Coconut oil is widely recognized as both a dietary staple and a common topical agent. Its reputation for offering various health benefits, including a natural ability to fight microbes, has driven its popularity. The commercial market offers different types of coconut oil, with the highly processed, refined version being the most common and affordable. The central question is whether this widely available refined oil retains the potent antibacterial properties associated with its unrefined counterpart.
The Key Antibacterial Components in Coconut Oil
The primary source of coconut oil’s germ-fighting ability lies in its unique fatty acid composition, dominated by medium-chain triglycerides. Specifically, lauric acid (C12) accounts for approximately 40 to 50 percent of the oil’s total fat content, making it one of the richest natural sources available.
When coconut oil is consumed or applied, the body’s enzymes, specifically lipases, hydrolyze lauric acid to form a monoglyceride called monolaurin. Both lauric acid and monolaurin are potent antimicrobial lipids. Their mechanism involves interacting with the protective lipid membrane surrounding certain bacteria. By disrupting this outer layer, they cause the bacterial cell wall to disintegrate, preventing the microbe from functioning and multiplying.
Defining Refined Versus Virgin Coconut Oil
The difference between refined and virgin coconut oil lies in the raw material and extraction methods. Virgin coconut oil is produced from fresh coconut meat, using methods like wet-milling or cold-pressing that rely on minimal heat exposure. This gentle processing preserves the oil’s natural aroma, distinct flavor, and a higher content of volatile compounds and antioxidants.
Refined coconut oil is typically extracted from dried coconut meat, known as copra. This process often involves high heat and sometimes chemical solvents to maximize oil yield. Following extraction, the oil undergoes refining, bleaching, and deodorization (RBD) to remove impurities, eliminate the strong odor, and produce a neutral flavor. This extensive processing creates an oil with a higher smoke point and a longer shelf life, making it suitable for industrial use and high-heat cooking.
Does Refining Compromise Antibacterial Strength?
The question of compromised strength centers on whether the harsh refining process damages the lauric acid content. While the RBD process strips away many volatile compounds, such as polyphenols and other micronutrients, the antibacterial power is largely preserved due to the inherent stability of the medium-chain fatty acids.
Lauric acid is a saturated fatty acid, making it chemically stable and resistant to heat degradation. The refining process, even reaching high temperatures during deodorization, does not significantly alter the oil’s primary fatty acid profile. Studies consistently show that lauric acid content remains nearly identical in refined and unrefined oils, retaining the high 40-50% concentration. Since lauric acid is the direct precursor to the active antibacterial agent monolaurin, the oil’s core ability to fight bacteria remains intact, even if the overall antioxidant capacity is diminished.
Practical Applications and Effectiveness Against Specific Bacteria
Because refined coconut oil retains its high lauric acid content, it remains effective in antibacterial applications. One common practice is oil pulling, where the oil is swished in the mouth to reduce oral bacteria. It is also frequently used topically for skin and minor wounds, allowing monolaurin to act directly on the microbial population.
The antibacterial action is most pronounced against Gram-positive bacteria, which have a single, thick cell wall easily disrupted by monolaurin. Research demonstrates efficacy against common pathogens such as Staphylococcus aureus and various Streptococcus species. However, coconut oil shows minimal effectiveness against Gram-negative bacteria, such as Escherichia coli and Salmonella typhi. These bacteria possess a complex outer membrane that shields their cell wall, making them more resistant to the disruptive action of the fatty acids.