Coconut oil (CO) has been known for centuries to have health benefits and is now seen as a functional food. Virgin CO (VCO) is antioxidant, antimicrobial, antiviral, antihypercholesterol and antithrombotic. Cold processing of VCO conserves the chemicals of coconuts, tocopherols, sterols, and squalene. It is 48-50% saturated medium chain fatty acid (lauric oil) and short chain fatty acids (capric, caproic, and caprylic acids.
This study is of the hepatoprotective effects of virgin coconut oil prepared by, either, dried- or fermented-processed methods. First, liver injury was induced in rats with paracetamol (PCM or acetaminophen.) The liver is frequently exposed to similar injury from environmental pollutants.
Some of the rats were pretreated with silymarin, a hepatoprotective, to compare to protection from VCO. Some of the animals pretreated with VCO received VCOA (dried-processed VCO) and some received VCOB (ferment-processed VCO.) VCOB was prepared using the probiotic, Lactobacillus plantarum. After the treatments, blood tests were done and liver biopsies were performed.
The rats which received normal saline water before the treatment with PCM had a significant increase in liver weight. Pretreatment with VCOA and VCOB at 10 ml/kg blocked the increased liver weight effect of PCM. Doses of 1 and 5 ml/kg had no effect. Silymarin had the same effect as VCOA and VCOB. 10 ml/kg of VCOA and VCOB and 100 mg/kg of silymarin prevented the elevation of blood factors which indicate liver damage when elevated.
The pathology slides of the PCM rats treated with saline, or 1 ml/kg VCOA or VCOB or 5 ml/kg VCOA or VCOB showed liver inflammation. The liver of rats that received 10 mg/kg of VCOA or VCOB had nearly normal liver structure. 10 mg/kg VCOA or VCOB or 100 mg/kg silymarin increased the viability of the liver cells.
Tests of liver injury include testing for liver weight increase and for liver enzymes in the blood. Liver enzymes enter the blood through damaged cell membranes. PCM in high doses increased liver weights and caused pathology evidence of cell damage. PCM is considered safe at low doses and toxic at high doses. It causes oxidation of lipids and alteration of proteins that leads to liver cell death.
Pretreatment with VCOA or VCOB significantly reduced blood enzyme levels, similar to the known hepatoprotective herbal extract of milk thistle (Silybum marianum,) silymarin. The method of protection of VCOs is unknown. The effect of protection by VCOs was seen only at the high level of 10 ml/kg and not at lower doses.
Glutathione is an important component of cells. It helps maintain proteins and lipids in the cells. Excessive toxicity results in oxidation of the glutathione. This results in lowered cell levels of glutathione.
Other herbs reported to be of use in liver damage include Angrographis paniculata, Aquilegia vulgaris (European columbine,) Picrorhiza kurroa (titka kul,) Silybum marianum (milk thistle,) Strychnos potatorum (Therran,) and Tridax procumbens (tridax daisy.)
CONCLUSION: VCOs, whether prepared by dried technique or fermented technique are hepatoprotective by an unknown mechanism.
NOTE: Coconut oil comes from the coconut palm (Cocos nucifera.) It is good cooking oil because it has a high smoke point of 360 degrees F. It does not easily become rancid.