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Osteoporosis Begins In Gut, Driven By Dysbiosis.

Updated: Aug 6, 2023

The Science

In the early phase of the emergence of research on Th17 cells, researchers realized that autoimmunity was being driven by these (relatively recently identified) Th17 cells, not (as had been long believed) Th1 cells.

Where osteopenia & osteoporosis are concerned, this research makes quite a convincing case for the role of tumor necrosis factor-positive (TNF+) Th17 cells migrating from the intestinal tract to the bone—driven by intestinal dysbiosis.

That's right, osteoporosis begins in the gut, driven by dysbiosis.

Loss of estrogen further encourages this migration.

The papers where this research initially appeared are Chen et al. (Frontiers in Microbiology, 2021) and Yu et al. (Journal of Clinical Investigation, 2021). A third paper discusses the implications of the JCI paper.

Two additional papers discuss the research on icariin, and salvia miltiorrhiza, and other natural substances (e.g., genistein) that promote osteoblast activity and inhibit osteoclastic activation (not that healthy bones don't need both—it's just the imbalance we're addressing).

The Take Home

This exciting new research hints at a more subtle and perhaps sophisticated understanding of the processes driving bone weakness and loss with age. While many enlightened folks long ago moved beyond the "calcium + vitamin D" supplementation paradigm. This fascinating new research even moves us past the protein sufficiency, K2, trace minerals template we've been working with for several years now. Can nothing be simple anymore?

  1. For starters, "Get to the root." Address & clean up the dysbiosis. This is not always easy, but a well-chosen combo antimicrobial product taken pretty religiously over the course of 1 or 2 months, has changed many a life. Additionally, since persistent microbial infiltration/infection in other so-called "hollow spaces" is also known to promote chronic Th17 cell proliferation and activation, suss out and treat these other "hollow space" infections; most notably, chronic sinusitis, chronic vaginitis, chronic UTIs and chronic lung inflammation.

  2. Support the Th1 response (which downregulates Th17— and also, conveniently, promotes osteoblastic activity). This is typically done with berberine (from the various yellow root & rhizome sources: Oregon grape, coptis, skullcap, phellodendron), baicalin (again, skullcap), sulforaphane (your home grown broccoli sprouts), ginger, echinacea, and a few others, often in combination.

  3. In addition to support for Th1, support for regulatory T cell functions ("T regs") is also likely to be helpful, to reduce inflammation and particularly the NFkB/STAT3 coactivation that connects inflammation with Th17 activation. This can be done with curcuminoids, resveratrol, fish oil, and a few others.

  4. Consider adding icariin (from the Oriental medicine herb Yin Yang Huo also known as epimedium) and salvia miltiorrhiza (from the Oriental medicine herb Dan Shen) to support osteoblasts and inhibit osteoclasts. Some may also wish to consider using a genistein-containing product, a soy-based phytoestrogen.

Many wise folks have already implemented fish oils, curcumin, sulforaphanes and even ginger into their everyday lives. So if you can only wrap your head around 1 or 2 of these interventions, first would be assessing and addressing the condition of your intestinal microbial balance. The second (although choosing between hormone balance and gut health is a choice of Sophie) would be optimizing hormone balance, whether through herbal & lifestyle tweaks or through (carefully vetted) BHRT.



Gut Microbiota and Bone Diseases: A Growing Partnership

Front Microbiol. 2022 May 6;13:877776. Chen Y, Wang X, Zhang C, et al.

Ovariectomy induces bone loss via microbial-dependent trafficking of intestinal TNF+ T cells and Th17 cells J Clin Invest. 2021 Feb 15;131(4):e143137. Yu M, Pal S, Paterson CW, et al.

From the gut to bone: connecting the gut microbiota with Th17 T lymphocytes and postmenopausal osteoporosis J Clin Invest. 2021 Mar 1;131(5):e146619. Lorenzo J.


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