Bovine Lactoferrin Health Benefits and as Treatment for H. Pylori, Acne and Interstitial Cystitis by Jeffrey Dach MD
A number of studies (see references below) show Lactoferrin added to Triple Therapy plus Bismuth (quadruple therapy) improves the eradication rate for H. Pylori infection in the stomach demonstrated by repeat H. Pylori breath test. The addition of probiotics is also useful.
What is Lactoferrin?
Lactoferrin is a glycoprotein found in milk, especially colostrum. It is usually derived from bovine milk and popular for immune and digestive support. Lactoferrin is also present in saliva, tears, and nasal secretions. Lactoferrin is in the transferrin family of proteins and binds iron, regulates iron absorption in the gut and deprives bacterial pathogens of iron. Lactoferrin is antibacterial, antiviral, antifungal, antioxidant, anti-inflammatory, and immune-modulating.
Lactoferrin supports the innate immune system, promotes beneficial gut bacteria, and may be useful as add on in iron deficiency anemia, respiratory infections, gut health, and even skin issues like acne.
Lactoferrin for Treatment of Acne
Lactoferrin, vitamin E (tocotreinol) and zinc is a good combination for acne treatmentto reduce inflammation, decrease sebum production (oil), and fight bacteria like Propionibacterium acnes. Lactoferrin helps decrease skin oil (sebum) and specific skin surface lipids (like triacylglycerols) that contribute to breakouts. Lactoferrin is anti-inflammatory and antimicrobia, targeting Propionibacterium acnes (now Cutibacterium acnes), the bacteria associated with acne. Lactoferrin regulates oil production in sebaceous (oil) glands. Studies using lactoferrin-enriched fermented milk or supplements (often with Vitamin E & Zinc) have shown significant reductions in inflammatory and total acne lesions. (see references below)
Lactoferrin for Treatment of Crohn’s Disease and Other GastroIntestinal Diseases
Alexander DB, Iigo M, Yamauchi K, Suzui M, Tsuda H. Bovine lactoferrin and Crohn’s disease: a case study. Biochemistry and Cell Biology. 2017 Feb;95(1):133-141. doi: 10.1139/bcb-2016-0107. Epub 2016 Nov 30. PMID: 28165294.
A 22-year-old male suffering from abdominal pain, repeated diarrhea, and weight loss visited the Digestive Disease Department of Nagoya City University Hospital on 19 December 2011. He was hospitalized and diagnosed with Crohn’s colitis. His Crohn’s Disease Activity Index (CDAI) was 415. Treatment by granulocyte apheresis, mesalazine, and adalimumab was started. His CDAI was 314 on 30 December and 215 on 5 January. A colonoscopic examination on 19 January showed almost complete remission in the transverse colon and marked remission in the rectum. Mesalazine therapy was stopped on 28 February, and the patient was instructed to self-inject 40 mg of adalimumab every other week. His CDAI was 50 on 10 April, indicating clinical remission. His last self-injection of adalimumab was on 24 April 2012, and he started taking 1 g of bovine lactoferrin (bLF) daily. His CDAI was 35 on 8 January 2013. He continued taking 1 g of bLF daily without any other treatment for Crohn’s disease. Laboratory blood tests on 7 September 2015 showed no sign of disease recurrence, and a colonoscopic examination on 23 October 2015 showed almost complete mucosal healing. This case indicates that ingestion of bLF to maintain Crohn’s disease in a remissive state should be further explored.
In 2025, Dr. Manuella Rizzi writes:
Due to its well-known antimicrobial, anti-inflammatory, and iron-chelating abilities, lactoferrin use has gained growing interest in the field of gastroenteric diseases, both as a preventive and supportive therapeutic intervention. Such interest rises from some key characteristics of lactoferrin. Firstly, this molecule is known to act as a bactericidal and bacteriostatic agent toward many Gram-positive and Gram-negative bacteria involved in gastroenteric disease pathogenesis (e.g., Enterococcus, Escherichia, Enterobacter, Helicobacter, Vibrio), thus helping in controlling bacterial infections. Secondly, it has been reported to act as a prebiotic compound, thus promoting the growth of specific probiotic strains and helping to reduce antibiotic-dependent gastrointestinal side effects and intestinal dysbiosis. Thirdly, lactoferrin has been proven to exert a barrier-stabilizing effect in both in vitro and in vivo models of intestinal barrier damage by restoring tight junction morphometry and reducing epithelial apoptosis. Lastly, it is well-known that lactoferrin is able to reduce pro-inflammatory marker (e.g., IL1, IL6, IL8, TNFα) expression, thus contributing to inflammation resolution and tissue damage recovery, as demonstrated in vitro, where lactoferrin administration has proven to be able to upregulate intestinal stem cells (Lgr5) and proliferation (Wnt/β-catenin) markers, and in vivo, where it successfully alleviated aflatoxin M1-induced intestinal barrier dysfunction [22,44,54,109,112,113,114]. Among the gastroenteric conditions for which lactoferrin has been successfully used as a therapeutic approach, there is Helicobacter pylori infection, which represents a major pathogenic factor for chronic gastritis and peptic ulcers [115,116,117,118]. The interest in lactoferrin’s potential therapeutic value in this context dates back to the end of the previous century, when the first studies evaluated its in vitro and in vivo effectiveness against H. pylori commercial strains and clinical isolates [55,118,119,120]. These data have since been confirmed using both in vitro and in vivo models based on antibiotic-resistant strains [115,121,122,123]. Since the uncontrolled use and abuse of antibiotics worldwide is the major cause of the emergence of antibiotic-resistant bacterial strains, thus strongly reducing year by year the successful eradication rate of this infection, the actual clinical approach to this condition is represented by triple or even quadruple therapies based on a mix of antibiotics and proton pump inhibitors [115,121,123,124]. Despite being effective, due to the considerable use of antibiotics, these approaches are associated with gastrointestinal side effects mainly related to the destruction of the resident microbial flora and the generation of a pro-inflammatory environment [116,119,122,125]. In this context, it is not surprising that several researchers focused their work on the discovery of novel interventions to eradicate H. pylori infection or, at least, reduce its antibiotic resistance. The positive preclinical results obtained using lactoferrin thus fostered the design of clinical trials aimed at investigating its effectiveness as an add-on to the standard triple/quadruple therapy (Table 3). As of now, some clinical trials, but not all, have demonstrated that lactoferrin’s addition to the proton pump inhibitor/antibiotic mix increased the successful eradication rate of the classical therapy by taking advantage of the different lactoferrin antibacterial mechanisms of action compared to antibiotics, thus maximizing the eradication effect. Moreover, lactoferrin supplementation (especially in combination with probiotics) has been proven to reduce the common side effects associated with classical eradication schedule, thus further supporting its use in managing H. pylori infection [115,117,121,124,125,126]. …At the time of writing, the only clinical evidence regarding lactoferrin use in IBD management is represented by a case report showing a long clinical (at least 3.5 years) and symptomatic (4.5 years) remission in a Crohn’s colitis patient supplemented daily with bovine lactoferrin [129].
