Reasons to Love Monolaurin - by Stephen Phillips, MD
Monolaurin is a truly amazing miracle of nature. I’ve publicly professed my love for this humble coconut oil-derived marvel on many occasions because it did for me what years of the strongest antibiotics failed to do. So first I’ll describe how it helped me and then delve into the many astonishing benefits, along with an important warning, of this unassuming, easily-missed remedy for so many of life’s ills.
Monolaurin, also known as glycerol monolaurate, is a medium-chain, fatty acid molecule—Technically a 12-carbon fatty acid monoester for both of you reading this right now who think organic chemistry is cool—And it has incredible properties. In addition to the metabolic and neurologic benefits we derive from medium-chain fatty acids, monolaurin goes many steps further—It has an enormous spectrum of antimicrobial activity against disease-causing bacteria, viruses, parasites, and fungi.
Lauric acid, a close chemical cousin to monolaurin, is a medium-chain fatty acid found in coconut oil and breast milk. Although lauric acid also has in vitro antimicrobial properties, monolaurin is far more potent. As such, monolaurin is effective in vivo—It protects mice from bacterial infection, whereas coconut oil, which is rich in lauric acid, does not.
Monolaurin is naturally occurring in human breast milk at 20 times the concentration found in cow’s milk, and for good reason—We’re helpless little drooling cherubs when we’re born. In the first few months of life, our immune systems are not well-developed, leaving us susceptible to infections from pretty much everything.
How awesome of Mother Nature to provide a fix for that.
As some of you may know, but many probably don’t, I got very sick from a bug bite—My illness broke me in nearly every conceivable way. More than just disabled from the daily routines of life due to maiming arthritis in most every joint, I was bedbound for over a year, unable to walk, sit up on my own, or lift my arms against gravity. Profoundly anemic with nightly fevers to 102F, and having lost 50 lbs, my resting heart rate was 120, going up to 180 with attempts to stand. Despite having told my story publicly so many times, it’s still difficult to admit to myself that I likely skirted the edges of death for the better part of 6 months. My personal medical history is included in one chapter of Chronic, a book devoted to the exploration of the usually-undiagnosed infections that underlie and cause a broad swath of chronic illnesses, most of which are often labeled as autoimmune.
Autoimmune diseases are veritable black holes in medical science. My diagnoses, most of which were “autoimmune,” included spondylitis, rheumatoid arthritis, uveitis, hemolytic anemia, fever of unknown origin, and POTS, among so many others. All are descriptive diagnoses, which means that they paint a picture of an illness but bring us no closer to figuring out its root cause. It’s shocking for most people to learn what chronic infections, many spread by bug bites (termed vector-borne infections), can do.
Happily, the majority of those who contract one or more of these myriad infections will never get as sick as I did. We’re evolutionarily adapted to fight them off fairly well—But still, there are tipping points. Many of us will be asymptomatic or minimally symptomatic until acquiring yet another, often more virulent, infection,—The straw that breaks the camel’s back—Or until something dysregulates our immune response, like Covid can do.
In my experience, reactivation of previously asymptomatic chronic infections is turning out to be a significant contributor to Long Covid. One example of a common, chronic bacterial infection spread by bug bites, which spans the continuum from asymptomatic to potentially fatal disease, is bartonellosis:
“Bartonellosis are diseases caused by any kind of Bartonella species. The infection manifests as asymptomatic bacteremia to potentially fatal disorders.”
I’m not saying that SARS-Cov2 isn’t sticking around in Long Covid patients, as there’s good evidence that it does. But I am saying that what we are recognizing as Long Covid is a complex process, likely involving multiple reactivated infections due to the immune dysregulation from persistent SARS-Cov2.
Long Covid has given scientists a window seat into the looking glass of chronic illness—They just have to peer deeply, past their own reflections—To see what lurks beneath.
Once the unseen is recognized, monolaurin becomes more valuable than gold and diamonds. To me, it’s like a trusted friend.
As I was getting sick, I noticed that I’d worsen each afternoon. It would begin each day with pain at 2:00 pm. By 4:00 pm I was forced to retreat to bed, my memory foam prison, lying flat under two blankets, alternately shaking with cold or drenched with sweat. And there I would lie, on the brink of consciousness, racked with pain for several hours until at last symptoms would relent on their own by around 10:00 pm. Such was my life for almost two years.
When I finally puzzled out my illness and how to treat it after 25 doctors failed me, several antibiotics were effective after over a year’s worth of others were a miserable waste of time. I got my life back and returned to medical practice in 2013, but I still couldn’t completely shake my afternoon flares. Albeit much tamed in both severity and duration since antibiotics, I’d still get daily chills, like I was coming down with the flu, at 2:00 pm each day and by about 6:00 pm they were gone.
Since more of the antibiotics that had helped me didn’t resolve these remaining afternoon chills, I just accepted that this was my life going forward. It was far better than having been bed-bound, plagued by what I could only describe as malaria-like symptoms. And for that I was grateful.
Then in about 2016, my brother Jeff, may he rest in peace, recommended monolaurin to me. I’d never heard of it. When I asked how he knew about it, he just said, “I know things.” He was an attorney—I’m still not sure how he found out about it, but I’m forever thankful that he did.
When I took monolaurin, I experienced a flare of chills and flu-like symptoms so severe that I had to stop it after 2 days. Along with the chills, I also had a recurrence of severe heartburn (GERD) which prompted me to resume prescription meds for it that had long since been discontinued.
GERD was an old symptom of mine that I’d almost forgotten—I didn’t include all the details of my illness in Chronic because my personal story was too long to fit into a single chapter—It could have been its own book. So I won’t be able to include them all here either, but to summarize—When I got sick, in addition to everything else I went through, I also developed abdominal pains that wrenched me into a fetal position, severe GERD, and IBS symptoms. When I was treated with antibiotics that didn’t help my illness, my GI symptoms didn’t improve. When I found antibiotics that did help my illness, they helped everything, including my GI symptoms. GERD was a thing of the past for several years, until monolaurin brought it roaring back.
