Your Fascia Doesn’t Recognize You as a Hunter
Hyaluronan (hyaluronic acid) deficiency is silencing your ancestral repair signals
Morning stiffness and wrinkling skin are usually naturalized as obligatory aging. When you aren’t recognized by your fascia as a hunter, this atrophy accelerates. This vital connective tissue is a functional composite of collagen and hyaluronan, where collagen provides the high-tensile scaffolding and hyaluronan serves as the visco-elastic lubricant that permits low-friction sliding. Your fascia evolved to expect an ancestral supply and signal that initiate structural restoration, signals our ancestors received in massive doses but are now erased from our plates.
The Silence of the Modern Plate
Official dietary guidelines disregard hyaluronan because the molecular signal has effectively vanished from the modern plate. Neither the FDA nor the EFSA provides daily estimates, masking an institutional blind spot where modern diets provide only a residual 3 to 6 milligrams daily[1].
Modern diets valorize skeletal muscle, such as skinless chicken and lean steaks. These tissues contain just 1 to 2 milligrams of hyaluronan per 100 grams; a standard steak provides a scant 5 milligrams[2]. Plants contain none.
The Ancestral Hyaluronan Baseline
Anthropological data from the Hadza, Ju/’hoansi, and Aché attest how whole-animal consumption maintained high hyaluronan levels[3]. By consuming the skin, marrow, and organs that we often throw away today, these groups made use of the richest sources of connective tissue available.
Our ancestors lived through cycles of plenty and hardship. During lean times, people on the savanna relied more on gathered plants. Still, they would have picked up some hyaluronan by getting marrow out of bones and eating small game, probably in the range of 10 to 40 milligrams. Bone broth is the last clear trace of that older pattern of eating, when connective tissues were a regular part of the diet.
A successful hunt fundamentally changed these ancestral proportions. An animal’s fascial networks, skin, and synovial fluid are saturated with hyaluronan, holding roughly 50 to 150 milligrams per 100 grams[4]. By utilizing the whole animal, the tribe transitioned their biological baseline into a high-saturation state, reaching a daily intake range of 150 to 350 milligrams[5].
Hunter vs. Gatherer Mode
Modern diets stall the system in a permanent gatherer mode. Because the fascia no longer recognizes the hunt, it de-prioritizes structural restoration, causing the chronic stiffness we mistake for aging. Ancestrally, dietary hyaluronan operated as a metabolic governor. Consumption of a fresh kill triggered hunter mode, providing the sustained biological command and the necessary building blocks to repair the micro-architectural tears of the hunt through large-scale fascial remodeling[6].
Bioavailability
A basic bioavailability problem makes the simple idea that swallowed hyaluronan travels straight to the fascia much harder to support. Its size alone prevents direct delivery to tissue. In its natural high-molecular-weight form, hyaluronan is already an enormous biopolymer, with a molecular mass that exceeds what the intestine can typically transport. It can also bind up to 1,000 times its own weight in water, which makes its effective size even larger by creating a huge hydrodynamic volume. As a result, native hyaluronan has little to no systemic bioavailability, because the intestinal epithelium acts as a size-selective barrier that keeps these large polymer chains from entering the bloodstream and reaching target tissues[7].
Unlocking the Hunter Mode Supply and Signal
Your microbiome governs this transition. By enzymatically cleaving high-molecular-weight hyaluronan, specialized bacteria simulate the structural fragmentation of the hunt, releasing the specific fragments required to bypass the intestinal barrier and trigger the hunter mode signal[8]. This fermentation process nourishes the gut lining as a premium prebiotic thereby optimizing the Firmicutes-to-Bacteroides ratio.
Exogenous fragments alleviate the biosynthetic burden of de novo hyaluronan production, optimizing systemic metabolic efficiency[9]. Once absorbed, these fragments act as both the substrate supply for hyaluronan production and the biological signal for repair.
Your fascial receptors recognize the hunter through two different inputs. First, high-velocity movement initiates a signaling burst; mechanical shear tears local hyaluronan to release the precise fragment sizes that bind and trigger CD44 receptors[10]. Second, dietary polymers provide a sustained signal.
These large molecules act like a microbial bioreactor, fermenting slowly in the colon and supplying fascial receptors with a steady stream of fragments[11]. Their ongoing presence at the CD44 receptor helps maintain the hunter mode signal, which stimulates fibroblast proliferation and the production of new collagen and hyaluronan. In turn, this supports the structural remodeling needed to repair accumulated mechanical wear[12].