Rizzi, Manuela, et al. “Lactoferrin, a Natural Protein with Multiple Functions in Health and Disease.” Nutrients 17.21 (2025): 3403.
Lactoferrin in the Treatment of Interstitial Cystitis
Interstitial cystitis (IC) is a painful bladder syndrome (PBS). This is a chronic condition characterized by suprapubic pain associated urinary frequency and urgency. Mainstream medicine has no curative treatment. A 2024 study by Dr. Luigi Rosa from Italy showed 90% efficacy in releiving symptoms of IC in 21 women over 18 weeks of treatment with Lactoferrin and Sodium Bicarbonate (an alkalinizing agent). The IL-6 inflammatory marker decreased with treatment.
Rosa, Luigi, et al. “Lactoferrin in the treatment of interstitial cystitis: a retrospective pilot study.” Biochemistry and Cell Biology 102.6 (2024): 506-514.
Interstitial cystitis (IC), defined as a painful bladder syndrome (PBS), is a chronic condition that manifests itself as a suprapubic pain associated with an enhancing of frequency/urgency of urination, and for which there is no cure. Here, we present a retrospective pilot study on women affected from IC/PBS and treated with bovine lactoferrin (bLf). A total of 31 women, affected (20) or unaffected (11) from hereditary thrombophilia (HT), presented the median of 6 episodes of IC/PBS during the 6 months before the study. Treatment consisted of 17 weeks of orally administered Valpalf® capsules, containing bLf plus sodium bicarbonate and citrate. Out of 31 patients, only 3 women had one episode of IC/PBS during the follow-up period, while no episode was observed in 28 women. In the HT group, a significant decrease in both serum IL-6 and D-dimers was found after Valpalf® treatment. Moreover, in Valpalf®-treated women, cystoscopy revealed a global improvement in the appearance of the bladder, especially in term of inflammation/irritation and presence of Hunner ulcers. Even if our results must be corroborated by randomized double-blinded controlled trials on a larger number of patients, our observations indicate that bLf treatment is efficient in relieving IC/PBS symptoms, without side effects.
blood samples were taken from each HT woman in the morning before breakfast and serum IL-6 levels and D-dimers before and after Valpalf treatment were determined by each HT woman at different laboratories in Italy.
IL-6 is a well-established urinary inflammatory marker in IC/BPS, especially for the severe form,
Patients’ treatments: The patients suffering from IC/PBS were treated with Valpalf alone. As reported in Conte et al. (2023) for the patients suffering from recurrent cystitis, the best therapeutic scheme consisted in five capsules of Valpalf (200 mg of bLf plus sodium bicarbonate and citrate) for 7 days (three capsules in the morning and two in the afternoon) before meals to avoid the gastric degradation (Rosa et al. 2020), two capsules of Valpalf for 30 days (one in the morning and one in the afternoon before meals), and one capsule in the morning before meals for 90 days. Follow-up started from the week after the end of treatment (18th week) until further 16 weeks. (Note: sodium bicarbonate and citrate alkalinize the urine)
The therapeutic regimen was the same we recently applied for the patients suffering from recurrent cystitis (Conte et al. 2023), consisting of 5 capsules of Valpalf for 7 days, followed by 2 capsules for 30 days and 1 capsule for 90 days. Follow-up started from the week after the end of treatment (18th week) for an additional 16 weeks.
90% Cure Rate
The absence of IC/PBS episodes was evaluated based on the lack of clinical symptoms such as the decrease of subpubic pain, frequency and urgency of urination. At the end of
follow-up, 28/31 (90.3%) of women undergoing Valpalf treatment reported no IC/PBS episodes during the treatment and across the follow-up period, whereas the remaining 3 (9.7%) experienced only one episode of IC/PBS across time (Fig. 2A).
