Although I told you where to get the naringin product, remember at the time I also advised against it in favor of whole grapefruit juice or extract. They don't know exactly which compound inhibits the P450 enzyme/CYP3A4 isomer, so you are better to take the juice/extract.
Studies that I have read say that ingestion of one 8oz double-strength/16oz regular strength with a compound, or three 8 oz glasses throughout the day (for a constant increased environment) will do the trick. One study I have read makes the supposition that grapefruit extract would work the same way, although it didn't actually test the theory.
However, don't forget, it will also delay/block absorption of certain classes of compounds that are sensitive to increased p-glycoprotein (a side-effect of grapefruit ingestion). So be careful if you are on other pharms/herbs.
Here's a tip: in addition to getting 100% grapefruit juice, get the bitterest brand you can buy; naringin/naringenin (which may be entirely or partly responsible for the effect we are looking at) has a very bitter taste -- many producers use enzymes to destroy the naringin/naringenin content in grapefruit juice to make it more palatable to the consumer.
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Interaction between drugs and grapefruit juice results in an increase in the oral bioavailability of drugs. For instance, the consumption of grapefruit juice led to a marked reduction of CYP3A4 activity in the small intestine and was associated with a five times increase in felodipine Cmax and tripled mean area under the curve (AUC) [3 and references therein]. However, the active components responsible for in vivo inhibition of CYP3A4 activity have yet to be fully determined. The predominant flavonoid in grapefruit juice is naringin and is likely to be one of the components in grapefruit that affects drug metabolism. In vitro studies reveal that flavonoids can inhibit microsomal oxidation of felodipine as well as nifedipine (12,13). However, naringin appears to be a weak inhibitor of microsomal felodipine oxidation and its aglycone, naringenin, may be a much more potent inhibitor (12). An in vivo study has demonstrated that the increase in felodipine AUC by naringin solution was much less than that observed with grapefruit juice, indicating that other factors were important (14). Further investigation using a naringin capsule formulation resulted in no change in mean or individual nisoldipine pharmacokinetics compared with water (15). A similar phenomenon occurs with quercetin, which is an inhibitor of CYP3A4. No in vivo inhibition of CYP3A4 mediated metabolism of nifedipine is produced after ingestion of a high dose of quercetin (16).
Recent studies have shown that in addition to flavonoids, other compounds in grapefruit juice might be involved in the drug interaction. A furanocoumarin, 6',7'-dihydroxybergamottin was currently found to be a potent inhibitor of CYP3A4 in liver microsomes (17). Several components of grapefruit juice were isolated from extracts with ethyl acetate and found to be inhibitors of human liver microsomal CYP3A4. These compounds were identified as furanocoumarin derivatives (18). Later, analysis of ethyl acetate extracts from grapefruit juice revealed the presence of several furanocoumarins of which bergamottin, the parent compound of 6',7'-dihydroxybergamottin, is the major one and was found to be a mechanism-based inactivator of CYP3A4 in human liver microsomes (19). Other components of grapefruit juice may also contribute to the interaction with CYP3A4. The other non-flavonoid components found in grapefruit juice such as limonin and obacunone, a triterpene-derived product, also reduced microsomal testosterone 6b-hydroxylation in human liver (18). ((What does this mean?))
12.
Guengerich, F.P. and Kim, D.H.,_ In vitro inhibition of dihydropyridine oxidation and aflatoxin B1 activation in human liver microsomes by naringenin and other flavonoids. Carcinogenesis, 11: 2275-2279, 1990.
13.
Miniscalco, A., Lundahl, J., Regårdh, C.G., Edgar, B. and Eriksson, U.G.,_ Inhibition of dihydropyridine metabolism in rat and human liver microsomes by flavonoids found in grapefruit juice. J Pharmacol Exp Ther, 261:1195-1199, 1992.
14.
Bailey, D.G., Arnold, J.M.O., Munoz, C. and Spence, J.D., Grapefruit juice-felodipine interaction: mechanism, predictability, and effect of naringin. Clin Pharmacol Ther, 53:637-642, 1993.
15.
Bailey, D.G., Arnold, J.M.O., Strong, H.A., Munoz, C. and Spence, J.D.,_ Effect of grapefruit juice and naringin on nisoldipine pharmacokinetics. Clin Pharmacol Ther, 54:589-594, 1993.
16.
Rashid, J., Mckinstry, C., Renwick, A.G., Dirnhuber, M., Waller, D.G. and George, C.F.,_ Quercetin, an in vitro inhibitor of CYP3A4, does not contribute to the interaction between nifedipine and grapefruit juice. Br J Clin Pharmacol, 36:460-463, 1993.
17.
Edwards, D.J., Bellevue, F.H. and Woster, P.M., Identification of 6',7'-dihydroxybergamottin, a cytochrome P450 inhibitor in grapefruit juice. Drug Metab Dispos, 24:128-129, 1996.
18.
Fukuda, K., Ohta, T. and Yamazoe, Y., Grapefruit component interacting with rat and human P450 CYP3A: possible involvement of non-flavonoid components in drug interaction. Biol Pharm Bull, 20: 560-564, 1997.
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