.
27. Gedik, N., Kabasakal, L., Sehirli, O., Ercan, F., Sirvanci, S., & Keyer-Uysal, M. (2005). Life Sci 76(22), 2593–2606.
28. Chung, L. Y. (2006). J Med Food 9(2), 205–213.
29. Kyo, E., Uda, N., Kasuga, S., & Itakura, Y. (2001). J Nutr 131(3s), 1075S–1079S.
30. Williams, F. M., Skinner, J., Spector, T. D., Cassidy, A., Clark, I. M., Davidson, R. M., et al. (2010). BMC Musculoskelet Disord 11, 280.
31. Josling, P., Adv. Ther. 2001, 18, 189–193.
32. Ziaei, S., Hantoshzadeh, S., Rezasoltani, P., Lamyian, M., Eur. J. Obstet. Gynecol. Reprod. Biol. 2001, 99, 201 –206.