Your CD44 receptors’ activation follows a sigmoidal curve instead of linear progression. Low background levels do nothing as the receptors require a bigger influx to cluster and trigger the repair cascade. When the receptors are saturated, adding more hyaluronan has no bigger effect. Taking ten times the clinical dose will not multiply your results ten times as the fascia is already in hunter mode[13].
Measurable Outcomes for Skin and Joints
Restoring the hunter mode signal reverses structural decline. Clinical trials show that taking 120 to 240 milligrams of oral hyaluronan per day can significantly improve skin hydration and elasticity while also reducing wrinkle depth. A systematic review of seven randomized controlled trials involving 291 patients found that this daily dose led to meaningful improvements in these key measures of skin health[14].
However, because these trials typically last only 8 to 12 weeks, they likely capture only the leading edge of structural repair. With the metabolic half-life of dermal collagen estimated at 15 years, these brief snapshots cannot measure the cumulative, decadal benefit of CD44-mediated collagen remodeling[15]. The visible restoration seen in months marks the inception of a decadal shift in the functional integrity of the internal fascia wrapping every muscle and organ.
Load-bearing joints show the most dramatic systemic repair. A systematic review covering 11 clinical trials and 597 patients found that taking 120 to 240 milligrams daily is the effective range for improving standardized osteoarthritis scores. At this dose, patients saw meaningful reductions in joint pain, stiffness, and physical dysfunction[16]. It also appears to restore support for synovial fluid and fascial signaling. As the extracellular matrix is rebuilt, these precursors help shift the body out of a cycle of chronic friction and back toward smoother, easier movement.
Stiff joints and sagging skin frequently reflect a system starved of hunter mode inputs, signaling a structural atrophy that we too often attribute solely to the passage of time. Restoring the supply and signal your fascia demands through bone broth (which contains other valuable substances as well) or clinical supplementation allows it to recognize the command for repair once more, ending the silence dictated by modern foodways. Restoring these ancestral proportions returns the system to hunter mode, restoring supple skin and vigorous joints.
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Neither the FDA nor the EFSA provides established recommended daily intakes or measurable epidemiological baselines for hyaluronan. The 3 to 6 milligram estimate is derived by Gemini 3.1 Pro from the standard Western consumption of skeletal muscle and the systemic exclusion of hyaluronan-dense connective tissues.
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Commercial meat analyses show that hyaluronan is virtually absent in muscle fibers, appearing only in trace amounts within intramuscular connective tissue. Nakano & Thompson (1996), Glycosaminoglycans of bovine skeletal muscle. Canadian Journal of Animal Science, 76(4).
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Traditional populations ate skin, marrow, and connective tissue to maintain systemic hyaluronan levels far exceeding modern consumption. Cordain et al. (2002), The paradoxical nature of hunter-gatherer diets. European Journal of Clinical Nutrition; and Hill & Hurtado (1996), Aché Life History.
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Skin, cartilage, and synovial fluid have far greater Hyaluronan concentrations compared to skeletal muscle. StatPearls (2024), Integumentary System
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This baseline estimates anthropological intake from Hadza and Aché hunting patterns. The 350 mg upper range derived by Gemini 3.1 Pro reflects the acute metabolic flux provided by the total utilization of large-game connective tissues.
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The hunter mode hypothesis refers to the rapid turnover and repair functions triggered by high-molecular-weight hyaluronan and mechanical stress. Williams et al. (2015), Disrupted homeostasis of synovial hyaluronic acid and its associations with synovial mast cell proteases. Arthritis Research & Therapy
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Intestinal permeability assays show that native high-molecular-weight hyaluronan (often >1,000 kDa) cannot passively traverse the intestinal epithelium, which typically restricts paracellular transport to molecules <1 kDa. Systemic bioavailability necessitates enzymatic cleavage into smaller fragments. Yu et al. (2023), Molecular weight and gut microbiota determine the bioavailability of orally administered hyaluronic acid. Carbohydrate Polymers
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Oral hyaluronan undergoes microbial fermentation to act as a novel prebiotic. See: Zheng et al. (2020), Hyaluronic Acid as a Novel Prebiotic: In Vitro Fermentation and Its Effects on Human Gut Microbiota. International Journal of Biological Macromolecules
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Making hyaluronan from scratch costs the body energy because it depends on activated sugar precursors such as UDP-glucuronic acid and UDP-N-acetylglucosamine. Hyaluronan fragments from outside the body may make that job easier by supplying material that is already partly processed, which could lower some of the ATP and enzyme work needed to build new hyaluronan. Laurent et al. (1997), Hyaluronan: its nature, distribution, functions and turnover. Journal of Internal Medicine