Given that this wasn’t my first rodeo, I recognized that both the chills and the GERD were part of a herxheimer reaction, a worsening of symptoms upon starting antibiotics in the setting of certain bacterial infections. Herxheimers have been stereotypically attributed to the treatment of spirochetal infections such as Lyme, syphilis, relapsing fever, and leptospirosis, but they’re also known to occur during the treatment of bartonellosis, brucellosis, Q fever (coxiella), and some other infections.
Not being a fan of suffering, but very much impressed with the severity of the herxheimer, I decided to re-treat with monolaurin, but starting at only a tiny dose and going up slowly—It comes as granules so it was very easy to titrate up. In this way, it was a painless experience for me, and after about 6 weeks or so, I was up to full dose and stayed on it for a while. About a month later, I looked at the clock one day, shocked to see that it was 4:00 PM and I didn’t have chills. Oh, and my GERD was gone too, this time for good.
(One important observation—Monolaurin capsules don’t work well in my experience, even at equivalent doses to the granules. I’m not sure why, but I think it may have something to do with the granules being sealed, possibly limiting oxidative degradation.)
I remember being stunned that this inexpensive, over the counter supplement did what so many powerful, expensive, and potentially dangerous antibiotics could not. As epiphanies go, this one ranked fairly highly. So I read everything I could about this inconspicuous substance, ruminated a bit about its presence in breast milk, and it all started to make sense. There’s a connectedness to how monolaurin works, an elegance that’s been honed over eons of evolution.
It’s rare in medicine that I stumble upon a win-win-win scenario. This is one of those times. Monolaurin is a cheap, readily available, non-prescription supplement that destroys a broad range of disease-causing bacteria, yet unlike almost all antibiotics, it has minimal to no impact on the beneficial bacteria of our microbiome. To the contrary, in animal studies across species, monolaurin has been demonstrated to upregulate the presence of beneficial GI flora.
Monolaurin not only has well-documented in vitro antibacterial action against a range of disease-causing bacteria, including Lyme and H. pylori bacteria, it also blocks some bacteria from producing toxins and chemicals involved in antibiotic resistance.
The very mechanism by which monolaurin destroys microbes is entirely different from how antibiotics work. The antibacterial actions of antibiotics are diverse, but they share one thing in common—Precision. By working on small but critical parts of bacterial processes—For example by inhibiting one specific part of the functioning of a ribosome—Antibiotics unfortunately allow for the development of resistance via mutation.
Monolaurin is horse of a different color. It works by disrupting the lipid membranes of microbes—Think of it like soap, because it works in a similar way. When you wash your hands, you’re disinfecting the majority of pathogens on your hands—A full onset attack against their lipid membranes, as opposed to the smart bomb effect of antibiotics. And so, like soap, monolaurin is not poised to foster bacterial resistance. Even when used at sub-therapeutic concentrations for over a year in vitro, monolaurin did not allow the development of resistance against it in Staph aureus, a bacteria which is notorious for its ability to develop antibiotic resistance.
In all these years of people washing their hands, soap-resistant pathogens have not become a major problem—The same should hold true for monolaurin. If it works, it should continue to work.
And because of its unique soap-like mode of action, it’s also active against a range of biofilms, the importance of which cannot be overstated—Bacteria within biofilms are up to 5000 times more resistant to antibiotics compared to the same bacteria floating freely—So this is a very big deal.
Like anything in medicine, monolaurin isn’t helpful for everyone—But out of all the supplements I’ve come across, this has been one of the most useful for my patients and myself.
In Part 2, I’ll be reviewing the antiviral, antiparasitic, antifungal, and immunomodulatory actions of monolaurin
This is Part 2 of my series professing my love for monolaurin, a substance made from coconut oil which has extraordinarily broad antimicrobial activity—Against bacteria, viruses, parasites, and fungi. Yet precise when it needs to be, it spares the beneficial bacteria of our microbiome. The breadth and selectivity of its reach is impressive, but how it works is even more so—Not at all like antibiotics, it doesn’t allow for the development of antimicrobial resistance.
It’s no wonder that monolaurin is naturally occurring in breast milk, to lend a helping hand when our immune systems are under-developed. This inexpensive, over-the-counter supplement truly is a little marvel of evolution.
For context, please start reading in Part 1, where I give an overview of monolaurin, my personal experience with it, and describe its discerning antibiotic action against almost exclusively disease-causing bacteria. Here in Part 2, I’ll review its antiviral activity, which is kind of awe-inspiring.
I’d planned on including its antifungal, antiparasitic, and immunomodulatory effects here as well, but I ran out of room—The viral contribution to chronic illness is just so large that it became an article unto itself—So I’m looking forward to including the antifungal, antiparasitic, and immunomodulatory data in Part 3. Hopefully it will fit and I won’t need a Part 4.
As of this writing, emergency rooms have been crowded with a surge of patients suffering from respiratory viral infections, largely influenza and RSV. Add in another wave of Covid and you’ve got what they’re calling a ‘tripledemic’—Covid, flu, and RSV:
“Hospitals across the U.S. are grappling with Covid, flu and RSV cases in a situation that’s pushing doctors and nurses to the brink.”
If only there was a cheap, safe, over-the-counter product that had antiviral activity against all three of these viruses. If only…
For the past 80 years, it’s been well-known that lauric acid, the fatty acid from which monolaurin is made, has in vitro antiviral activity against influenza. More recent data has shown lauric acid’s activity against RSV in an animal model. And since lauric acid has generally less potent antimicrobial action than its famous monoglyceride derivative, if you’d assumed that monolaurin has powerful activity against RSV and multiple strains of both influenza A & B—You’d be right. That data is explored in the paragraphs below.
But what about Covid? I remember at the start of the pandemic when The Integrated Chemists of The Philippines made the bold and prescient recommendation that coconut oil and its derivative monolaurin should be considered for the treatment of Covid.
Coronaviruses are enveloped, so it makes sense that monolaurin would work against the entire family—Covid included. Compatible with this, out of dozens of potential Covid treatments tested, computer modeling predicted monolaurin to have stronger activity against SARS-CoV2 than almost all others.
At around that same time, research conducted in The Philippines demonstrated efficacy of virgin coconut oil (VCO), which is about 50% lauric acid, against SARS-CoV2:
“results from the Philippines Department of Science and Technology (DOST) laboratory studies on VCO and COVID-19, which found that VCO decreased viral load for mild to moderate cases of COVID-19 60 to 90%.”
