Lactoferrin: Promising Strategy for Better Bone and Joint Health - Combats Osteoporosis and Osteoarthritis

Over the last ten years, lactoferrin, a natural bioactive glycoprotein from milk, has stirred considerable interest in the field of bone health. (1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16) Lactoferrin limits inflammatory messenger molecules to reduce inflammation and reduce catabolic (tearing down) activity in the body. This includes a calming down of the destructive action of osteoclasts, the cells responsible for excessive bone resorption that leads to osteoporosis. This anti-catabolic effect not only helps people with osteoporosis but it also prevents the cartilage degradation seen in people who suffer from osteoarthritis. (17,18)

Lactoferrin, a multifunctional protein of the innate immune defense system.

Now, with solid evidence (19,20,21) that lactoferrin also enhances anabolic (bone building) activity in bones, it is currently one of the hottest and most promising neutraceutical on the market for combating osteoporosis. Lactoferrin's anabolic (building) effect on bone stems from its ability to reduce inflammation and osteoclastic activity, and also by improving osteoblast cell activity for enhanced bone formation.

Lactoferrin is one of those few molecules that is known to effect both the osteoclasts and the osteoblasts in the remodeling activity of bone...AND it is NOW in OsteoStim. OsteoStim already includes a stellar list of natural vitamins, herbs, and bioactive ingredients shown to help balance bone remodeling through a reduction in osteoclastic activity and a boost in osteoblastic bone-building action. This OsteoNaturals product has just gotten better.

1. Blais, A., Malet, A., Mikogami, T., et al. Oral bovine lactoferrin improves bone status of ovariectomized mice. Am J Physiol Endocrinol Metab 2009:296(6):E1281-8.
2. Bharadwaj, S., Naidu, A.G., Betageri, G.V., et al. Milk ribonuclease-eriched lactoferrin induces positive effects on bone turnover markers in postmenopausal women. Osteoporos Int 2009; Sept 20(9):1603-11.
3. Guo HY, Jiang L, Ibrahim SA, et al. Orally administered lactoferrin preserves bone mass and microarchitecture in ovariectomized rats J Nutr. 2009;139(5):958–6.
4. Cornish J, Callon KE, Naot D, et al. Lactoferrin is a potent regulator of bone cell activity and increases bone formation in vivo. Endocrinology. 2004;145(9):4366–74.
5. Lorget F, Clough J,Oliveira M, Daury MC, Sabokbar A,Offord E. Lactoferrin reduces invitro osteoclast differentiation and resorbing activity. Biochem Biophys Res Commun. 2002;296(2):261–6. 
6. Takayama Y, Mizumachi K. Effect of bovine lactoferrin on extracellular matrix calcification by human osteoblast‐like cells. Biosci Biotechnol Biochem. 2008;72(1):226–30. 
7. Takayama Y, Mizumachi K. Effect of lactoferrin‐embedded collagen membrane on osteogenic differentiation of human osteoblast‐like cells. J Biosci Bioeng. 2009;107(2):191–5. 
8. Yagi M, Suzuki N, Takayama T, et al. Effects of lactoferrin on the differentiation of pluripotent mesenchymal cells. Cell Biol Int. 2009;33(3):283–9. 
9. Grey A, Banovic T, Zhu Q, et al. The low‐density lipoprotein receptor‐ related protein1is a mitogenic receptor for lactoferrin in osteoblastic cells. Mol Endocrinol. 2004;18(9):2268–78. 
10. Grey A, Zhu Q, Watson M, Callon K, Cornish J. Lactoferrin potently inhibits osteoblast apoptosis,viaanLRP1‐independent pathway. Mol Cell Endocrinol. 2006;251(1–2):96–102. 
11. Grey A, Zhu Q, Watson M, Callon K, Cornish J. Lactoferrin potently inhibitsosteoblastapoptosis,viaanLRP1‐independent pathway. Mol Cell Endocrinol. 2006;251(1–2):96–102. 
12. Naot D, Chhana A, Matthews BG, et al. Molecular mechanisms involved in hemitogenic effect of lactoferrin in osteoblasts. Bone. 2011;49(2):217–24.  
13. Hou, J.M., Chen, E.Yl, Wei, S.C., et al. Lactoferrin inhibits apoptosis through insulin-like growth factor 1 in primary rat osteoblasts. Acta Pharmacol Sin 2014;35(4):523-30. 
14. Onubushi, T., Kawazoe, A., Miyauchi, M., et al. Molecular mechanisms of the inhibitory effects of bovine lactoferrin on lipopolysaccharide-mediated osteoclastogenesis. J Biol Chem 2012;287(28):23527-36.
15. Ying, X., Cheng, S., Wang, W., et al. Effect of lactoferrin on osteogenic differentiation of human adipose stem cells. Int Orthop 2012;36(3):647-53.
16. Montesi, M., Panseri, S., Iafisco, M., et al. Coupling hydroxyapatite nanocrystals with lactoferrin as a promising strategy to fine regulate bone homeostasis. PloS One 2015;10(7);e0132633
17. Ahmadinia, K., Yan, D., Ellman, M., Im, H.J. The anti-catabolic role of bovine lactoferricin in cartilage. Biomol Concepts 2013;4(5):495-500.
18. Kim, J.S., Ellman, EB,. An, HS., et al. Lactoferricin mediates anabolic and anti-catabolic effects in the intervertebral disc. J Cell Physiol 2012;227(4):1512-20.
19. Amini AA, Nair LS. Lactoferrin: a biologically active molecule for bone regeneration. Curr Med Chem. 2011;18(8):1220–9. 
20. Li, W., Zhu, S., and Hu. J., Bone regeneration is promoted by orally administered bovine lactoferrin in a rabbit tibial distraction osteogenesis model. Clin Orthop Relat Res 2015; 473(7):2383-93. 
21. Zhang, W., Guo, H., Jing, H., et al. Lactoferrin stimulates osteoblast differentiation through PKA and p38 pathways independent of lactoferrin’s receptor LRP1. J Bone Miner Res 2014;29(5):1232-43.

