BITTER MELON (Momordica charantia): This edible gourd should be every physician’s “go-to” plant for the 16 million or more Americans with high-normal glucose readings or ‘boderline diabetic/metabolic syndrome patients.
Preliminary evidence suggests bitter melon’s hypoglycemic action can be explained through several independent mechanisms: for one, it has been shown to increase peripheral glucose oxidation as well as glucose tolerance and insulin signaling in induced insulin resistance models (Sridhar MG, et al: Br J Nutr. 2008;99(4):806-12. Basch E, et al. Am J Health Syst Pharm. 2003;60:356-9). It also decreases hepatic gluconeogenesis, while increasing glycogen synthesis.
Bitter Melon increases insulin output from the pancreas, and it also provides a unique compound called polypeptide-P, which is an insulin mimetic with a similar structure to bovine insulin (Krawinkel MB, Keding GB. Nutr Rev. 2006;64(7 Pt 1):331-7).
Bitter Melon slices.
Compounds produced by this intriguing gourd have been shown to reduce triglyceride levels in a dose-dependent manner in animal trials (Jayasooriya AP, et al. J Ethnopharmacol. 2000;72:331-6). Though we don’t yet have human data corroborating this effect, the animal studies suggest that bitter melon may have a role in reducing cardiovascular risk, particularly in people with diabetes or metabolic syndrome.
Bitter melon products are typically standardized to their constituents, momordicosides and charantin, and usually dispensed in 500-600 mg doses, twice daily, following meals. As it does have an insulin mimetic action, it may be necessary to adjust the dose of concurrently prescribed hypoglycemic drugs.