Felodipine is a calcium channel blocker used in the treatment of congestive heart failure, hypertension and
Raynaud’s Syndrome. Test tube studies indicate that Quercetin inhibits the enzyme in the liver that is responsible
for the breakdown of felodipine. This may result in higher, more potentially dangerous levels of felodipine in the
bloodstream, although no human reports of adverse ef ects have been reported to date.25
1. Murray M. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing; 1996. p. 320-31.
2. Beyer-Meyers A, et al. Diminished sugar cataractogenesis by quercetin. Exp Eye Res 1979; 28(6): 709-16
3. Chaudry PS, et al. Inhibition of human lens aldose reductase by flavonoids, sulindac, and indomethacin. Biochem Pharmacol. 1983; 32:
1995-98
4. Havsteen B. Flavonoids, a class of natural products of high pharmacological potency. Biochem Pharmacol 1983;32:1141-8.
5. Middleton E. The flavonoids. Trends Pharmaceut Sci 1984;5:334-8.
6. Ferrandiz ML, Alcaraz MJ. Anti-inflammatory activity and inhibition of arachidonic acid metabolism by flavonoids. Agents Action
1991;32:283-7.
7. Middleton E, Drzewiedi G. Flavonoid inhibition of human basophil histamine release stimulated by various agents. Biochem Pharmacol
1984;33:3333-8.
8. Middleton E, Drzewieki G. Naturally occurring flavonoids and human basophil histamine release. Int Arch Allergy Appl Immunol
1985;77:155-7.
9. Amella M, Bronner C, Briancon F, Haag M, Anton R, Landry Y. Inhibition of mast cell histamine release by flavonoids and bioflavonoids.
Planta Medica 1985;51:16-20.
10. Pearce F, Befus AD, Bienenstock J. Mucoal mast cells, III. Effect of quercetin and other flavonoids on antigen-induced histamine
secretion from rat intestinal mast cells. J Allergy Clin Immunol 1984;73:819-23.
11. Busse WW, Kopp DE, Middleton E. Flavonoid modulation of human neutrophil function. J Allergy Clin Immunol 1984;73:801-9.
12. Yoshimoto T, Furukawa M, Yamamoto S, Horie T, WatanabeKohno S. Flavonoids: Potent inhibitors of arachidonate 5-lipoxygenase.
Biochem Biophys Res Common 1983;116:612-8.
13. Chaundry PS, Cambera J, Juliana HR, Varma SD. Inhibition of human lens aldose reductase by flavonoids, sulindac and indomethacin.
Biochem Pharmacol 1983;32:1995-8.
14. Varma SD, Muzuno A, Kinoshita JH. Diabetic cataracts and flavonoids. Science 1977;195:87-9.
15. Elangovan V, et al. Studies on the chemopreventative potential of some naturally-occurring biovlavonoids in 7,12-
dimethylbenz(a)anthracene-induced carcinogens in mouse skin. J Clin Biochem Nutr 1994;17:153-60.
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16. Verma AK, Johnson JA, Gould MN, Tanner MA. Inhibition of 7,12-dimenthylbenz(a)anthracene and N-nitrosomethyl urea induced rat
mammary cancer by dietary flavonol quercetin. Cancer res 1988;48:5754-5758.
17. Stavric B. Quercetin in our diet: from potent mutagen to probable anticarcinogen. Clin Biochem 1994;27:245-8.
18. Larocca LM, Giustacchini M, Maggiano N, Ranelletti FO, Piantelli M, Alcini E et al. Growth-inhibitory effect of quercetin and presence of
type II estrogen binding sites in primary human transitional cell carcinomas. J Urol 1994;152:1029-33.
19. Castillo MH, Perkins E, Campbell JH, et al. The effects of the bioflavonoid quercetin on squamous cell carcinoma of head and neck
origin. Am J Surg 1989: 351-5
20. Kuo SM. Antiproliferative potency of structurally distinct dietary flavonoids on human colon cancer cells. Cancer Letter 1996;110:41-8.
21. Tarayre JP, Lauressergues H. Advantages of a combination of proteolytic enzymes, flavonoids and ascorbic acid in comparison with
non-steroid anti-inflammatory agents. Arzneim Forsch 1077;27:1144-9.
22. Hirono I, Ueno I, Hosaka S, Takanashi H, Matsushima T, Sugimura T et al. Carcinogenicity examination of quercetin and rutin in ACI rats.
Cancer Lett 1981;13:15–21.
23. Kato K, et al. Lack of promotive effect of quercetin on methlazoxy acetate carcinogenesis in rats. J Toxicol Sci 1984;9:319-25.
24. Kato K, et al. Absence of initiating activity by quercitin in the rate liver. Ecotoxicol Environ Safety 1985;10:63-9.
25. Healthnotes online. Healthnotes Inc, 2000.
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S-Adenosylmethionine (SAM)
General Features
S-Adenosylmethionine (SAM) is an important methyl donor (CH3) in the transmethylation reactions required for the
synthesis of DNA bases, creatine, glutathione, neurotransmitters (i.e. melatonin), phosphatidylcholine, and for liver
detoxification reactions.
In the body, SAM is synthesized from methionine and ATP. Methionine, required for the synthesis of SAM, is obtained
from diet, or produced from homocysteine, which accepts a methyl group (CH3) from vitamin B12; that was transferred
to vitamin B12 from folic acid originally. Thus the synthesis of methionine and SAM are primarily dependant upon an
adequate nutritional status of folic acid and vitamin B12.1,2,3
Curiously, high doses of methionine do not increase levels of SAM, but rather are associated with some degree of
toxicity.4 The most natural way to optimize endogenous synthesis of S-Adenosylmethionine is to ensure adequate
intake of folic acid, vitamin B12 and protein.3 Of clinical significance is the fact that SAM supplementation on its own
has been shown to provide significant results in depression, osteoarthritis, fibromyalgia and liver disorders.5
Clinical Applications and Mechanism of Action