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Treatment Sequence with Osteoporosis Medications Matters

The effects of medications on bone can be dramatic. Glucocorticoids (e.g. prednisone and dexamethasone) for inflammation, thiazolidinediones (e.g. Avandia and Actos) for type 2 diabetes, and proton pump inhibitors (e.g. Prevacid and Nexium) all can lead to dramatic bone loss. In fact, bone loss can be so profound from drug therapy that it is very important to talk with your doctor about any possible impact on skeletal health when being prescribed a new medication.

Medications specific to osteoporosis treatment can also be very powerful. Many people are aware that drugs for osteoporosis can cause both minor and severe adverse effects. [The most common drugs available for the treatment of osteoporosis are the antiresorptive bisphosphonates (alendronate, risedronate, ibandronate and zoledronic acid) and Prolia (denosumab), and the anabolic Forteo (teriparatide - TPTD).] Most of these drugs can even lead to increased risk for fracture when taken for three or more years. But what many people don't realize is that these drugs are so powerful that it REALLY matters WHICH medication your doctor prescribes first. He or she needs to choose the RIGHT medication for the job...the FIRST time. Guessing is not good here. Getting it wrong can lead to life-threatening consequences. Unlike an antibiotic that can be changed if the first one doesn't seem to be working to kill off an infection, antiresorptive osteoporosis medications can limit the effectiveness of the anabolic drug TPTD...so order is everything when selecting which of these drugs to use in each individual case.

When someone has severe bone loss and they have sustained fractures, it is common to put them on a sequential treatment program of TPTD (the only anabolic drug therapy currently available) for two years followed by a course of treatment with an antiresorptive bisphosphonate or denosomab. This sequential drug therapy can have dramatic and positive results for reducing fracture risk when drug therapy is warranted.

But what if a person with osteoporosis were to be treated initially with a bisphosphonate and THEN, due to a lack of response (no improvement in bone mineral density (BMD) to the antiresorptive drug, was then prescribed TPTD? Is this a wise protocol? Can this sequence lead to increased fracture risk? This is exactly what Dr. Felicia Cosman of Helen Hayes Hospital in NY set out to evaluate. The importance of proper drug sequencing is the subject of her recent perspective in this months issue of the Journal of Bone and Mineral Research.

In a perspective reviews study, Dr. Cosman concluded the following:

1) When selecting a treatment protocol for someone with severe bone loss, if no osteoporosis drug therapy has been used before, Dr. Cosman recommends TPTD anabolic therapy first (if appropriate) followed by antiresorptive therapy.

2) She goes on to say,"...our observations clearly highlight that the common practice of providing patients with first-line antiresorptive therapy and then only after patients have an inadequate BMD response and/or an intercurrent fracture to switch to TPTD is not the optimal utilization of anabolic treatment." Dr. Cosman explains that this is extremely important especially when someone sustains a hip fracture. She states that to transition to TPTD after a course of antiresorptive therapy "might in fact lead to a transient loss of strength in cortical sites, including the other hip. This is critically important in patients with a recent fracture where we know the risk of a second imminent fracture is extremely high..."(Hip fractures are a common cause of premature death. Over 50% of people who fracture a hip will die within the year.) For these cases she recommends concurrent treatment with an antiresorptive agent and TPTD instead of sequential therapy. 

