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The Gut-Bone Connection

At-a-Glance:

  • Research uncovered direct and indirect connections between the intestines and bones.
  • You can now address this important underlying component of bone health. 
  • Intestinal chronic inflammation, malabsorption, dysbiosis, and medications stimulate bone destruction. 
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    By Dr. John Neustadt

    Over the last decade, research has uncovered direct and indirect connections between the intestines and bones. This helps explain why gastrointestinal issues contribute to bone loss and empowers us to address this important underlying component of bone health. 

    In the general population, about 43% of adults 50 years and older have some bone loss. When someone has a gastrointestinal issue, their risk for bone loss is even higher. Up to 60% of people with Celiac disease and up to 77% of people with irritable bowel disease (IBD) have bone loss.1-3 In fact, a low bone density test can be the only presenting symptom of celiac disease.4

    Regardless of the label applied to the condition, the common underlying causes of bone loss in all these situations are chronic inflammation, malabsorption, dysbiosis, and medications.

    Chronic Inflammation
    Immune cells produce molecular signals that regulate inflammation. These are called cytokines, and they directly influence bone health. Pro-inflammatory cytokines increase bone-destroying osteoclast cells in bone. These include tumor necrosis factor-alpha (TNF-alpha) and interleukins (e.g., IL-1, IL-6, IL-7, IL-8, and IL-11). Chronic inflammation is a recognized aspect of gastrointestinal diseases, such as irritable bowel syndrome (IBS), Crohn’s disease, and Ulcerative Colitis.5,6 

    Medications have been developed to help reduce inflammation, such as glucocorticoids (e.g., prednisone, dexamethasone); however, these and other medications are potent bone-destroyers.7-9 Multiple clinical trials concluded that MK4 supports healthy bone density in people taking glucocorticoids. In one two-year clinical trial with 60 men and women ages 15-57 years taking prednisone, bone density was maintained in those also taking MK4 (45 mg/day). Those who only took prednisone saw their bone density decrease by 3.19%.10

    Malabsorption
    Intestines act as a barrier and filter. They block the absorption of harmful molecules while allowing healthy ones, like amino acids, flavonoids, vitamins, and minerals, to pass through. This molecular trafficking is crucial for keeping substances that can cause heart disease, bone loss, and other problems out of your bloodstream. 

    Like holes in a sieve, your intestines block particles larger than a certain size under healthy conditions. Chronic inflammation damages the intestinal lining and creates a “leaky gut” situation that allows larger particles to get through. The immune system sees this situation as a threat and releases pro-inflammatory cytokines to deal with it. However, those cytokines also travel to the bones, activate bone-destroying osteoclasts, and decrease bone density.11

    Intestinal inflammation also decreases the absorption of healthy nutrients. Nutrient deficiencies are common in patients with Celiac disease, Crohn’s disease, Ulcerative Colitis, and other gastrointestinal conditions. These include vitamin K, vitamin D, iron, selenium, copper, zinc, folic acid, vitamin B1, vitamin B6, and vitamin B12. In fact, more than half of all patients with Crohn’s disease and Ulcerative Colitis have nutritional deficiencies.12-16

    Medications used for some of these conditions can also contribute to malabsorption and nutritional deficiencies. Acid-blocking medications, like proton pump inhibitors (PPI), decrease the absorption of calcium, magnesium, vitamin B12, other B vitamins, and iron.17, 18 

    Deficiencies of micronutrients (vitamins and minerals) contribute to bone loss because it deprives the bones of the needed raw materials. Taking high-quality dietary supplements to help maintain healthy levels of nutrients. I recommend the products I created for my patients, including Supreme Multivitamin, FerroSolve, Osteo-K, and Osteo-K Minis

    Dysbiosis
    Your gut contains a mind-boggling number of microorganisms. The human intestines are composed of ten trillion to one hundred trillion microorganisms. Their collective genome contains at least 100 times as many genes as your genome, representing 500-1000 species.19, 20 

    The links between the gut microbiome, bone, and systemic health are irrefutable. Intestinal dysbiosis increases inflammation, damages the intestinal lining, and has been observed in people with bone loss.21

    While human studies are lacking, animal studies show that replenishing helpful bacteria with probiotics promotes bone health. Mice studies have shown that the gut microbiome is a major regulator of bone mass, and the vitamins gut bacteria produce may regulate bone matrix quality.22, 23 

    In a four-week study with mice surgically put into menopause by removing their ovaries, which reduced their estrogen, a multistrain probiotic improved bone mass, decreased gut permeability, and reduced systemic inflammation. This study also had a group of mice that weren’t in menopause and had normal estrogen. In this group, the probiotic also increased bone mass. The probiotic blend contained strains of Bifidobacterium breve, Bifidobacterium longum, Bifidobacterium infantis, Lactobacillus acidophilus, Lactobacillus plantarum, Lactobacillus paracasei, Lactobacillus bulgaricus, and Streptococcus thermophilus, which are in NBI’s Belly Rescue product.24

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    References

    1 Mosca C, Thorsteinsdottir F, Abrahamsen B, et al. 2022;110(6):641-648. 

    2 Pollak RD, Karmeli F, Eliakim R, et al. 1998;93(9):1483-90. 

    3 Bjarnason I, Macpherson A, Mackintosh C, et al. 1997;40(2):228-33. 

    4 Bommu VJL, Mirza L. 2021;13(12):e20602.

    5 Ng QX, Soh AYS, Loke W, et al. 2018;11:345-349.

    6 Saez A, Herrero-Fernandez B, Gomez-Bris R, 2023;24(2). 

    7 Canalis E, Mazziotti G, Giustina A, et al. 2007;18(10):1319-28. 

    8 Card T, West J, Hubbard R, et al. 2004;53(2):251-5.

    9 Van Staa TP, Laan RF, Barton IP, et al. 2003;48(11):3224-9. 

    10 Yonemura K, Fukasawa H, Fujigaki Y, et al. 2004;43(1):53-60. 

    11 Paray BA, Albeshr MF, Jan AT, et al. 2020;21(24).

    12 Lai Y, Masatoshi H, Ma Y, et al. 2021;12:791565.

    13 Fletcher J, Cooper SC, Ghosh S, 2019;11(5).

    14 Ghishan FK, Kiela PR. 2017;46(4):797-808. 

    15 Nowak JK, Grzybowska-Chlebowczyk U, Landowski P, et al. 2014;4(1):4768. 

    16 Rondanelli M, Faliva MA, Gasparri C, et al. 2019;55(7).

    17 Thong BKS, Ima-Nirwana S, Chin KY. 2019;16(9).

    18 Qorraj-Bytyqi H, Hoxha R, 2018;6(3):442-446. 

    19 Eckburg PB, Bik EM, Bernstein CN, et al. 2005;308(5728):1635-8. 

    20 Gill SR, Pop M, Deboy RT, et al. 2006;312(5778):1355-9. 

    21 Akinsuyi OS, Roesch LFW. 2023;11(3):e00322-23. 

    22 Sjögren K, Engdahl C, Henning P, et al. 2012;27(6):1357-67.

    23 Guss JD, Taylor E, Rouse Z, et al. 2019;127:146-154. 

    24 Li JY, Chassaing B, Tyagi AM, et al. 2016;126(6):2049-63. 

     

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