About a year later in 2021, a randomized controlled trial of VCO in Covid patients demonstrated quicker resolution of illness along with a lowering of the C-reactive protein (CRP), which is known to be a marker for Covid severity:
“VCO group showed more rapid relief from symptoms of COVID-19 and a significant higher reduction in mean CRP levels compared to the Control group after 28 days.”
And around that same time in 2021, further supportive evidence of monolaurin’s activity against Covid continued to accumulate from other sources as well—In an article from the medical journal Nature—Higher monolaurin blood levels were found to be associated with better outcomes in the midst of the first Covid wave in Italy:
“Circulating monolaurin, which has well-known antiviral and antibacterial properties, was higher in protected subjects, suggesting a potential defensive role against SARS-CoV-2 infection…monolaurin levels were twice as high in subjects protected from SARS-CoV-2 infection.”
For decades, the scientific community has known that monolaurin has broad in vitro antiviral activity against enveloped viruses—It was tested against 14 of them over 40 years ago in the now famous work of Hierholzer and Kabara.
And the results demonstrated remarkable antiviral activity:
“Monolaurin is a monoglyceride of lauric acid and is a naturally occurring fatty acid ester with general antibacterial and antifungal properties…we felt it was important to measure the virucidal effects of these compounds on representatives of the major groups of human enveloped (lipid-containing) viruses…all viruses were reduced in infectivity by >99.9%.”
Other researchers have found similar findings for medium-chain monoglycerides (i.e. monolaurin):
“Medium-chain saturated and long-chain unsaturated fatty acids inactivated visna virus and other enveloped viruses causing more than a 3000-fold to 10,000-fold reduction in virus titer. 1-Monoglycerides and ethers of medium-chain fatty acids were more antiviral than the corresponding free fatty acids. Antiviral fatty acids were found to affect the viral envelope, causing leakage and, at higher concentrations, a complete disintegration of the envelope and the viral particles.”
Visna virus, a retrovirus, is a cousin to HIV. It causes a slowly progressive, invariably fatal disease in sheep. Retroviruses are some of the most mysterious and scary viruses out there—It’s comforting to know that they may have an Achille’s heal, or more aptly an Achille’s envelope—Susceptible to the action of monolaurin.
In a study reproducing the findings of Hierholzer and Kabara in regard to monolaurin’s activity against HSV-1, researchers also found that monolaurin has powerful antiviral action against vesicular stomatitis virus (VSV), a cousin to the infamous rabies virus. So of course I began wondering if monolaurin has ever been used as an adjunctive treatment for rabies—I couldn’t find any data on its use, but given the nearly 100% lethality of rabies once symptoms develop—Why the hell not?
An important take-home message is that just like baldness or eye color in people, traits run in viral families too. If monolaurin affects one or two viruses of a family, it’s likely to have impact against other members of the extended family-tree as well. For example, monolaurin has antiviral activity against HIV, mumps, yellow fever, and Zika viruses in vitro—Is there a pattern here?
Well since visna virus is a retroviral cousin to HIV, I think that it was predictable that monolaurin would have action against HIV as well. To extend this further, both yellow fever and Zika viruses are from the same viral family, so could we make the prediction that monolaurin would work against another member of that family, like hepatitis C virus (HCV)?—Yes, I think so—Unsurprisingly, lipids from human breast milk inactivate HCV.
I remain humbled by what we already know about monolaurin—That it has activity against an enormous list of disease-causing enveloped viruses. But I’m even more impressed by its potential—It’s thought work against enveloped viruses in general, a phenomenally large group—The vast majority of which have never been tested for monolaurin susceptibility.
I’d say that safe, broad-spectrum antivirals with direct antiviral activity are rare, but they’re more than that—They’re unicorns. That’s part of the many reasons why monolaurin is so ridiculously impressive.
Innocuous antivirals are hard to find because it’s difficult to isolate and target viral processes from those of the infected host cell:
“Why are there so few antivirals? The answer boils down to biology, and specifically the fact viruses use our own cells to multiply. This makes it hard to kill viruses without killing our own cells in the process.”
Covid has taught us many hard lessons, one of the most obvious being that we don’t have enough antivirals—And they’re not easy to come by. So to find some that act broadly across viral families, the hunt has been shifting to medications that work on host systems taken over by viruses, rather than against the viruses themselves.
The good news about herpes viruses, if there ever is such a thing to be said about this miserable viral family, is that they’re all enveloped—Which means that monolaurin may have activity against the entire group. The bad news about herpes viruses is that the diseases they stereotypically cause represent just the tips of very large icebergs—The damage they do to our species is massive and outside the scope of this article, but I’ll touch on a few biggies.
When most people think herpes, cold sores come to mind, which are caused by HSV—But a cold sore is probably the least harmful thing caused by this virus. Other viruses in the herpes family include EBV, CMV, HHV-6, and VZV. All told, these viruses are among the most common to chronically infect humans, causing a world of hurt.
Coronary artery disease, caused by atherosclerosis, is the leading cause of death in the Western world. HSV is associated with well-documented increased risks of atherosclerosis (AS) in a meta-analysis of 17 studies of HSV-1 and 7 studies of HSV-2:
“17 studies were available for meta-analysis of HSV-1 infection and AS risk and seven studies for meta-analysis of HSV-2 infection and AS risk. Subjects exposed to HSV-1 infection exhibited an increased risk of AS (OR = 1.77; 95% CI: 1.40–2.23; P < 0.001)…HSV-2 positive subjects demonstrated significantly increased AS risk (OR = 1.37; 95% CI: 1.13–1.67; P < 0.005)”
And HSV is not the only herpes virus that increases the risks of vascular disease—VZV does as well. VZV can present acutely as chickenpox and come back later in life as shingles, also known as herpes zoster (HZ).
In this study, having had HZ was associated with an increased risk of both heart attacks and stroke for up to more than a decade after an outbreak of shingles:
“HZ is associated with higher long‐term risk of a major cardiovascular event. These findings suggest there are long‐term implications of HZ and underscore the importance of prevention.”
The mechanism by which VZV increases vascular risk has been at least partially defined as being due to the upregulation of pro-inflammatory cytokines leading to clots. Sound familiar?—Similar mechanisms are involved in clotting disorders due to Covid.