An analysis restricted to HT patients revealed that 18 out of 20 patients (90%) did not manifest IC/PBS episodes at the end of follow-up period (p < 0.001), whereas 2 patients (10%) experienced a single episode each, one during the Valpalf treatment and one during the follow-up period (Fig. 2B). Concerning the remaining non-HT women, 10 out of 11 patients (90.1%) did not manifest IC/PBS episodes (p < 0.001), while only 1 patient showed one episode during the follow-up period (Fig. 2C). These results indicate the efficacy of bLf in alleviating IC/PBS symptoms.
A further analysis on the remaining 11 non-HT women revealed the same trend (p < 0.001) (Fig. 2C). Ten out of 11 patients (90.1%) did not manifest IC/PBS episodes, while only 1 patient showed one episode of IC/PBS during the follow-up period (Fig. 2C).
Note: HT=hereditary thrombophilia (a tendency to form blood clots)
Reduction in IL-6 and D-Dimer
In the present study, the anti-inflammatory activity of bLf (Bovine Lactoferrin) was highlighted in term of a significant reduction of both IL-6 and D-dimers in HT women. Before the treatment, HT women showed serum IL-6 and D-Dimers levels of 81.0 ± 9.8 pg/mL and 774.8 ± 142.4 ng/mL, respectively. After Valpalf treatment, these levels significantly decrease (33.5 ± 6.2 pg/mL for IL-6 and 228.8 ± 56.4 ng/mL for D-Dimers)
Description Mosiac Plus 30 capsules (by Pharmaguida/Pharmalite)
Description of Valpalf. Ingredients: Valpalf [lactoferrin 200 mg per capsule (milk protein, lactose), sodium citrate, sodium bicarbonate], HPMC capsule; anti-caking agent: magnesium salts of fatty acids. Gluten free. Valpalf [lactoferrin ( milk proteins, lactose ), sodium citrate, sodium bicarbonate], capsule in HPMC; anti-caking agent: magnesium salts of fatty acids.
Instructions for use: It is recommended to take one capsule a day. Each capsule contains 200 mg of lactoferrin. To be swallowed with water or by opening it, dissolving the contents in a little water or other drink (tea, fruit juice, milk, yogurt) at room temperature.
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Conte, Antonietta Lucia, et al. “Effect of bovine lactoferrin on recurrent urinary tract infections: in vitro and in vivo evidences.” Biometals 36.3 (2023): 491-507.
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Lotz, Martin, et al. “Interleukin-6 and interstitial cystitis.” The Journal of urology 152.3 (1994): 869-873.
We analyzed the presence of the cytokine interleukin-6 in urine samples from interstitial cystitis patients. Interleukin-6 was significantly elevated in patients with interstitial cystitis (169.29 +/- 90.81 pg./ml. versus 34.8 +/- 6.35 pg./ml. in controls). Representative urine samples were analyzed with specific antibody to interleukin-6 and greater than 80% of the biological activity was neutralized. These cytokine measurements were then compared with clinical parameters and interleukin-6 levels correlated positively with the pain scores. Studies on the potential cellular origin of interleukin-6 showed increased levels in spontaneously voided urine but not in ureteral urine, which was collected during cystoscopy, suggesting that interleukin-6 is the product of activated cells in the bladder. This finding is supported by in situ hybridization analyses, which showed that interleukin-6 messenger ribonucleic acid expressing cells are located in the interstitium and epithelial layer, and within blood vessels. The implications of these findings for interstitial cystitis pathogenesis are discussed.
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COVID Associated Cystitis Is Real – IC Awareness Month
September 1, 2021 By Jill Osborne|August 31st, 2021|Awareness, Our Blog, Research|
Dhawan, Ananya, et al. “COVID-associated cystitis: the culprit behind the bladder woes post-COVID infection? A review.” International Urology and Nephrology 55.10 (2023): 2367-2372.
Wittenberg, Sophie, et al. “Prolonged impacts of COVID-19-associated cystitis: A study on long-term consequences.” World journal of clinical cases 11.33 (2023): 7987.
Virno, Trevor, et al. “COVID-19-Associated Cystitis: De Novo Urinary Urgency Following SARS-CoV-2.” Cureus 17.12 (2025).
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Lactoferrin as Antiviral and Anti-Spike Protein Agent
In 2022, Dr. Antimo Cutone used a spike protein containing pseudo-virus to study the use of Lactoferrin as an Anti-viral agent, as an Anti-Spike protein agent, and suggested Lactoferrin as adjuvant in treating C0\/1D-l9 infection, writing:
SARS-CoV-2 causes C0\/1D-l9, a predominantly pulmonary disease characterized by a burst of pro-inflammatory cytokines and an increase in free iron. The viral glycoprotein Spike mediates fusion to the host cell membrane, but its role as a virulence factor is largely unknown. Recently, the antiviral activity of lactoferrin against SARS-Co\/-2 was demonstrated in vitro and shown to occur via binding to cell surface receptors, and its putative interaction with Spike was suggested by in silico analyses. We investigated the anti-SARS-CoV-2 activity of bovine and human lactoferrins in epithelial and macrophagic cells using a Spike-decorated pseudovirus. Lactoferrin inhibited pseudoviral fusion and counteracted the deleterious effects of Spike on iron and inflammatory homeostasis by restoring basal levels of iron-handling proteins and of proinflammatory cytokines IL-1β and IL-6. Using pull-down assays, we experimentally proved for the first time that lactoferrin binds to Spike, immediately suggesting a mechanism for the observed effects. The contribution of transferrin receptor 1 to Spike-mediated cell fusion was also experimentally demonstrated. In silico analyses showed that lactoferrin interacts with transferrin receptor 1, suggesting a multifaceted mechanism of action for lactoferrin. Our results give hope for the use of bovine lactoferrin, already available as a nutraceutical, as an adjuvant to standard therapies in C0\/1D-l9.
