“And It’s Tasty Too!”
Well, maybe not that tasty, but I couldn’t help flashing on the “I Love Lucy” comment. There are so many good things being discovered about lactoferrin.
It is pretty exciting to see how the lactoferrin in mother’s milk kills a wide range of yeasts and fungi. It is especially pleasing for many people to see how it is very effective at killing the causative agent of Candida in its different forms. It is also well known for its ability to kill gut parasites and lowers gut inflammation found in conditions such as Ulcerative Colitis, Crohn’s and Diverticulitis.
As an additional bonus, it can be used by itself but has also been shown in many clinical studies to radically increase the ability of standard treatments if a person wishes to combine it with a doctor’s plan. Wow, that is flexibility! You can go natural or combine lactoferrin with standard treatments if you prefer – and there is plenty of lactoferrin studies for a doctor to appreciate!
We include several of those reports in our Candida Yeast Infection articles but will include some here, as well as some abstract summaries. First, let’s look at some Wikipedia comments. They say lactoferrin and lactoferricin (that’s what the digestive system turns lactoferrin into when taken orally) inhibit in vitro growth of Trichophyton mentagrophytes, which are responsible for several skin diseases such as ringworm.(1)
What’s more important is that lactoferrin also acts against candida alvicans, a diploid fungus (a form of yeast) that causes opportunistic oral and genital infections in humans.(2) Fluconazole has long been used against Candida albicans, which resulted in emergence of strains resistant to this drug (not good). However, a combination of lactoferrin (with fluconazole) can act against these fluconazole-resistant strains of Candida albicans as well as other types of candida. These include: C. glabrata, C. krusei, C. parapsilosis and C. tropicalis.(3) Of course, a naturalist might say, “Why not just use lactoferrin?”
Antifungal activity is observed for sequential incubation of Candida with lactoferrin and then with fluconazole, but not vice versa (this might indicate that it is the lactoferrin doing most of the work).
Administration of lactoferrin through drinking water to mice with weakened immune systems and symptoms of aphthous ulcer reduced the number of Candida albicans strains in the mouth and the size of the damaged areas in the tongue.(4) Oral administration of lactoferrin to animals also reduced the number of pathogenic organisms in the tissues close to the gastrointestinal tract.
Candida albicans could also be completely eradicated with a mixture containing lactoferrin, lysozyme and introakonazol in HIV-positive patients who were resistant to other antifungal drugs.(5) Such antifungal action when other drugs deem inefficient is characteristic of lactoferrin and is especially valuable for HIV-infected patients.(6) Contrary to the antiviral and antibacterial actions of lactoferrin, very little is known about the mechanism of its antifungal action. Lactoferrin seem to destroy the cell wall and binds the plasma membrane of C. albicans.(7)
Only apo-lactoferrin (the form we use) is effective against Candida. Working synergistic with other antifungals, or by itself, lactoferrin is fungicidal strains of Candida – including the hard to treat C. krusei. Prevents Candida turning hyphal, biofilms from forming and may break down existing biofilms.
Lactoferrin detaches Candida from mucosal linings and stimulates immune response against Candida in the small intestine. This, potentially, not only helps to kill off Candida, but prevents future relapse. It is effective in treating H. pylori gastritis and kills a number of pathogenic bacteria, viruses and parasites for good measure.
As a bonus, lactoferrin stimulates growth of good bacteria such as Lactobacilli and Bifidobacteria – and it does not contain casein so will not cause a milk allergy.
Clinical Comments & Abstracts
(Here are some clinical tidbits you may be interested in.)
(Apo-lactoferrin is the way to go.) “Five oral isolates each of Candida albicans and Candida krusei were studied for their sensitivity to the fungicidal effect of human lactoferrin. Significant inter- and intraspecies variations were observed and with most isolates the sensitivity of C. krusei to lactoferrin was greater than that of C. albicans. Fungicidal activity of lactoferrin was dose-dependent and observable only with the iron free form of the molecule (apo-lactoferrin). http://www.ncbi.nlm.nih.gov/pubmed/8141667
As we said, apo-lactoferrin is fungicidal. Lactoferrin boost the immune response to Candida, and feeds good bacteria. This latest evidence shows that lactoferrin helps fight fungus no matter where it exists in the body. This systemic antifungal action of lactoferrin is strong, and can be useful when added to another systemic antifungals. This is especially seeing as lactoferrin has been shown in laboratory experiments to have a particularly strong synergy with azole antifungals.
(Natural lactoferrin is good, drugs may not be so good.) “Pre-incubation of Candida in tunicamycin (an agent that inhibits the synthesis of yeast cell-wall mannoproteins) and subsequent exposure to apo-lactoferrin enhanced the antifungal activity, whilst addition of ergosterol (a yeast cell-wall component) to the assay suspension had no significant effect. These results, taken together, indicate that apo-lactoferrin, an important component of saliva, interacts with cell-membrane constituents of C. albicans such as mannoproteins, and may modulate the effect of topical antifungal agents commonly prescribed for oral candidoses. http://www.sciencedirect.com/science/article/pii/0003996994900264
In this study of skin fungus in guinea pigs, oral lactoferrin reduced the severity of symptoms. http://www.ncbi.nlm.nih.gov/pubmed/11020258
Only iron free apo-lactoferrin was effective in inhibiting Candida in this study. Lactoferrin also prevented Candida turning hyphal (in absence of iron). It was effective for a number of isolates of C. albicans, krusei and tropicalis.” Here, lactoferrin inhibited hyphal growth in azole resistant strains of Candida. http://www.ncbi.nlm.nih.gov/pubmed/9660988
“Another problem with Candida overgrowth is that it sticks to mucosal linings and spreads like a weed. A study with vaginal mucosal lining cells showed that lactoferrin not only significantly reduces Candida from sticking; it actually helps detach Candida if it has already latched on! This finding is likely to apply to other mucosal linings such as the lungs, sinuses, and digestive tract.”
1. Mazurier J, Spik G (1980). “Comparative study of the iron-binding properties of human transferrins. I. Complete and sequential iron saturation and desaturation of the lactotransferrin”. Biochim. Biophys. Acta 629 (2): 399–408.
2. Shongwe MS, Smith CA, Ainscough EW, Baker HM, Brodie AM, Baker EN (1992). “Anion binding by human lactoferrin: results from crystallographic and physicochemical studies”. Biochemistry 31 (18): 4451–8.
3. Broc JHk, De Sousa M (1989). Iron in immunity, cancer, and inflammation. New York: Wiley.
4. Bennett RM, Davis J (1982). “Lactoferrin interacts with deoxyribonucleic acid: a preferential reactivity with double-stranded DNA and dissociation of DNA-anti-DNA complexes”. J. Lab. Clin. Med. 99 (1): 127–38.
5. Bagby GC, Bennett RM (1982). “Feedback regulation of granulopoiesis: polymerization of lactoferrin abrogates its ability to inhibit CSA production”. Blood 60 (1): 108–12.
6. Mantel C, Miyazawa K, Broxmeyer HE (1994). “Physical characteristics and polymerization during iron saturation of lactoferrin, a myelopoietic regulatory molecule with suppressor activity”. Adv. Exp. Med. Biol. 357: 121–32.
7. Levay PF, Viljoen M (1995). “Lactoferrin: a general review”. Haematologica 80 (3): 252–67.