And not to be outdone, CMV also likely causes vascular disease:
“…high levels of CMV antibodies were found to be associated with clinically manifest atherosclerotic disease, suggesting that a periodically activated latent infection or a continuously active infection is present in patients with atherosclerosis…Of particular significance is the recent finding that heart transplant recipients, who are immunosuppressed, and who are also actively infected with CMV, are prone to develop accelerated atherosclerosis in the transplanted organ.”
And CMV-DNA has been demonstrated more frequently in atherosclerotic plaques vs healthy tissue samples:
“The presence of CMV-DNA in aortic plaques is associated with increased risk of atherosclerosis. CMV infection may be considered as an independent risk factor for this event.”
Multiple lines of evidence link HSV to Alzheimer’s. For example, positive HSV antibodies over time, especially antibodies demonstrating reactivated infection, are associated with Alzheimer’s.
Plus, HSV-1 DNA has been demonstrated in amyloid plaques of Alzheimer’s patients’ brains:
“We discovered a striking localization of herpes simplex virus type 1 DNA within plaques…”
And in a study of 8,362 newly diagnosed HSV patients, those who went untreated had a 256% increased risk of subsequent dementia about a decade later, compared to 25,086 non-HSV controls. Of note, the use of anti-herpes antivirals prevented dementia by up to 91%, with a dose response relationship to longer durations of treatment:
“This analysis revealed an adjusted hazard ratio of 2.564 (95% CI: 2.351-2.795, P < 0.001) for the development of dementia in the HSV-infected cohort relative to the non-HSV cohort. Thus, patients with HSV infections may have a 2.56-fold increased risk of developing dementia. A risk reduction of dementia development in patients affected by HSV infections was found upon treatment with anti-herpetic medications (adjusted HR = 0.092 [95% CI 0.079-0.108], P < 0.001). The usage of anti-herpetic medications in the treatment of HSV infections was associated with a decreased risk of dementia.
And perhaps the most impressive findings yet—Researchers made a mini-brain in the test tube, introduced HSV-1 into it, and watched as changes occurred that are typical of Alzheimer’s:
“Growing evidence implicates pathogens in AD development, with herpes simplex virus type I (HSV-1) gaining increasing attention as a potential causative agent. Here, we describe a multidisciplinary approach to produce physiologically relevant human tissues to study AD using human-induced neural stem cells (hiNSCs) and HSV-1 infection in a 3D bioengineered brain model. We report a herpes-induced tissue model of AD that mimics human disease with multicellular amyloid plaque–like formations, gliosis, neuroinflammation, and decreased functionality”
Whereas the causal link between HSV and Alzheimer’s has been strong, data linking VZV with dementia has been inconsistent. Although VZV vaccination is associated with a reduction of dementia, implying that VZV may play a role, VZV infection itself has not been conclusively linked.
To help clarify these discrepancies, the same researchers who studied HSV-1 in a brain model also studied VZV in a mini-brain in the test tube. They evaluated VZV both on its own, and in a co-infection model with HSV-1. They found that in contrast to HSV-1, VZV did not induce the classic Alzheimer’s findings—But they found that VZV could reactivate a silent HSV-1 infection, thus inducing HSV-1 to cause changes typical of Alzheimer’s:
“Cells infected with VZV did not show the main AD characteristics, Aβ and P-tau accumulation, which HSV-1 does cause, but did show gliosis and increased levels of pro-inflammatory cytokines, suggesting that VZV's action relating to AD/dementia is indirect. Strikingly, we found that VZV infection of cells quiescently infected with HSV-1 causes reactivation of HSV-1 and consequent AD-like changes, including Aβ and P-tau accumulation.”
Epstein-Barr Virus (EBV) infects greater than 90% of the world’s adult population. When most people think EBV, infectious mononucleosis (mono) comes to mind, as EBV is the most common cause of mono. Although mono is much worse than a cold sore, it too is just the tip of the iceberg of the damage EBV can do.
EBV infection has been closely linked to the development of multiple sclerosis (MS):
“The findings strongly suggest that EBV is part of the chain of events that leads to most cases of MS. However, EBV in itself is not sufficient to trigger MS.”
“Part of the chain of events” means that EBV on its own is not associated with MS—Mono is the key. In developed countries, where EBV infection is typically delayed until adolescence, it often causes mono. Rates of MS are 20-40 times higher in developed countries than those were EBV infection occurs in early childhood, when it only causes mild illness. Please check out MS—The Infection Connection, Part 1 and Part 2, to go for a deep dive into this topic.
EBV is very adept at causing cancer—Thankfully, the human immune system is fairly well-suited to picking off these cancers before they can establish a foothold, but unfortunately 100,000’s of cancers still arise each year globally from EBV. “Seemingly innocent” is an appropriate way to describe this incredibly nasty virus:
“Epstein-Barr virus (EBV), a gamma-1 herpesvirus, is carried as a life-long asymptomatic infection by the great majority of individuals in all human populations. Yet this seemingly innocent virus is aetiologically linked to two pre-malignant lymphoproliferative diseases (LPDs) and up to nine distinct human tumors; collectively these have a huge global impact, being responsible for some 200,000 new cases of cancer arising worldwide each year.”
Monolaurin has antiviral activity against HIV. The natural question that follows—Can monolaurin effectively treat HIV in patients?
In the first small study to evaluate this, monolaurin and coconut oil both demonstrated favorable effects in HIV patients. There were only 15 patients total—Five per treatment group—Two groups received monolaurin, one group received coconut oil. By the end of the study, 10 out of 15 patients had a reduced viral load and CD4+ T lymphocyte counts increased in 7 out of 15 patients.
Many years later, another small study was done—This time 40 HIV patients were divided into receiving virgin coconut oil (VCO) x 6 weeks vs control. VCO consumption led to significantly higher average CD4+ T lymphocyte counts versus control.
Research in macaques has found monolaurin to be innocuous to cervical tissue and not harmful to normal vaginal flora, even with long term use. Multiple studies of intra-vaginal monolaurin have demonstrated that macaques were protected from repeated high dose exposures to SIV, the monkey virus analog to HIV.