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High-velocity movement generates mechanical shear forces that physically cleave hyaluronan into signaling fragments. Grimmer et al. (2003), Mechanical loading and the extracellular matrix. Journal of Applied Physiology
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High-molecular-weight hyaluronan transits to the colon to act as a “microbial bioreactor” where species like Bacteroides salyersiae release bioactive oligosaccharides. Radioactive tracer studies confirm these fragments persist in target tissues for 24 to 48 hours. Yu et al. (2024), A keystone gut bacterium promotes the absorption of dietary hyaluronic acid. Carbohydrate Polymers; Kimura et al. (2016), Absorption of Orally Administered hyaluronan. Journal of Medicinal Food; and Zhang et al. (2024), The gut microbiota-joint axis in health and disease. Science Bulletin
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Hyaluronan fragments induce endogenous production by binding to CD44 receptors. See: Stern et al. (2006), Hyaluronan fragments: An information-rich system. European Journal of Cell Biology
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Biophysical modeling confirms that hyaluronan binding to CD44 exhibits positive cooperativity, creating a steep, sigmoidal dose-response curve. Receptors require a minimum threshold of ligand density to initiate clustering, and quickly reach an absolute saturation plateau where additional hyaluronan provides no further cellular signaling or biological effect. Wolny et al. (2010), Analysis of CD44-hyaluronan interactions in an artificial membrane system: Insights into the distinct binding properties of high and low molecular weight hyaluronan Journal of Biological Chemistry; and Dubacheva et al. (2015), Designing multivalent probes for tunable superselective targeting. Proceedings of the National Academy of Sciences
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Oral hyaluronan improving skin hydration, elasticity, and wrinkle depth gets shown by the a systematic meta-analysis of Michelotti et al. (2023), Oral intake of a specific sodium hyaluronate: A systematic review and meta-analysis. Nutrients
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The efficacy of oral hyaluronan in reducing pain and improving joint function, demonstrating significant improvements across standardized osteoarthritis metrics (such as WOMAC and VAS scores) gets confirmed by the systematic review of Minoretti et al. (2024), Oral Hyaluronic Acid in Osteoarthritis and Low Back Pain: A Systematic Review. Mediterranean Journal of Rheumatology
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The efficacy of oral hyaluronan in reducing pain and improving joint function, demonstrating significant improvements across standardized osteoarthritis metrics (such as WOMAC and VAS scores) gets confirmed by the systematic review of Minoretti et al. (2024), Oral Hyaluronic Acid in Osteoarthritis and Low Back Pain: A Systematic Review. Mediterranean Journal of Rheumatology.
I don’t object to the AI writing, but I would really appreciate it if you’d include your process for creating this. It seems to be written purely to advocate this position; if you didn’t prompt the model to look at the evidence skeptically, then I think the reader should be very skeptical.
Less wrong asks us to write to inform, not to persuade. Models do write to persuade by default, because most of their training data does.
I think it would be vastly more useful if you carefully prompted the model to critique its own arguments and the research it’s basing them on. Models have limited metacognitive skills relative to humans, so humans can scaffold them to fill that weakness.
Lesswrong is far better for not using the advocacy model of epistemology that much of the world uses. That confuses everyone and makes finding truth far harder than asking each person to be objective and balanced in their thinking and presentation.
(Comment written without AI and not much editing) As far as dealing with AI writing having a field where you explain how you used the AI is probably a better idea than having a policy that requires putting the LLM tags around LLM writing.
The impulse to write the post came from me a two weeks looking at hyaluranon supplement at the drogery store and being skeptical of it doing anything because I was skeptical that it is bioavailable. At that point I did query a model and it told me there are multiple trials that so show clinical effects. Then I was in a discussion with Benque where he argued for glycine deficiency where one of the arguments is that our ancestors got a lot more because they what connective tissue and there was an open question about the merits of straight glycine vs a more natural source.
From there I ran a lot of deep research queries. Often in both Gemini and ChatGPT, sometimes just Gemini as it’s less limited in the amount of deep research I could run.
There are a lot of complex issues to write about around bone broth and it’s ingredients so I had an idea of maybe writing 3-4 posts and focusing the first one hyaluranon. I see the fact that hyaluranon isolated from the other factors does have the clinical effect in the trials as a justification for why it’s justified to take it as one chunk even when I think that glycine, hydroxyprolyl-glycine, prolyl-hydroxyproline, glucosamine, chondroitin and dermatan also have some significance. There’s a bit about elastin that’s not in bone broth but in connective tissue in skin that I’m unsure about.
When running the queries I found the variation between hunter gathers, and from that came the “hunter mode” idea . That label is as far as I can see original to my work.