Cutone, Antimo, et al. “Lactoferrin binding to SARS-CoV-2 spike glycoprotein blocks pseudoviral entry and relieves iron protein dysregulation in several in vitro models.” Pharmaceutics 14.10 (2022): 2111.
SARS-CoV-2 causes COVID-19, a predominantly pulmonary disease characterized by a burst of pro-inflammatory cytokines and an increase in free iron. The viral glycoprotein Spike mediates fusion to the host cell membrane, but its role as a virulence factor is largely unknown. Recently, the antiviral activity of lactoferrin against SARS-CoV-2 was demonstrated in vitro and shown to occur via binding to cell surface receptors, and its putative interaction with Spike was suggested by in silico analyses. We investigated the anti-SARS-CoV-2 activity of bovine and human lactoferrins in epithelial and macrophagic cells using a Spike-decorated pseudovirus. Lactoferrin inhibited pseudoviral fusion and counteracted the deleterious effects of Spike on iron and inflammatory homeostasis by restoring basal levels of iron-handling proteins and of proinflammatory cytokines IL-1β and IL-6. Using pull-down assays, we experimentally proved for the first time that lactoferrin binds to Spike, immediately suggesting a mechanism for the observed effects. The contribution of transferrin receptor 1 to Spike-mediated cell fusion was also experimentally demonstrated. In silico analyses showed that lactoferrin interacts with transferrin receptor 1, suggesting a multifaceted mechanism of action for lactoferrin. Our results give hope for the use of bovine lactoferrin, already available as a nutraceutical, as an adjuvant to standard therapies in COVID-19.
Eker, Furkan, et al. “The potential of lactoferrin as antiviral and immune-modulating agent in viral infectious diseases.” Frontiers in immunology 15 (2024): 1402135.
Andreu, Sabina, et al. “Liposomal lactoferrin exerts antiviral activity against HCoV-229E and SARS-CoV-2 pseudoviruses in vitro.” Viruses 15.4 (2023): 972.
Manzoni, Paolo, et al. “Lactoferrin supplementation in preventing and protecting from SARS-CoV-2 infection: Is there any role in general and special populations? an updated review of literature.” International Journal of Molecular Sciences 25.19 (2024): 10248.
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Lactoferrin Heals Leaky Gut:
Here are three influential and widely cited studies (including in vitro, in vivo, and mechanistic work) demonstrating lactoferrin’s role in improving intestinal barrier function (often referred to as healing “leaky gut” or reducing intestinal permeability). These support effects on stimulating epithelial cell proliferation/differentiation, increasing tight junction proteins (e.g., claudin-1, occludin, ZO-1), and sealing gaps. Direct clinical evidence for decreasing serum zonulin is limited and often tied to colostrum (which contains lactoferrin), but related barrier improvements align with reduced permeability markers.
Hirotani Y, et al. (2019). The In Vitro Protective Role of Bovine Lactoferrin on Intestinal Epithelial Barrier. Molecules, 24(1):148. doi: 10.3390/molecules24010148. PMID: 30621198.
Full-text URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC6337092/
This in vitro study using human intestinal epithelial crypt (HIEC) and Caco-2 cells showed bovine lactoferrin significantly increased expression of tight junction proteins (claudin-1, occludin, ZO-1) at mRNA and protein levels, reducing permeability and strengthening barrier function. It highlights lactoferrin’s promotion of epithelial integrity, relevant to leaky gut repair.
Zong X, et al. (2016). Porcine lactoferrin-derived peptide LFP-20 protects intestinal barrier by maintaining tight junction complex and modulating inflammatory response. Biochemical Pharmacology, 104:74-82. doi: 10.1016/j.bcp.2016.01.013. PMID: 26808210.
Full-text URL: Available via ScienceDirect (or institutional access).
In LPS-challenged models (in vitro IPEC-J2 cells and in vivo mice), a lactoferrin-derived peptide increased zonula occludens-1, occludin, and claudin-1 expression, reduced permeability/apoptosis, and preserved barrier integrity against inflammation—directly supporting sealing of gaps and epithelial protection.
Liu J, et al. (2023). The Role of Lactoferrin in Intestinal Health. Pharmaceutics, 15(6):1749. doi: 10.3390/pharmaceutics15061749. PMID: 37376181.
Full-text URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC10304194/
This comprehensive review synthesizes evidence (including preclinical and clinical data) on lactoferrin’s promotion of intestinal epithelial proliferation, differentiation, tight junction enhancement, and barrier repair. It notes dose-dependent stimulation of enterocyte growth and maturation, aligning with reduced permeability in conditions like leaky gut.
These studies collectively provide strong mechanistic support for lactoferrin’s barrier-protective effects, primarily through upregulation of tight junctions and epithelial regeneration. While direct human trials specifically measuring serum zonulin reduction with isolated lactoferrin are emerging (often confounded by colostrum studies showing zonulin decreases), the barrier improvements imply similar outcomes. Evidence is robust in preclinical models, with growing translational support.
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Lactoferrin increases BDNF
- Chen Y, et al. (2015). Lactoferrin promotes early neurodevelopment and cognition in postnatal piglets by upregulating the BDNF signaling pathway and polysialylation. Molecular Neurobiology, 52(1):256-269. doi: 10.1007/s12035-014-8856-9. PMID: 25146846.