“This larger and more extensive study of GML as a topical microbicide documents its previously reported efficacy against repeated high-dose vaginal challenge in the SIV-rhesus macaque non-human primate model of HIV-1 transmission to women…We chose this exceptionally rigorous high dose challenge, rather than repeat low dose exposures…The 2x109 copies of SIV RNA in our challenges was two orders of magnitude higher than the highest semen levels of 107 copies of viral RNA/ml associated with high rates of transmission… For comparison, while topical integrase inhibitors have recently been reported to protect 5/6 macaques against repeat low dose vaginal challenges, the challenge doses used were ~ 1000 fold lower than the ones we used in the high dose challenges.”
Even a cursory review of the scientific literature indicates that monolaurin has immense potential against a wide array of important viruses. And the medical field is profoundly lacking broad spectrum antivirals, so you’d think that this would be shouted from the rooftops. But monolaurin has barely been studied in human clinical trials. I’m no fan of big pharma—This is one of the many reasons.
If monolaurin was patentable, I don’t think you’d have enough fingers and toes to count all the large randomized controlled trials that would be done evaluating this amazing gem against all sorts of acute and chronic viral infections. But there’s no money in it, and so they likely won’t be done unless we have a foundational shift in how research is performed in the world—Not holding my breath.
My 2-cents from clinical practice—I’ve seen many patients over the years derive great benefits from the use of monolaurin for recurrent cold sores, as well as chronic bacterial infections.
From my personal and professional experience, as well as the existing medical research, I think monolaurin is amazing—I just wish things were different and it could have its moment to shine in large, well-designed human trials.
Join me in Part 3 to explore monolaurin’s antifungal, antiparasitic, and immunomodulatory effects
What’s so special about monolaurin? Well, how much time ya got?
What I thought would be a short article about one of nature’s impressive little marvels, turned into a multi-part series—The more I researched this amazing substance, the more profound my admiration for it became.
So welcome to Part 3 of this longform piece about what might just be the most under-promising, over-delivering, easy-to-fall-in-love-with supplement out there.
And although I had meant for this to be the final installment for this series, Substack just sent me that note again—”Post too long for email”—so I’ve broken this into a Part 3 and a Part 4 to stay within the email limit.
Part 3 focuses on monolaurin’s antiparasitic activity & Part 4 will be all about monolaurin’s antifungal and immunomodulatory actions. But please start reading at Part 1 for important context if you’re new to this series.
I’ve often said that if I wasn’t a doctor, I’d do something professionally with monolaurin, EMDR, or Costco (Who doesn’t like Costco?—Just check out their return policy—90 days, even for electronics!!)—Such is my passion for all three. No, I’m not employed by Costco—If only…
But my love for monolaurin runs deep—As reviewed in Part 1, its amazingly selective antibacterial action results in the destruction of disease-causing bacteria while sparing the beneficial ones of our microbiome. And as reviewed in Part 2, its remarkably broad-spectrum antiviral activity against a huge array of enveloped viruses, examples of which include Covid, influenza, RSV, all herpes viruses, HIV, and countless others, is almost the stuff of legend. And here in Part 3, I’ll review its antiparasitic actions.
Monolaurin has got to be one of the hardest working supplements on the planet.
Public health misdeeds come in different flavors, all of them unpalatable. A ubiquitous scourge on our species that goes unnoticed—That tastes bad enough. But when it’s actively ignored, even mocked, resulting in serious health consequences—There’s not enough sugar in the world to coat that bitter pill.
I only became aware that US physicians dismiss domestically-acquired parasitic infections with a collective sigh of boredom while writing Chronic. We interviewed countless infectious disease researchers, and I kept hearing the same refrain—In developing countries, parasitic infections are taken seriously, but in the US they’re ignored. And they’re right—Trying to find a US parasitologist who tries to puzzle out these infections is like trying to find a 1980 Fiat without rusted fenders.
Parasitic infections are so overlooked here that they’re actually referred to as “neglected” diseases in medical parlance:
“Chagas disease, cysticercosis, and toxoplasmosis affect millions of people in the United States and are considered neglected parasitic diseases. Few resources are devoted to their surveillance, prevention, and treatment.”
Initially I found it hard to believe that docs would turn a blind eye to such potentially serious infections, but then it all clicked. I’ve sometimes wondered why patients report that the discussion of parasitic infections occurs almost exclusively in the alternative medicine realm—But where else could it occur? When patients ask their primary care docs about the possibility of parasitic infections, I hear that it’s often met with an eye roll.
Parasitic infections are legion— Some being among our most deadly and difficult to treat diseases—They constitute an enormous global health burden:
“Parasites are extremely common, and are responsible for some of the world's most deadly illnesses, from dysentery and diarrhea to malaria…It's estimated that at least half of all known species are parasitic…cause millions of deaths and billions of infections in humans every year…”
So why, despite causing widespread disability and death—Certainly deserving of not only our respect, but also our awe and righteous concern—Are parasites the Rodney Dangerfield of infectious diseases?
“With my doctor, I don't get no respect. I told him I want a vasectomy. He said with a face like mine, I don't need one.”—Rodney Dangerfield
Parasites are not only common in the United States, they cause significant disease. Ok, so we don’t have sleeping sickness or elephantiasis like they do in Africa—It’s not a contest—But we do have many parasitic infections in the US that result in public health ramifications. It’s bad enough that acute parasitic infections are missed and dismissed on a regular basis—The status of chronic disease related to parasitic infection is even worse—It’s completely off the radar screens of almost all docs.
For example, to focus on one of the many parasites we have in the United States for a second—Toxoplasmosis is common, globally distributed, infecting about 33% of the world’s population and 11% of the US population. Yet in the US, this disease is still described by the tip of its iceberg—Usually a mild clinical course in people with normal immune systems and potentially life-threatening in immunocompromised folks. But toxoplasma sets up lifelong infection, even in immunocompetent people—What’s it doing during that time?
It’s been known for decades that parasitic infections result in immunosuppression. When we talk about suppressing the immune system, the first thing that usually comes to mind is the increased risk of acquiring routine infections. For example, mice harboring chronic toxoplasmosis are more susceptible to sepsis than control mice. But does this happen in humans?—I think it could—Toxoplasma is a single-celled parasite which is a distant cousin to malaria. And malaria, which is proven to induce immunosuppression in humans, also increases the risk of human sepsis.
