Busting Biofilms - Monolaurin and Biofilm Control

Last Updated: March 28, 2019 | First Published: July 9, 2018
Reviewed by: Dr. Ahmed Zayed, M.D.

Monolaurin Biofilm Disruptor

Busting Biofilms

By forming a collective in biofilms, bacteria and fungi survive and guarantee their growth and expansion [Ref #1]. Bacteria and fungi thrive in biofilms because of the large number of species present -allowing the biofilm to endure and adapt. If a toxic substance is presented, the biome mutates by choosing the most adaptable species which often leads to antibiotic resistance. Biofilms often cause infections that are complex, chronic, and immune to antibiotic treatment. The effects of contamination are often widespread and costly: from clinical treatment infections to outbreaks like salmonella [Ref #2] and recurring fungal infection.

Monolaurin and Disrupting Biofilms

Because of its antibiotic resistance, researchers need to look for other ways to control biofilms and monolaurin may be one of these alternative forms of treatment.

Monolaurin is a natural compound, commonly found in coconut oil, known for its antibacterial and antiviral properties [Ref #3]. Various studies have demonstrated impressive benefits of Monolaurin as a biofilm disruptor which include:

  • Prevention of diseases caused by certain types of Salmonella [Ref #4]

    • Monolaurin has been found effective in some strains of salmonella with single lipopolysaccharide layers. The lipopolysaccharide layers of biofilms are responsible for adhesion, growth, and protection of bacterial and fungal culture. Monolaurin's antibacterial properties can act as a biofilm disruptor in this layer.

  • Stops fungal growth in the mycelium by targeting digestive enzymes [Ref #5]

    • The mycelium is responsible for feeding the fungal biofilm through several digestive enzymes. Trehalose is one of the digestive enzymes responsible for both growth and adaptation. Without trehalose, the mycelium cannot get any nutrition. Monolaurin is potent against trehalose. Its antifungal properties allow it to stop both the growth and the mutation of the fungi mycelium.

  • Inhibits bacterial genes that are responsible for releasing toxins.

    • Monolaurin also fortifies host cells from toxic shock.

  • Attacks fungi and yeasts without affecting the body’s PH

    • Fungal infections in the female reproductive system are complicated to treat. Most antifungals damage the mycelium but have the side effect of destabilizing the body's PH. Monolaurin is able to destroy fungal infections without disrupting the body’s natural acidic levels.

  • Alters biofilm formation

    • By changing biofilm formation, monolaurin breaks down the defense structure of biofilms.

  • Improves immune system function

    • Biofilms' antibiotic resistance can be difficult for patients who are immunocompromised. Monolaurin has the added benefit of activating T-cells needed to fight infection without triggering autoantibodies.


Biofilm infections are complex and costly. As biofilms learn to adapt, alternative forms of treatment are necessary. Monolaurin is at the frontline of the treatment needed to disrupt biofilms. As research on the compound's properties grows, so are the chances of controlling biofilm infections.


  1. Høiby, Niels et al. “The Clinical Impact of Bacterial Biofilms.” International Journal of Oral Science 3.2 (2011): 55–65. PMC. Web. 16 June 2018.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469878/

  2. Giaouris, Efstathios et al. “Intra- and Inter-Species Interactions within Biofilms of Important Foodborne Bacterial Pathogens.” Frontiers in Microbiology 6 (2015): 841. PMC. Web. 16 June 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4542319/

  3. Seleem, Dalia et al. “ In Vitro Evaluation of Antifungal Activity of Monolaurin against Candida Albicans Biofilms.” Ed. Pankaj Goyal. PeerJ 4 (2016): e2148. PMC. Web. 16 June 2018.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924139/

  4. Mueller, Elizabeth A., and Patrick M. Schlievert. “Non-Aqueous Glycerol Monolaurate Gel Exhibits Antibacterial and Anti-Biofilm Activity against Gram-Positive and Gram-Negative Pathogens.” Ed. Gunnar F Kaufmann. PLoS ONE10.3 (2015): e0120280. PMC. Web. 16 June 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370562/

  5. Parente-Rocha, Juliana Alves et al. “Antifungal Resistance, Metabolic Routes as Drug Targets, and New Antifungal Agents: An Overview about Endemic Dimorphic Fungi.” Mediators of Inflammation 2017 (2017): 9870679. PMC. Web. 16 June 2018.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5485324/