Cosman, F., Nieves, JW., and Dempster, DW. 2017. Treatment sequence matters: anabolic and antiresorptive therapy for osteoporosis. J Bone Miner Res 32(2):198-202.

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OsteoStim is Available

Our new shipment of OsteoStim has finally arrived. For four years now, OsteoStim has been

instrumental in helping many people turn around their declining bone mineral density and regain confidence in the strength of their skeleton. Once again they can wake up with the peace of mind that their bones will get them through the day without breaking. And now...OsteoStim is not only back in stock, but it is better than ever. Here is what we did to improve OsteoStim:

OsteoStim update: 

• We have enhanced the formula with the addition of Bioferrin® 1000 (a product of Glanbia Nutritionals), a low-iron form of lactoferrin called apolactoferrin.
  Clinical research demonstrates lactoferrin, a purified bioactive glycoprotein found naturally in milk, is anabolic to bone. Lactoferrin has been shown to reduce inflammation, stimulate the immune system, improve gut health, and best of all strengthen bones. Lactoferrin stimulates the production of osteoblasts to enhance bone formation while inhibiting osteoclasts (cells that destroy bone). The addition of lactoferrin to our OsteoStim makes this product by far the product of choice when searching for bone-health supplements.
• OsteoStim is GMO free!

We are confident you will find these changes make our OsteoStim even better! As always, the mission of OsteoNaturals is to provide the best nutrition products possible for skeletal health.  

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OsteoStim: Now has Apolactoferrin

On March 8th you will finally be able to place your order for OsteoStim. It has been a long arduous

process, but getting things right sometimes takes time...and this certainly took more time than expected. From procuring ingredients, to manufacturing, and even to printing labels, we seemed to run into production delays all the way. But production is finally complete and we are just waiting for labels to be affixed to the bottles and shipped. We couldn't be more excited about the final product.

As many of you know from previous Newsletters, OsteoStim will now contain another ingredient. In an ongoing effort to bring you the most effective nutrition product available for improving skeletal health, we have added a low-iron form of lactoferrin to OsteoStim.

Lactoferrin is a naturally occurring glycoprotein found in milk. It is an important part of the immune system and helps the body's innate immune defense fight against harmful bacteria, viruses, and fungi. In addition to its antimicrobial activity, lactoferrin also helps normalize bone remodeling activity as seen in the reduction of bone resorption markers (N-telopeptide and deoxypyridinoline) and increase in bone formation markers (osteocalcin and alkaline phosphatase). (1) 

With its normalizing impact on the immune system, lactoferrin reduces chronic systemic inflammation (2) which is common in people suffering from osteoporosis. This type of inflammation is often the cause of excessive osteoclastic bone resorption and bone loss. Lactoferrin not only reduces osteoclastic activity but it is one of the few compounds that can also stimulate osteoblast cells for improved bone formation. (3) The reason we see so much periodontal disease, small bowel bacterial overgrowth, candida infections, joint inflammation, muscle pain, elevated blood sugar, depression, and fatigue in patients with osteoporosis is because these are all signs and symptoms of chronic systemic inflammation. But if we reduce the chronic inflammation (and lactoferrin does a great job at this) we also REDUCE EXCESS OSTEOCLASTIC BONE RESORPTION and improve bone, and overall, health.

But...there is one drawback to lactoferrin, especially in postmenopausal women. Lactoferrin increases iron levels in the body. With no more blood loss from monthly periods, postmenopausal women should not be taking in excess iron. For this reason, we are using a special form of lactoferrin called Bioferrin 1000 (Bioferrin is a registered trademark of Glanbia Nutritionals). Bioferrin 1000 is a low-iron form of lactoferrin called apolactoferrin. In fact, for each 100 grams of Bioferrin 1000 there is less than 15 milligrams iron. In three capsules of OsteoStim there is a therapeutic dose of 250 milligrams apolactoferrin which makes this dosage virtually iron free.

We are very proud to be able to provide you with this product.


1) Bharadwaj, S., et al. 2009. Milk ribonuclease-enriched lactoferrin induces positive effects on bone turnover markers in postmenopausal women. Osteoporosis Int 20(9):1603-11.

2) Bharadwaj, S., et al. 2010. Inflammatory responses improve with milk ribonuclease-enriched lactoferrin supplementation in postmenopausal women. Inflammatory Research 59(11):971-8.   

3) Naot, D., et al. 2005. Lactoferrin - A novel bone growth factor. Clinical Medicine & Research 3(2):93-101.

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