Full-text URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC4510916/
This highly referenced study showed that dietary bovine lactoferrin supplementation in postnatal piglets significantly upregulated BDNF mRNA and protein levels in the hippocampus, activated downstream signaling (e.g., phosphorylated CREB), and improved cognitive performance in maze tests. It establishes lactoferrin’s role in enhancing the BDNF neurotrophic pathway for neuroplasticity and cognition. - Yang C, et al. (2014). Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviate early weaning diarrhea in postnatal piglets. The Journal of Nutritional Biochemistry, 25(8):834-842. doi: 10.1016/j.jnutbio.2014.03.015. PMID: 24824862.
Full-text URL: Available via ScienceDirect (or institutional access).
In piglets supplemented with higher doses of lactoferrin, intestinal mRNA expression of BDNF was significantly upregulated (P<0.05), alongside improvements in gut maturation and reduced diarrhea. This study links lactoferrin to BDNF elevation in the gut-brain axis context. - Paesano R, et al. (2014). Protective effects of maternal nutritional supplementation with lactoferrin on growth and brain metabolism. Pediatric Research, 75(5):616-623. doi: 10.1038/pr.2014.16. PMID: 24213624.
Full-text URL: Available via Nature (or institutional access).
Maternal bovine lactoferrin supplementation in a model of intrauterine growth restriction normalized altered hippocampal BDNF transcript levels in offspring, alongside other neuroprotective effects on brain metabolites and receptors. This supports lactoferrin’s ability to preserve or enhance BDNF in compromised neurodevelopment.
These studies provide robust preclinical evidence (frequently cited in reviews on lactoferrin’s neuroprotective effects) for lactoferrin’s upregulation of BDNF, primarily through transcriptional and signaling mechanisms. Human clinical data on direct BDNF increases remain limited and emerging.
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Lactoferrin Antifungal Properties (Anti-Candida)
Here are three widely cited studies (foundational and frequently referenced in reviews and meta-analyses on lactoferrin’s antimicrobial properties) demonstrating lactoferrin’s (primarily bovine or derived peptides) potent antifungal activity against Candida species, including reduction of fungal growth, disruption of biofilm formation, and synergy with conventional antifungals (e.g., azoles like fluconazole, amphotericin B). These support its potential as an adjunct in antifungal regimens.
Kuipers ME, de Vries HG, Eikelboom MC, Meijer DK, Swart PJ. (1999). Synergistic fungistatic effects of lactoferrin in combination with antifungal drugs against clinical Candida isolates. Antimicrobial Agents and Chemotherapy, 43(11):2635-2641. doi: 10.1128/AAC.43.11.2635-41. PMID: 10543740.
Full-text URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC89536/
This highly cited in vitro study showed that human and bovine lactoferrin (especially apo-lactoferrin) exhibited direct fungistatic activity against multiple clinical Candida isolates, reducing growth significantly. Combinations with fluconazole, amphotericin B, and 5-fluorocytosine demonstrated pronounced synergy (up to 50% enhanced inhibition), allowing lower doses of antifungals while achieving complete growth inhibition—highlighting lactoferrin’s role in overcoming resistance and enhancing regimens.
Fernandes KE, Carter DA. (2020). The antifungal activity of lactoferrin and its derived peptides: mechanisms of action and synergy with drugs against fungal pathogens. Frontiers in Microbiology, 8:2. doi: 10.3389/fmicb.2017.00002. (Wait, year is 2017; full cite: Fernandes KE, Carter DA. (2017).)
Full-text URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC5241296/
This comprehensive review (widely cited for mechanistic insights) synthesizes evidence that bovine lactoferrin and peptides (e.g., lactoferricin B) directly reduce Candida growth via iron sequestration, membrane disruption, and apoptosis-like effects. It details disruption of biofilm virulence factors and strong synergy with azoles and amphotericin B, positioning lactoferrin as a promising adjunct to combat resistant strains.
Bellamy W, Takase M, Wakabayashi H, Kawase K, Shimamura S. (1993). Killing of Candida albicans by lactoferricin B, a potent antimicrobial peptide derived from the N-terminal region of bovine lactoferrin. Medical Microbiology and Immunology, 182(2):97-105. doi: 10.1007/BF00189377. PMID: 8412834.
Full-text URL: Available via Springer (or institutional access).
A seminal, highly referenced study demonstrating that lactoferricin B (from bovine lactoferrin) potently kills Candida albicans (effective at 18-150 μg/ml), reducing fungal growth and viability through direct membrane damage. Later citations extend this to biofilm inhibition and synergy, establishing lactoferrin derivatives as powerful antifungals suitable for combination therapy.
These studies provide strong evidence across direct growth inhibition, biofilm interference, and synergistic enhancement, making lactoferrin a valuable addition to antifungal protocols, especially against resistant Candida. Preclinical data is robust, with growing support for clinical translation.
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Lactoferrin Prevents Upper Respiratory Infections
Ali, Akbar Shoukat, et al. “Lactoferrin reduces the risk of respiratory tract infections: A meta-analysis of randomized controlled trials.” Clinical nutrition ESPEN 45 (2021): 26-32.
Background: Lactoferrin (Lf) is one of the key immunomodulatory substances found naturally in various body fluids, such as saliva, tears, and breast milk, and forms a vital part of the innate
defense against invading pathogens. Various studies have demonstrated antibacterial, antifungal, and antiviral properties of Lf and its protective role against respiratory tract infections (RTIs). The
present meta-analysis aims to elucidate the association of Lf administration in reducing the risk of RTIs by systematically reviewing the data from randomized controlled trials (RCTs).
