Coconut oil reduces testosterone induced prostate hypertrophy


Coconut oil reduces testosterone induced prostate hypertrophy
by Anthony Roberts

Coconut oil is generally eschewed by health conscious consumers due to its high percentage of saturated fat. However, a recent study (*conducted on rodents) gives us good reason to think that steroid users ought to consider adding it to their diets (along with other, less saturated fats, of course). In this study, Sprague-Dawley rats were separated into several groups, and administered testosterone, either with or without coconut oil (at two different doses, high and low). When the animals were sacrificed, the ones who had been given testosterone with the higher dose of coconut oil, had lower prostate weights as well as a lower prostate:bodyweight ratio. The researchers speculate that this could be as a result of the notable levels of lauric and myristic acid found in the fat (which are the same acids found in saw palmetto, which has also been used successfully to treat benign prostate growth).

J Pharm Pharmacol. 2007 Jul;59(7):995-9.
Effects of coconut oil on testosterone-induced prostatic hyperplasia in Sprague-Dawley rats.
de Lourdes Arruzazabala M, Molina V, Más R, Carbajal D, Marrero D, González V, Rodríguez E.
Source

Centre of Natural Products, National Centre for Scientific Research, Cubanacán, Playa, Havana City, Cuba. lourdes.arruzazabala@cnic.edu.au

Abstract

Benign prostatic hyperplasia (BPH) is the benign uncontrolled growth of the prostate gland, leading to difficulty with urination. Saw palmetto lipid extracts (SPLE), used to treat BPH, have been shown to inhibit prostate 5a-reductase, and some major components, such as lauric, myristic and oleic acids also inhibit this enzyme. Coconut oil (CO) is also rich in fatty acids, mainly lauric and myristic acids. We investigated whether CO prevents testosterone-induced prostate hyperplasia (PH) in Sprague-Dawley rats. Animals were distributed into seven groups (10 rats each). A negative control group were injected with soya oil; six groups were injected with testosterone (3 mg kg(-1)) to induce PH: a positive control group, and five groups treated orally with SPLE (400 mg kg(-1)), CO or sunflower oil (SO) (400 and 800 mg kg(-1)). Treatments were given for 14 days. Rats were weighed before treatment and weekly thereafter. Rats were then killed and the prostates were removed and weighed. CO (400 and 800 mg kg(-1)), SPLE (400 mg kg(-1)) and SO at 800 mg kg(-1), but not at 400 mg kg(-1), significantly reduced the increase in prostate weight (PW) and PW:body weight (BW) ratio induced by testosterone (% inhibition 61.5%, 82.0%, 43.8% and 28.2%, respectively). Since CO and SPLE, but not SO, contain appreciable concentrations of lauric and myristic acids, these results could be attributed to this fact. In conclusion, this study shows that CO reduced the increase of both PW and PW:BW ratio, markers of testosterone-induced PH in rats.

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