Immune suppression from parasites is also notably important from the perspective of the multiple infections most of us carry asymptomatically or minimally symptomatically, throughout our lives.
Take Lyme for example—20% of German’s in their 70’s are infected with Lyme bacteria. These are not people diagnosed with Lyme disease, but rather people who carry the infection without significant symptoms. What happens if they become immunocompromised, whether purposely with the use of prescription medications, or immunosuppressed by chance, by the acquisition of Covid or a parasitic infection? Do these infections become symptomatic?
And although the prevalence of Lyme is similarly high in countless areas around the world, where Lyme isn’t common there are other endemic chronic bacterial infections, such as tuberculosis, bartonellosis, brucellosis, and many others. Do these cause more disease as well when the hapless human acquires a parasite by eating a salad whose lettuce should have been washed a bit better?
We know that immunosuppression from the commonly prescribed tumor necrosis factor alpha inhibitors, Humira, Remicade, Enbrel, and Simponi, is associated with worse outcomes in the treatment of early Lyme. We also know that immune dysregulation from Covid can reactivate latent infections, and that parasitic infections result in complex and varied interactions with other infections, including bacteria, often enhancing their ability to cause disease.
A meta-analysis of 9 studies found that those with toxoplasmosis had a 3.3 times higher risk of having rheumatoid arthritis (RA), with remarkably good statistical power—The odds of this finding being a chance result would be less than 1 in 10,000. This leads to some critical questions: Does toxoplasmosis directly cause RA? Does it indirectly cause RA by inducing immunosuppression, worsening disease states due to other pathogens, like bartonella, which then cause RA? Or does immune dysregulation related to RA, and the often purposeful pharmacologic immune suppression during RA treatment, increase the likelihood of toxoplasmosis acquisition?
Such a tangled web—The complex immunologic interplay between parasites and their hosts is still poorly understood. Parasites suppress, or more accurately put, manipulate the immune response to survive—They have lots of immunologic tricks up their sleeve:
“…important strategies used by representative protozoa and helminths to overcome, evade, resist, suppress, and/or manipulate the host immune apparatus/mechanisms that are directed against them…”
The next thing that usually comes to mind when people talk about immune suppression is the increased risk for cancer. Although it’s well known that some parasites can cause certain types of cancer, they’re not usually thought to do this from the perspective of generalized immune suppression, but rather from the perspective of chronic inflammation of the areas they infect. And paradoxically, there’s evidence in mouse studies that malaria, toxoplasmosis, and infection by a parasite called neospora can have anti-cancer effects due to reversal of the immune suppression induced by cancer.
Huh?!—I thought parasites induced immune suppression—They do, but it’s not a one-way street. Parasites are adept at variably manipulating the immune response to increase their survival and procreation. This is a perfect example of why we should approach science with humility—Something many researchers don’t do on their missions to prove what they think is correct. I can imagine that a parasite infecting a host who has cancer would benefit from that host’s prolonged survival, thereby allowing the parasite time to propagate—Just my own theory—But I see an evolutionary benefit here.
And if you think that’s weird, I’ll top that. Put this one in the category of “sounds too weird to be true, but...” As per CDC:
“We were amazed when we found this new type of disease – tapeworms growing inside a person essentially getting cancer that spreads to the person, causing tumors,”
You read it correctly. Tapeworms got cancer, and then the tapeworm cancer spread to the person. In this case, it resulted in a tragic fatal outcome.
“The growth pattern was decidedly cancer like, with too many cells crowded into small spaces and quickly multiplying. But the cells were tiny – about 10 times smaller than a normal human cancer cell…eventually finding DNA from H. nana tapeworms in the man’s tumor in mid-2013. Unfortunately, the man died 72 hours later.”
And it’s not only the immune response that parasites manipulate, they have the uncanny ability to influence host behavior to further their survival—Some of which includes what I think of as creepy parasitic mind control. For example, some parasites induce crickets to commit suicide by jumping into a body of water so they can exit the body of the cricket to reproduce. Some can also force caterpillars and ladybugs to protect the parasites’ offspring.
When it comes to mammals, perhaps the most often cited example of parasitic mind control is in toxoplasmosis, which causes mice and rats to become paradoxically attracted to cat urine, making them easy prey:
The protozoan parasite Toxoplasma gondii blocks the innate aversion of rats for cat urine…In mice and rats, latent Toxoplasma infection converted the aversion to feline odors into attraction…”
And humans are not immune to parasitic infections changing our behavior. There is a hefty treasure trove of articles linking parasitic infections to psychiatric illness, yet most psychiatrists I’ve spoken to haven’t heard of it—Or if they have, it’s a vague memory from med school or a board exam question.
I can’t count the initially awkward conversations I’ve had with psychiatrists on this topic—But given that most of these doctors tend to be an open-minded bunch, the talks have usually ended with “Sounds interesting, send me any data you have.” After sending them information, this has typically been followed by a call from an excited psychiatrist a week or so later—”I had no idea that this was a thing!!”
It’s definitely a thing:
“We conducted a systematic review to try to shed some light on the association between parasite infection and mental illnesses. Our results displayed a clear relationship between the two. From the reviewed papers we found that an individual was four times more likely to develop a mental illness when testing positive for a parasite infection. Furthermore, nearly sixty percent of the overall participants from the papers with a mental illness also were infected with parasites.”
And humans are also not immune to other puppet master-like effects from parasites. Malaria parasites make infected people smell better to mosquitoes, thus increasing malaria’s transmissibility:
“The parasite that causes malaria can change the way you smell, making you more attractive to mosquitoes…”
Monolaurin and lauric acid, the fatty acid from which monolaurin is derived, have documented antiparasitic activity against a range of protozoan single-celled parasites and least one helminth parasite. In many cases, there action is comparable, or superior to, that of metronidazole, a commonly used pharmaceutical antiparasitic.
For example, lauric acid has antiparasitic activity against giardia which is about equal to metronidazole:
“…anti-giardial, with an LD50 concentration comparable to that of metronidazole, the drug of choice in the treatment of giardiasis”
Other researchers have found similar efficacy findings—Monolaurin is comparable to metronidazole in the treatment of both giardia and entamoeba in experimentally infected hamsters—And it displayed synergy with metronidazole when combined—The two together were more effective than either on its own.