Methods: We systematically searched PubMed, Cochrane Library, Medline & CINAHL, Turning Research into Practice (TRIP), ProQuest Theses & Dissertations Databases, and China National Knowledge Infrastructure (CNKI) from inception till March 15, 2021. The primary outcome measure was a reduction in respiratory illness; decrease in frequency, symptoms, and duration. Random-effects model was used to estimate the odds ratio (OR) and 95% confidence interval (CI).
We used Cochrane’s risk-of-bias tool version 2 (RoB-2) to appraise the risk of bias of included RCTs.
Results: A total of nine RCTs were eligible for this review, of which six were included in the meta-analysis. Overall, two studies demonstrated a high risk of bias. The meta-analysis revealed a significantly reduced odds of the development of respiratory infections with the use of Lf relative to the control (pooled odds ratio = 0.57; 95% confidence interval 0.44 to 0.74, n=1,194), with sufficient evidence against the hypothesis of ‘no significant difference’ at the current sample size.
Conclusions: The administration of Lf shows promising efficacy in reducing the risk of RTIs. Current evidence favours Lf fortification of infant formulas. Lf may also have a beneficial role in managing symptoms and recovery of patients suffering from RTIs, and have potential for use as an adjunct in COVID-19, however warrants further evidence from a large well-designed RCT
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Lactoferrin Anti-Cancer Activity
León-Flores, D. B., et al. “Anticancer potential of lactoferrin: Effects, drug synergy and molecular interactions.” BioMetals (2025): 1-2
Lactoferrin, a glycoprotein present in mammals, is of significant interest due to its pleiotropic behavior, demonstrating a broad spectrum of biological activities such as antimicrobial, antioxidant, anti-inflammatory, immunomodulatory, and anticancer effects. In this review, we examine the current knowledge of Lf’s role in cancer. In addition, it exhibits a synergistic effect along with conventional drugs, potentially enhancing their efficacy and, at the same time, reducing the side effects associated with most traditional therapies.
Bolesławska, Izabela, et al. “Lactoferrin—A Regulator of Iron Homeostasis and Its Implications in Cancer.” Molecules 30.7 (2025): 1507.
Słoka, Joanna, et al. “Mesalazine and Lactoferrin as Potential Adjuvant Therapy in Colorectal Cancer: Effects on Cell Viability and Wnt/β-Catenin Pathway.” Current Issues in Molecular Biology 47.5 (2025): 327.
The aim of this study was to evaluate the effect of a mesalazine (MES) and lactoferrin (LACT) combination on the viability of CRC cells and healthy intestinal epithelial cells, as well as to assess the expression profile of target genes within the Wnt/β-catenin pathway. Additionally, this study aimed to preliminarily analyze the mechanism of action underlying the combined effects of these compounds. In this study, we used three CRC cell lines (HCT-116, DLD-1, and HT-29) along with the healthy intestinal epithelial cell line CCD 841 CoN. These cells were treated with MES and LACT separately, as well as in combination. We demonstrated that the combination of MES and LACT reduced the viability of CRC cells more effectively than either compound alone, while slightly increasing the viability of normal intestinal epithelial cells. The synergistic effect of MES and LACT may serve as a foundation for developing new treatment strategies for CRC, utilizing compounds with a high safety profile.
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Buy Jarrow Formulas freeze-dried apolactoferrin product (often 250mg per capsule) has good efficacy for iron regulation and immunity, and preservation of the protein’s structure. Buy on Amazon.
Buy Pure Encapsulations Colostrum 40% IgG : Buy Pure Encapsulations Colostrum, derived from USDA certified dairy farms in the US, is standardized to contain 40% IgG (immunoglobulins) and is a concentrated source of lactoferrin.
Suggested Instructions: Bovine Lactoferrin 30 min after breakfast and dinner, and the Probiotic supplement 1 h after breakfast and dinner.
Potent Anti-Obesity Effects of Lactoferrin and reduction in CRP
Ono, Tomoji, et al. “Potent anti-obesity effect of enteric-coated lactoferrin: decrease in visceral fat accumulation in Japanese men and women with abdominal obesity after 8-week administration of enteric-coated lactoferrin tablets.” British journal of nutrition 104.11 (2010): 1688-1695.
They were given 300 mg of enteric coated lactoferrin per day for 8 weeks (or placebo). After 8 weeks, the lactoferrin group LOST weight (-1.5 kg or 3.3 lb) while the control group GAINED weight (+1 kg or 2.2 lb). Those taking lactoferrin also saw greater waist + hip circumference loss than the control. Most striking of all was that the lactoferrin group markedly shed visceral fat. They lost over 12% of their visceral fat, while the control lost under 2%. Total fat area was reduced by more than double in the lactoferrin group. CRP DROPPED in the lactoferrin group by 1 mg/L, while it increased in the control by nearly 3.
Other Benefits of Lactoferrin:
1. Lactoferrin binds to and inactivates LPS. Thus, along with Berberine prevents “leaky gut” , insulin resistance, inflammation, and obesity.
Drago-Serrano, Maria Elisa, et al. “Lactoferrin-lipopolysaccharide (LPS) binding as key to antibacterial and antiendotoxic effects.” International immunopharmacology 12.1 (2012): 1-9.
2. Lactoferrin has direct anti-inflammatory effects (inhibits NF-κB, ICAM-1, VCAM-1, etc.). Inflammation directly promotes insulin resistance and fat gain.
