Ben Doughty
Exploring how hyaluronan dynamics shape developmental timing, aging, and disease. 💧
OSF: osf.io/sd5g4/
- Cancer and aging may resist “cures” for the same reason: they aren’t diseases of parts, but of the biological environment those parts live in.
- When survival depends on danger, bodies harden. When survival depends on cooperation, bodies soften. Modern humans may be shaped less by predators and more by protection, not just culturally, but biologically.
- I’ve written a essay outlining a framework I’ve been developing around hyaluronan, development, and tissue timing. bendoughty1.substack.com/p/the-hyalur...
- Mistimed metabolic maturation may accelerate aging.
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- We talk about “self-domestication” in animals and early humans. But rarely ask whether it’s accelerated since industrialization, especially in men. Safer environments and better nutrition change development.
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- Reposted by Ben DoughtyI am happy to share this article, entitled "The importance of Biological Theory". It is my inaugural editorial as the new Editor-in-Chief of @biologicaltheory.bsky.social . In these complex and challenging times, theory is more important now than ever. Enjoy! doi.org/10.1007/s137...
- Inflammaturation: a term I’m using for when inflammation-linked signals act as premature maturation cues. Aging is framed as chronic inflammation. Development as growth and plasticity. But what if some inflammation advances developmental timing?
- Reposted by Ben DoughtyHow do cells orchestrate themselves to achieve a directional movement as a group? Hi, I’m @sayukihirano.bsky.social. In this thread, I’ll highlight key mechanisms of how cells communicate with each other to perform directional collective migration.
- Reposted by Ben Doughty“Doctors won’t tell you this, but you don’t need medication for a tapeworm—all you need is the natural power of friction,” Robert F. Kennedy Jr. said as he dropped to the floor, lifted his legs high, and dragged his ass along the White House carpet during a press conference.
- Perineuronal nets (PNNs) are often described as the brain’s “plasticity brakes.” They condense around certain neurons—especially fast-spiking inhibitory interneurons—and mark the closure of critical periods for learning and circuit refinement.
- Very interesting preprint
- Hyaluronan underlies the emergence of form, fate, and function in human cardioids biorxiv.org/content/10.64898/20…
- Here’s an idea I’ve been working on, I jokingly call it the Hyaluronan Terrain Hypothesis. It was either that or the wet soil hypothesis. osf.io/sd5g4/
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- Long-lived animals often tolerate hypoxia (diving, burrowing, low-O₂ habitats). Hypoxia upregulates hyaluronan production, likely biasing toward longer chains, yet HA molecular weight is barely studied across species. Crocodilians are a rare exception, with reports of elevated HMW-HA.
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- Reposted by Ben DoughtyNot an alien, they have been around here for awhile: Crinoids! #LetsChangeThat
- An interesting preprint: "A role for heavy chain-modification in protecting hyaluronan from free radical fragmentation during inflammation." www.biorxiv.org/content/10.6...
- A possible metabolic link is substrate availability: high glucose increases the sugars needed to make hyaluronan. In insulin-resistant states, more glucose is diverted into pathways like hexosamine biosynthesis pathway, expanding UDP-sugar pools used for HA. HA accumulation is reported in diabetes.
- What's interesting is that hydrogen peroxide can easily travel out into the ECM. It's also produced and released by immune cells during inflammation. On its own, hydrogen peroxide isn't very effective at breaking down hyaluronan.
- Reposted by Ben DoughtyModern biology research is biased towards investigating genes that are widely conserved and present in humans. What about genes that ARE widely conserved but NOT present in humans? Can genes missing from humans tell us something about what makes our biology different from that of other animals? 1/8
- RHAMMΔ163 and telomerase regulation pubmed.ncbi.nlm.nih.gov/40661163/
- Here's what I'm thinking: There’s evidence that fully or partially knocking out TMEM2 / hyaluronidase causes developmental problems, including in the heart. So you can’t just aggressively modify hyaluronan turnover during early development without consequences. I'm thinking - metabolism.
- Regenerate Hyaluronan: Prime tissue with HA precursors (UDP-sugars), then apply a brief HIF-2α–leaning pseudohypoxic pulse under low-ROS conditions without drifting into HIF-1α. Repeat. Possible?
- Extracellular matrix proteolysis maintains synapse plasticity during brain development. Seems Hyaluronan turnover would be required for plasticity www.nature.com/articles/s41...
- Surely the boomers have noticed..
- Speculative idea: Sulforaphane helps protect CD44, reducing HA breakdown and receptor shedding + activates NRF2 Starch-heavy diets push glycolysis, supplying substrate to make long chains I can imagine a previous human with rock hard skin, we would look like babies in comparison