These coconut oil derivatives are also effective against a range of other single-celled parasites. For example, monolaurin was more effective than metronidazole against blastocystis and lauric acid has antiparasitic activity against leishmania (although caprylic acid, also found in coconut oil and human breast milk, in this case worked better).
Lauric acid also has antiparasitic activity against Trichomonas vaginalis, a parasitic sexually transmitted infection that both women and men can acquire—Yes, men can get this infection too:
“a sexually transmitted infection associated with infertility, gestational complications, predisposition to cervical and prostate cancer, and increased risk of human immunodeficiency virus (HIV) transmission and infection. Metronidazole, the only drug available for treating, has dubious efficacy, high toxicity, it is contraindicated in first trimester of pregnancy and drug-resistant cases are increasing. Thus, there is an urgent need for the development of alternative strategies to combat trichomoniasis…Lauric acid inhibited the proliferation of T. vaginalis in a dose-dependent manner after 24h of treatment.”
This is all noteworthy because as mentioned above, metronidazole can cause significant toxicity, including altered mental status, seizures, lack of coordination, and neuropathy. It also causes cancer in rodents, which prompted a black box warning about this in its FDA prescribing information.
In regard to helminths, lauric acid destroys a type of nematode that parasitizes plants. This parasite is not known to cause human disease, but its eggs have been carried by humans in our GI tracts. I’m including this information because whereas there is a good amount of research documenting monolaurin and/or lauric acid’s antiparasitic activity against single-celled parasites, there is a dearth of research testing monolaurin against parasitic worms.
Since monolaurin’s mechanism of action against bacteria and viruses results in extraordinarily broad coverage, from the studies demonstrating antiparasitic activity against multiple different single-celled parasites, I think it’s reasonable to expect a similarly broad class effect against other single-celled parasites not yet tested. But I don’t think that the one study I found demonstrating anti-nematode activity is enough to draw any conclusions about its activity against other helminths.
We desperately need advances in the treatments for helminths, and part of that research should include testing monolaurin’s activity. So if there are any parasitologists reading this, you know what to do :)
Please join me for Part 4, where I plan to review the antifungal and immunomodulatory activity of monolaurin, coming soon.
This is the last installment of this multi-part series about one of the most fascinating supplements I’ve yet to encounter. If you’ve read the previous parts of this series, I’m sure you’ve figured out by now that I seriously love monolaurin—And I have lots of good reasons.
This inexpensive derivative of lauric acid, a primary component of coconut oil, is available without a prescription. But as it is for the best things in life, price and accessibility are not metrics for worth. And for some patients, myself included, monolaurin has been an absolute game changer, catapulting us along on the journey back to good health.
In Part 1, I cover monolaurin’s uncanny activity against only disease-causing bacteria, while sparing the beneficial ones of our microbiome. In Part 2, I review its shockingly broad antiviral activity. In Part 3, I review its promising activity against a global scourge—Parasites. And here in Part 4, I’m reviewing its antifungal and immunomodulatory actions.
These parts build upon themselves sequentially, so please start with Part 1 for the context needed to understand my affection for monolaurin. Otherwise you might be thinking, “Why is this guy oohing and aahing over this stuff? It’s nothing special.”
I don’t fawn over every supplement that comes along—Quite the opposite. When I was at my sickest, unable to even sit up in bed on my own, out of desperation I spent thousands on over-the-counter remedies that didn’t work. So truth be told, I’m a bit jaded. But monolaurin is the real deal. It doesn’t work for everyone—Nothing does—But from what I’ve seen, it’s by far one of the most the most impressive non-prescription options out there.
From nutritious food to dandruff to deadly threat, there are lots of different fungi out there. Of the 4 million or so fungal species, only about 2000 are edible. Even less, about 300, cause human disease. Some fungal infections cause only minor medical conditions—Like athlete’s foot or dandruff—But some others are killers. And we have only a few precious weapons against them:
“The four main classes of antifungal drugs are the polyenes, azoles, allylamines and echinocandins.”
And drug resistance is developing broadly against this tiny antifungal arsenal.
“The number of antifungal classes is small, and resistance is becoming a much more frequent problem”
Azoles are some of the most commonly used antifungals due to their favorable pharmacokinetic and safety profiles. But their frequent use has resulted in antifungal resistance that keeps me up at night—95% of some virulent fungal samples tested in Vietnam were resistant to azoles. This should be a wake-up call as to what awaits us soon in the rest of our very small world. High-level antifungal resistance across multiple disease-causing fungi will likely come sooner than most expect, as it’s already a grave problem here in the US with candida and aspergillus. Candida auris burst onto the world stage in 2009—Resistant to multiple antifungals, its mortality rate in the United States is a staggering 30-60%.
These fungal grenades are exploding in slow motion, unseen but everywhere, under our collective, oblivious noses.
“…there are possibly 300 million people infected with fungal diseases worldwide and 1.6 million deaths every year—more than malaria, as many as tuberculosis. Just in the U.S., the CDC estimates that more than 75,000 people are hospitalized annually for a fungal infection, and another 8.9 million people seek an outpatient visit, costing about $7.2 billion a year.”
And now for the inconvenient truth that pharmaceutical companies don’t want you to hear: Although some of these fungal infections can infect and kill patients with normal immune systems, it’s no secret that the immunocompromised are more at risk. And we’ve become a purposely immunosuppressed society. It started slowly about 15-20 years ago, but over the past decade it’s become absolutely flagrant—If you’re in doubt about this, all it takes is a quick look to friends and family and you’ll likely find at least a few on immunosuppressive drugs.
Immunosuppression is a massively profitable never-ending annuity for pharma, with projections for continued financial growth years into the future. Is it a coincidence that Candida auris exploded as a pathogen at around the same time we became societally immunocompromised?—I don’t think so.
“A decade or so ago, it was common to think of immunosuppression as an uncommon condition, applying to patients with HIV, some cancer patients on chemotherapy, transplant recipients, or patients with rare genetic disorders. That is no longer the case. Immunosuppression is now common in the treatment of inflammatory and autoimmune disorders.”
