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Monolaurin/ Lauric acid
Technical information on Lauricidin® (monolaurin):
The antiviral, antibacterial, and antiprotozoal properties of lauric acid and monolaurin have been recognized for nearly three decades by only a small number of researchers: their work, however, has resulted in 50 or more research papers an numerous U.S. and foreign patents. Prof. Dr. Jon J. Kabara performed the original seminal research in this area of fat research. Kabara (1968) first patented certain fatty acids (FAs) and their derivatives (e.g., monoglycerides (MGs) can have adverse effects on various microorganisms. While nontoxic and approved as a direct food additive by the FDA, monolaurin adversely affects bacteria, yeast, fungi, and enveloped viruses.
Kabara found that the properties that determine the anti-infective action of lipids are related to their structure: e.g., free fatty acids & monoglycerides. The monoglycerides are active;
diglycerides and triglycerides are inactive
. Of the saturated fatty acids, lauric acid has greater antiviral activity than either caprylic acid (C-8), capric acid (C-10), or myristic acid (C-14).
Fatty acids and monoglycerides produce their killing/inactivating effects by several mechanisms. An early postulated mechanism was the perturbing of the plasma membrane lipid bilayer. The antiviral action attributed to monolaurin is that of fluidizing the lipids and phospholipids in the envelope of the virus, causing the disintegration of the microbial membrane. More recent studies indicate that one antimicrobial effect in bacteria is related to monolaurin's interference with signal transduction/toxin formation (Projan et al 1994). Another antimicrobial effect in viruses is due to lauric acid's interference with virus assembly and viral maturation (Hornung et al 1994). The third mode of action may be on the immune system itself (Witcher et al, 1993).
Hierholzer and Kabara (1982) first reported the antiviral activity of the monoglyceride of lauric acid (monolaurin) on viruses that affect humans.. They showed virucidal effects of monolaurin on enveloped RNA and DNA viruses. This work was done at the Center for Disease Control of the U.S. Public Health Service. This study was carried out using selected virus prototypes or recognized representative strains of enveloped human viruses. All these viruses have a lipid membrane. The presence of a lipid membrane on viruses makes them especially vulnerable to lauric acid and its derivative monolaurin. These initial findings have been confirmed by many other studies.
Research has shown that enveloped viruses are inactivated by added fatty acids and monoglycerides in both human and bovine milk (Isaacs et al 199 1). Others (Isaacs et al 1986, 1990, 1991, 1992; Thormar et al 1987) have confirmed Kabara's original statements concerning the effectiveness of monolaurin.
Some of the viruses inactivated by these lipids are the measles virus, herpes simplex virus (HSV-1 and -2), herpes family members (HIV, hepatitis C, vesicular, stomatitis virus (VSV), visna virus, and cytomegalovirus (CMV). Many of the pathogenic organisms reported to be inactivated by these antimicrobial lipids are those know to be responsible for opportunistic infections in HIV -positive individuals. For example, concurrent infection with cytomegalovirus is recognized as a serious complication for HIV positive individuals (Macallan et al 1993).
Thus, it would appear imperative to investigate the practical aspects and the potential benefit of a nutritional supplement such as monolaurin (Lauricidin®) for microbial infected individuals. Until now few nutritionists in mainstream nutrition community seem to have recognized the added benefit of antimicrobial lipids in the support of infected patients. These antimicrobial fatty acids and their derivatives are essentially nontoxic to man. According to the published research, lauric acid is one of the best "inactivating" fatty acids, and its monoglyceride is even more effective than the fatty acid alone (Kabara 1978, Sands et al 1978, Fletcher et al 1985, Kabara 1985).
It should be emphasized that lauric acid cannot be taken orally because it is severally irritating.
Lauricidin® on the other hand, a derivative of lauric acid
to glycerol to form monolaurin, can be taken orally without any problem.
The lipid-coated (envelope) viruses, bacteria and other microorganisms are dependent on host lipids for their lipid constituents. The variability of fatty acids in the foods of individuals as well as the variability from de novo synthesis accounts for the variability of fatty acids in their membranes.
Monolaurin does not appear to have an adverse effect on desirable gut bacteria, but rather on only potentially pathogenic microorganisms. For example, Isaacs et al (1991) reported no inactivation of the common Esherichiacoli or Salmonella enteritidis by monolaurin, but major inactivation of Hemophilus influenza, Staphylococcus epidermis and Group B gram positive streptococcus.
The potentially pathogenic bacteria inactivated by monolaurin include Listeria monocytogenes, Staphylococcus aureus, Streptococcus agalactiae, Groups A, streptococci-gram-positive organisms, and some gram-negative organisms (Vibrio parahaemolyticus and Helicobacter pylori).
Decreased growth of Staphylococcus aureus and decreased production of toxic shock syndrome toxin-l was shown with monolaurin (Holland et al 1994). Monolaurin was 5000 times more inhibitory against Listeria monocytogenes than ethanol (Oh & Marshall 1993). In vitro monolaurin rapidly inactivate Helicobacter pylori. Of greater significance there appears to be very little development of resistance of the organism to the bactericidal effects (Petschow et al 1996) of these natural antimicrobials.