Yami, Hojjat Allah, et al. “The immunomodulatory effects of lactoferrin and its derived peptides on NF‐κB signaling pathway: A systematic review and meta‐analysis.” Immunity, inflammation and disease 11.8 (2023): e972.
Lactoferrin and its derived peptides can be considered potent prophylactic and therapeutic candidates against inflammation‐associated diseases by targeting the NF‐kB pathway.
- Antimicrobial, antiviral, anti-tumor, anti-bacterial, anti-fungal [1] [2] [3] [4] [5]
- Reduces fatty liver caused by high fat diet [7]
- Protects against alcohol induced liver injury [8]
- Reduces histamine release [9]
- Reduces fatty liver caused by high fructose diet [10]
- Protect against Endotoxin, Septic Shock, Cytokine Reaction [12] [17]
- Viral inhibition [15]
- Alleviates constipation [16]
Header Image: Cows at Ashridge Park, Hertfordshire, England. October 25, 2025. Author: Simon Burchell. CC 4.0 Courtesy of Wikimedia Commons
Links to Articles with Related Interest:
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Hashimoto’s Thyroiditis Caused by H. Pylori
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Links and References:
1) Di Mario, Francesco, et al. “Use of bovine lactoferrin for Helicobacter pylori eradication.” Digestive and Liver Disease 35.10 (2003): 706-710.
Study: Adding lactoferrin to 7-day triple therapy achieved 100% H. pylori eradication vs just 76.9% with antibiotics alone (23% improvement in cure rate) The mechanism: lactoferrin binds iron that H. pylori needs to survive → disrupts bacterial biofilms → enhances antibiotic penetration → kills H. pylori → protects beneficial bacteria → prevents relapse Dose: 200mg lactoferrin, 3x daily (600mg total – must be 95%+ purity)
2) Choe, Yon Ho, et al. “Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa.” Journal of gastroenterology and hepatology 18.8 (2003): 980-985.
The lactoferrin sequestration in the gastric mucosa of HPIDA , H. pylori gastritis, and coexisting iron-deficiency anemia (HPIDA; n = 26) was remarkable, and this finding seems to give a clue that leads to the clarification of the mechanism by which H. pylori infection contributes to iron-deficiency anemia.
Husson, MARIE-ODILE, et al. “Iron acquisition by Helicobacter pylori: importance of human lactoferrin.” Infection and immunity 61.6 (1993): 2694-2697.
Okuda, Masumi, et al. “Bovine lactoferrin is effective to suppress Helicobacter pylori colonization in the human stomach: a randomized, double-blind, placebo-controlled study.” Journal of infection and chemotherapy 11.6 (2005): 265-269.
Hablass, Fahmy H., Sameh A. Lashen, and Eman A. Alsayed. “Efficacy of lactoferrin with standard triple therapy or sequential therapy for Helicobacter pylori eradication: A randomized controlled trial.” The Turkish Journal of Gastroenterology 32.9 (2021): 742.
Bovine lactoferrin could hasten the effectiveness of the proton-pump-based triple therapy or sequential therapy for H. pylori eradication.
Ciccaglione, Antonio Francesco, et al. “Bovine lactoferrin enhances the efficacy of levofloxacin-based triple therapy as first-line treatment of Helicobacter pylori infection: an in vitro and in vivo study.” Journal of Antimicrobial Chemotherapy 74.4 (2019): 1069-1077.
Yuan, Yuping, et al. “Recombinant human lactoferrin enhances the efficacy of triple therapy in mice infected with Helicobacter pylori.” International Journal of Molecular Medicine 36.2 (2015): 363-368.
Zullo, A., et al. “Quadruple therapy with lactoferrin for Helicobacter pylori eradication: a randomised, multicentre study.” Digestive and liver disease 37.7 (2005): 496-500.
Lu, Jacky, et al. “The innate immune glycoprotein lactoferrin represses the Helicobacter pylori cag type IV secretion system.” Chembiochem 22.18 (2021): 2783-2790.
Tolone, Salvatore, et al. “Evaluation of Helicobacter Pylori eradication in pediatric patients by triple therapy plus lactoferrin and probiotics compared to triple therapy alone.” Italian journal of pediatrics 38.1 (2012): 63.
Wang, Nannan, et al. “Bovine lactoferrin inhibits resistant Helicobacter pylori in vitro and protects gastric mucosal injury in vivo.” International Dairy Journal 147 (2023): 105770.
!!!!!!!!!!!!!! Best !!!!!!!!!!!!!!!!!
De Bortoli, Nicola, et al. “Helicobacter pylori eradication: A randomized prospective study of triple therapy: Versus: Triple therapy plus lactoferrin and probiotics.” Official journal of the American College of Gastroenterology| ACG 102.5 (2007): 951-956.
Bovine lactoferrin (bLf) in the diagnosis and therapy of various gut disorders (4, 5). BLF, a multifunctional iron-binding glycoprotein that is found in the milk, mucosal secretions (e.g., saliva, tears, bile), pancreatic and seminal fluids, and specific granules of the polymorphonuclear leukocytes in humans and bovines appears to be an
important factor in the host’s defence against a wide range of
bacteria.
Probiotics (Pbs) are also now widely accepted as useful agents in the prevention and treatment of pathological conditions such as infections of the small and large intestine. Temporary colonization of the gut with an appropriate probiotic strain promotes the state of eubiosis and can have a favorable immunomodulatory effect. Controlled clinical trials have demonstrated the efficacy of Pbs as first-line therapy for pathological conditions such as inflammatory bowel disease, irritable bowel syndrome, and gut virus infections (6).
