Coupling the cholesterol- and tumor-suppressive actions of palm oil to the impact of its minor constituents on 3-hydroxy-3-methylglutaryl coenzyme A reductase activity.

The impact of palm oil on cardiovascular disease and cancer may be explained by the mevalonate-suppressive action of constituent isoprenoid end products of plant secondary metabolism. Assorted monoterpenes, sesquiterpenes, carotenoids and tocotrienols down regulate, post-transcriptionally, 3-hydroxy-3-methylglutaryl coenzyme A reductase activity thereby modestly decreasing cholesterol synthesis and concomitantly decreasing LDL cholesterol. The reductase activity in tumor tissues differs from that of liver in being resistant to sterol feedback regulation. Tumor reductase activity retains sensitivity to the post-transcriptional regulation. As a consequence, the isoprenoid-mediated suppression of mevalonate synthesis depletes tumor tissues of two intermediate products, farnesyl pyrophosphate and geranylgeranyl pyrophosphate, which are incorporated post-translationally into growth control-associated proteins.