A number of fungi, yeast, and protozoa are also inactivated or killed by monolaurin. The fungi include several species of ringworm (Isaacs et al 1991). The yeast reported to be affected is Candida albicans (Isaacs et al 1991) The protozoan parasite Giardia lamblia is killed by monoglycerides from hydrolyzed human milk (Hemell et al 1986, Reiner et al 1986, Crouch et al 1991, Isaacs et al 1991).
Chlamydia trachomatis is inactivated by monolaurin (Bergsson et al 1998). Hydrogels containing monocaprin/monolaurin are potent in vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV-1 and bacteria such as Neisserian gonorrhea (Thormar 1999).
Lauricidin® vs. Coconut Oil
There is considerable confusion on the Internet about the biological and pharmacological effects between preformed monolaurin (Lauricidin®) and coconut oil (CNO) when taken orally. Statements have been made by a scientist and laypersons neither of whom have NEVER done any research on coconut oil, monolaurin or lauric acid.
There is confusion regarding the veracity of the following statements:
Coconut oil can be converted to monolaurin
Coconut oil is antiviral
Monolaurin is a trade mark
Monolaurin is lauric acid
All monolaurins are the same
MCTs are converted to active monoglycerides
Lauric acid can be ingested as a antiviral
Lauricidin® can be found in capsules
How did all of this start?
All of the discussion on the antimicrobial effects of certain lipids started with the seminal research of Dr. Kabara begun in 1966. He was the first to describe that lauric acid, known to be an active antibacterial agent, when esterified to glycerol to form a monoglyceride called monolaurin.
It is necessary to understand what a mono-, di-, and triglyceride is chemically. Below is the structure of a triglyceride.
H-C-OR sn1 position
H-C-OR sn3 position
Where sn# represents the glycerol carbon position, and R the kind of fatty acid attached to glycerol.
The removal of one-fatty acid (R) forms a diglyceride while the removal of two fatty acids results in the formation of a monoglyceride. Dr. Kabara’s findings confirmed by numerous other investigators indicted that while monoglycerides were biologically active the di- and triglycerides were not active.
That triacylglycerides and lauric acids found in coconut oil can be converted in the body to a pharmacologically active monoglyceride is parroted repeatedly on the Internet, state There are no studies that support the opinion that CNO or other lauric acid products form to any extent biologically active monoglycerides. While CNO is metabolized to monoglycerides and fatty acids, these by-products are not produced in a form or amount that would be biologically active. A technical explanation follows.
It needs to be recognized that monoglycerides are capable of being in two different isomers (
one of two or more molecules that have the same chemical composition but have different chemical structure and therefore different properties
The sn1 and sn3 monoglycerides are equivalent but different from that of the
-isomer. This difference is important in understanding how a oil (triglyceride) like CNO is metabolized.
Triglycerides from coconut or MCT oils in contrast to those in mother’s milk are hydrolyzed in the body to
-monoglycerides and free fatty acids. However, these monoglycerides and fatty acids are quickly resynthesized to inactive triacylglycerols after absorption into the enterocyte whereas sn1 (3)-monoglycerides are absorbed and not converted to the triglycerides.
The two isomeric monoglycerides (
and sn1 (3) follow two different metabolic pathways and therefore have different biochemical affects. This is important since triglycerides/diglycerides have been shown to be inactive as antimicrobial agents while the monoglycerides are active.
Often triglycerides containing the medium-chain fatty acids found in coconut oil or MCT oils are compared to those in mother's milk. Both are therefore considered to have the same nutriceutical effects. However to have similar nutriceutical affects both products need to be hydrolyzes
prior to digestion
from their triglyceride form to an active sn1 (3) monoglyceride and free fatty acid form. In the case of mother’s milk, the milk contains a lipase that converts the triglycerides to the sn1 (3) monoglycerides before absorption by the infant..
The only pertinent research on triglyceride metabolism can be found in an early paper by Mattson and Volpenhein (1964). They analyzed the amount of metabolites after feeding long chain fatty acid triglycerides synthesized with labeled fatty acids at various positions. From these studies, they concluded that hydrolysis of the dietary triglycerides in the intestinal lumen yielded 72 parts
-monoglycerides, 6 parts sn1 (3)-monoglycerides, and 22 parts free glycerol. The
-monoglycerides, approximately three-fourths of the dietary triglycerides, entered rat intestinal cells intact, and were reesterified to triglycerides.
From the above arguments, it is obvious that the yield of pharmacologically active sn1 (3) monoglyceride from coconut oil IF it is formed is no greater than 6% and probably less (~3%) when medium chain fatty acids (MCFAs) are considered. Since TAGs forms only ~6% of sn1 (3) monoglyceride , the amount of monolaurin formed would only be ~3%. Since I found that the usual level of Lauricidin® to be effective is between 3-9 grams/day, the intake of coconut oil would be 100-300 ml/day. This would be an unrealistic amount to take--plus the resulting diarrhea.
With Lauricidin®( sn1 (3) monolaurin) you get a product of highest purity and reasonable cost. Four to eight hundred percent less than monolaurin in capsules which have additives. Also Dr. Kabara, the discoverer of Lauricidin®, is available to answer any of your questions. No other supplement offers you more benefits and confidence.
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