One possible application that has attracted increasing interest
is the use of Pbs against H. pylori infection (7–10).
Patients were instructed to take the proton pump inhibitor 30 min before breakfast and dinner, the antibiotics and bLf 30 min after breakfast and dinner, and the Pb supplement 1 h after breakfast and dinner.
OBJECTIVES: Helicobacter pylori is causally associated with gastritis and peptic ulcer diseases. Recent data (meta-analysis) have demonstrated that triple therapy with amoxicillin, clarithromycin, and a proton pump inhibitor has an eradication rate of only 74–76% and new therapeutic protocols may be necessary. The aim of this study was to examine whether adding bovine lactoferrin (bLf) and probiotics (Pbs) to the standard triple therapy for H. pylori infection could improve the eradication rate and reduce side effects.
METHODS: H. pylori infection was diagnosed in 206 patients: in 107 based on an upper endoscopy exam and a rapid urease test, and in 99 by means of the H. pylori stool antigen-test and the C13 urea breath test
(C13 UBT). The patients were randomized into two groups: 101 patients (group A) underwent standard triple eradication therapy (esomeprazole, clarithromycin, amoxicillin), while 105 patients (group B) underwent a modified eradication therapy (standard triple eradication therapy plus bLf and Pb). Successful eradication therapy was defined as a negative C13 UBT 8 wk after completion of the treatment. Results were evaluated by intention-to-treat (ITT) and per-protocol (PP) analysis.
Data were evaluated and considered positive when P < 0.05.
RESULTS: At the end of the study 175/206 patients showed negative C13 UBT results. According to intention-to-treat analysis, the infection was eradicated in 73/101 patients from Group A and in 93/105 from Group B. PP analysis showed 73/96 patients from Group A and 93/101 from Group B to have been successfully treated. More patients from group A than from group B reported side effects from their treatment (P < 0.05).
CONCLUSIONS: The results of our study suggest that the addition of bLf and Pbs could improve the standard eradication therapy for H. pylori infection—bLf serving to increase the eradication rate and Pbs to
reduce the side effects of antibiotic therapy.
https://pubmed.ncbi.nlm.nih.gov/9200282/
Nakao, K., et al. “Gastric juice levels of lactoferrin and Helicobacter pylori infection.” Scandinavian journal of gastroenterology 32.6 (1997): 530-534.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10144760/
Imoto, Ichiro, et al. “Antimicrobial effects of lactoferrin against Helicobacter pylori infection.” Pathogens 12.4 (2023): 599.
Lactoferrin (LF) may suppress bacteria growth by depriving them of iron and exerts bactericidal activity by enhancing the permeability of the bacterial membrane [33]. In addition, LF degradation by pepsin releases lactoferricin (LFcin), another potent antibacterial peptide [32,34]. Interestingly, LFcin was reported to inhibit the urease activity of H. pylori [32]. The production of ammonia by urease released by H. pylori is a critical factor that allows the bacterium’s survival in the stomach’s acid environment [35]. Reports also support the antiviral effects of LF. It may inhibit viral penetration into host cells by binding to cell surface proteoglycans, binding to viral proteins, or interfering with intracellular viral transport [26,33]. In addition to the direct effect of LF on H. pylori, its anti-inflammatory activity may also explain the therapeutic properties of LF in H. pylori-associated pathology including gastric injury [36,37,38,39]. LF may also modulate the inflammatory response by interacting with immune cell surface receptors, regulating intracellular signal pathways, and controlling the production of inflammatory cytokines and the oxidant activity of iron [40,41,42,43]. In addition, evidence suggests that LF may exhibit anticancer activity by inhibiting the migration and proliferation and inducing apoptosis of cancer cells [26,44,45].
Lactoferrin and Acne vulgaris
Kim, Jungmin, et al. “Dietary effect of lactoferrin-enriched fermented milk on skin surface lipid and clinical improvement of acne vulgaris.” Nutrition 26.9 (2010): 902-909.
Mueller, Edgar A., et al. “Efficacy and tolerability of oral lactoferrin supplementation in mild to moderate acne vulgaris: an exploratory study.” Current medical research and opinion 27.4 (2011): 793-797.
Chan, Heidi, et al. “A randomized, double‐blind, placebo‐controlled trial to determine the efficacy and safety of lactoferrin with vitamin E and zinc as an oral therapy for mild to moderate acne vulgaris.” International journal of dermatology 56.6 (2017): 6
86-690.
ALKady, O. H., et al. “Assessment of Serum Lactoferrin Level in Patients with Acne Vulgaris.” Benha Journal of Applied Sciences 5.5 part (2) (2020): 247-250.
Su, Yuanting, Wei Cui, and Hongquan Wei. “Influence of lactoferrin on Propionibacterium acnes‐induced inflammation in vitro and in vivo.” Dermatologic Therapy 33.6 (2020): e14483.
Hassoun, Lauren A., and Raja K. Sivamani. “A systematic review of lactoferrin use in dermatology.” Critical Reviews in Food Science and Nutrition 57.17 (2017): 3632-3639.
Su, Yuan‐Ting, et al. “Lactoferrin regulates sebogenesis and inflammation in SZ95 human sebocytes and mouse model of acne.” Journal of cosmetic dermatology 22.4 (2023): 1361-1368.
Faruga-Lewicka, Wioleta, and Marek Kardas. “The role of vitamin D, omega acids, antioxidants, berberine, probiotics, lactoferrin and inositol in acne.” Farm Pol 78.11 (2022): 667-672.
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