How physicians and patients have been led down the primrose path of short-term symptom relief in exchange for a lifetime of chronic illness and the increased risk for opportunistic infections and cancers is outside the scope of this happy little monolaurin article. But when profits come before patients in the pursuit of perpetually treating symptoms while not addressing the cause of chronic illness—That’s a recipe for disaster. Not sure how to turn this train around, but I’m hoping this resonates with someone out there who does…
So here we are, with a larger and ever-increasing chunk of our population being intentionally immunosuppressed—And hand in hand with that surge, we now face a serious increase in the burden of disease, death, and healthcare costs due to fungal infections.
An enormous and growing public health threat, commonly cited examples of antifungal resistance include infections caused by aspergillus and candida, both of which can be lethal in immunocompromised people. But the problem is more expansive, almost embarrassingly so, than what is commonly recognized—Even ringworm is becoming resistant to antifungals. You may be thinking “Ringworm, big deal [yawn]” as you’re reading this, but even this lowly tinea fungus, usually trivial to those with normal immune systems, can kill immunosuppressed people.
It makes me want to pull out the last several hairs from my ever-so-slightly balding head, that despite the well-documented broad antifungal activity of monolaurin and its related medium-chain fatty acids, these compounds have not been developed by the pharmaceutical industry as antifungals. But should I be surprised?
“Drug companies are incentivised [British spelling] to profit not to improve health, says report.”
As described in the previous parts of this series, but I’ll repeat briefly here if you haven’t yet read them, lauric acid makes up about 50% of the lipid content of coconut, is the medium-chain fatty acid from which monolaurin is derived, and has broad spectrum antimicrobial activity, including action against fungi.
“…lauric acid is highly effective against candida albicans, staphylococcus aureus and aspergillus flavus”
This has been reproduced by multiple researchers against multiple species of molds:
The antifungal activity of three fatty acids (lauric, myristic, and palmitic acids) and their monoglycerides (monolaurin, monomyristic acid, and palmitin, respectively) against Aspergillus and Penicillium species in a model system was investigated…Fatty acids and their monoglycerides inhibited mold growth…”
And not unlike its vast antibacterial and antiviral reach, the breadth of monolaurin’s antifungal activity is similarly impressive, destroying 16 fungi belonging to different groups and having different cell wall compositions.
Amazingly, monolaurin has activity against both fluconazole-resistant strains of candida as well as candida biofilms.
“The MIC and MFC of monolaurin against the fluconazole-resistant strain 96901 were found to be much lower than those of fluconazole…suggesting a strong antifungal potential against fluconazole resistant strains…findings indicate a strong potential antifungal activity of monolaurin against C. albicans biofilms.”
And when I say amazingly, I mean it. Being active against fungal biofilms is a very big deal.
“One of the defining characteristics of biofilms is their increased resistance to antimicrobial agents. Fungi have been reported to be up to 1000-fold more resistant to antifungal agents than planktonic free-floating cells…”
This is emblematic of the unique advantages inherent to monolaurin—It’s fundamentally different than a standard antifungal or antibiotic, neither of which are adept at combatting a biofilm infection. Monolaurin is different—It’s detergent-like action helps, effectively, to wash biofilms away. And it’s not just in the test tube—Monolaurin has demonstrated activity against candida biofilms in mice as well.
I’ve always said that if I had to choose between a wonderful antimicrobial or a stellar immune system, I’d go with my immune system every day of the week. But in this case we may not have to choose—Monolaurin works both sides of the issue as an immunomodulator, which can be a confusing term, even for scientists.
“Immunomodulators are medications used to help regulate or normalize the immune system.”
Monolaurin’s effect on the immune system is all about nuance and duality, dampening some parts while augmenting others, with the net outcome being that it helps fix an abnormal immune response. These complex immunologic effects are separate from its antimicrobial activity. In a nutshell, monolaurin works as an anti-inflammatory, but not to the point of being immunosuppressive—Quite the opposite—Overall it improves immune function.
For example, it mitigates the negative inflammatory effects of a high fat diet and also alleviates inflammatory colitis in mice. In chickens, monolaurin improves all of the following: Anti-oxidant status, intestinal mucosal barrier function, and immunity against pathogens. And in multiple other animal models, monolaurin improves the immune response.
And in yet another example of monolaurin being a true immunomodulator, when added to the bovine viral diarrhea virus (BVDV) vaccine (Sorry, but I just have to take a second to comment on this dumb, redundant name—Bovine diarrhea virus would have been plenty, thanks for listening), monolaurin increases efficacy of the vaccine while reducing side effects compared to the standard adjuvant:
“BVDV causes reproductive, enteric, and respiratory diseases. Vaccination is essential in increasing herd resistance to BVDV spread….It was found that the BVD inactivated vaccine with 1% and 2% monolaurin elicited higher neutralizing antibodies that have longer-lasting effects (nine months) with no reaction at the injection site in comparison to the commercial vaccine adjuvanted by aluminum hydroxide gel.”
And along these same viral lines, in the case of HIV, immune system activation increases both the risk of disease acquisition and progression, whereas immune modulation decreases these risks. And here monolaurin prevents monkeys from contracting SIV, a cousin to HIV.
Lastly, a personal observation about papercuts. Invariably, I’d noticed that since childhood, mine would get red, inflamed, and on the verge of infection the day after the cut, and then begin to heal a day or two after that. This progression of events occurred no matter what disinfection interventions I tried—A thorough wash with soap and water, using alcohol swabs, antibiotic ointments, Band-Aids—All to no avail. Even the various oral antibiotics I was on over the years for bartonellosis didn’t put a dent in this pattern.
And then a few years ago I tried monolaurin—And the clouds parted and the sun shone down—Ever since, my papercuts have healed without a hint of drama. Was this turn around due to monolaurin’s immunomodulatory effects? Or due to its activity against bacterial biofilms? I think it’s probably both.
But I bring up this example because it’s a microcosm for monolaurin’s success when, in my experience, so many other things routinely fail. I’ll never forget the astonishment I felt when monolaurin helped me more completely than even the most powerful antibiotics we have in modern medicine. And I’ll never stop thanking my brother Jeff, may he rest in peace, for having recommended it to me.
From my personal and professional experience, I think it’s fair to say that monolaurin is one of nature’s most valuable gifts in our perpetual battle against the teeming microbes all around and within us.