In my system prompt I have a general command that Gemini is not supposed to edit the canvas without me giving explicit approval for an edit to avoid it digging in defending bad claims. When it comes to writing a new paragraph I feed the relevant deep research reports into the Gemini 3.1 Pro or Gemini 3 Thinking. I mostly used Pro for that.
I had a hypothesis that the effect of hyaluranon supplementation might be similar to the effect of warmup exercises that might be partly make the hyaluranon more fluid, that did not pan out when I did the relevant deep research queries.
Whenever one deals with complex biology, it’s necessary to make decisions about what details are valuable to include or not. I could for example have delved deeper into benefits for the microbiome, but that wasn’t a topic that felt central to the case I wanted to lay out.
After the first draft of the article was finished I did ask Gemini 3 Thinking to improve the article health conscious audience according to Larry McEnery principles of writing. This includes making the text more concise and removing fluff. In that process there were over 100 suggestions about how to change the text that I either approved or explained why they are a bad. From time to time I did ran a query asking whether anything in the article was scientifically inaccurate and fixed issues that came up.
For a while, one of the issues was that of course diets of hunter gathers could have been any mix between plant and animals, so that the model questioned the notion of there being two modes instead of something more gradual. I did add the paragraph about the sigmoidal activation curve rather late, which I think does justify the mode framing.
I did ask Justis for feedback via the LW feedback service and addressed a few concerns he had over the text.
I purposefully avoid giving specific recommendations about what dose to take even when the model would have thought that’s it’s valuable to give more specific recommendations, because I don’t have strong convictions about what dose is ideal.
I for one think that’s a great process and you should definitely include that in such a post to indicate how hard you worked to supply the metacognitive skills, judgment, and skepticism the LLMs tend to lack.
I think explaining that process would get more readers and buy-in; if you just say “some model spit this out” people won’t assume you’ve done that much careful work in prompting them to assemble something valid and meaningful.
I just went through a round of using LLMs for research, and my conclusion was that they need to be prompted to find flaws in methodology or interpretation in each paper individually. They’re too credulous in general. FWIW.
I think it would be ideal if you’d identified the alternate explanation Benquo gave; the lack of bioavailability seems like a glaring problem for your theory. But I also think that sort of problem is pretty likely in a thoroughly human-written post too, and it’s quite useful to write it anyway so that public discussion like that happens!
I’m uncertain whether I think supplementation is warranted (pending researching for possible side effects) given that exchange, so I’d love to see your further thoughts on that.
I did explicitly write about microbiome effects. The bioavailability paper Simec et al 2023 that Benquo mention does argue that their findings point towards systematic regulatory effects.
Most of what I wrote focuses on systemic regulatory action through CD44 activation. Benquo’s hypothesis of all effects being due to microbiome effects might be true, but it’s a contrarian position that’s not held by the people who actually did the bioavailability research. Simec does not even mention Benque’s hypnothesis as one worth considering an running experiments to see whether it’s true.
I do think Benque’s hypnothesis is valid enough that someone in the field should run an experiment, especially given that microbiome interventions can both help with skin and joint outcomes, but when writing a post like this, I think it’s fine to not be contrarian and go with the views of the people running the bioavailability experiments instead of making contrarian interpretations on them.
I think it’s more likely that that I’m going to argue a contrarian position instead of just going with the views that the scientists who are experts in the field hold when I’m written a human-written post, but I don’t think that’s an improvement. When it comes to writing like this, I think LLM’s helping grounding the argument from the perspective of domain experts is an improvement.
Sorry I hadn’t tracked your argument structure better.
I agree that you don’t need to take a contrarian position to make it a very worthwhile LW post. I was just suggesting that getting a good grip on the literature benefits from prompting your LLM assistant to take a contrarian view on each paper individually, to help you identify potential alternative explanations. I think many researchers’ interpretations of their research are pretty suspect, even though the research is going to be reported accurately. There’s a lot of motivated reasoning bias toward interpretations that make the research important.
But that’s a minor quibble. I think your methodology is exemplary for how to use LLMs to speed your research and writing, including prompting them to take a skeptical stance sometimes.
I hope to see more from you and others in this vein. I do think it’s important to say exactly how you used the LLMs; I trust this far more than if someone had just prompted Gemini to write this essay. You are supplying the metacognition, judgment, and executive function that the models currently lack.
I’m sorry this post didn’t wind up with a higher vote total. I think it was really good. I attribute this to suspicion from the community about a post that basically just says “some LLM wrote this” instead of saying how carefully you used combinations of LLMs as research and writing assistants.
I don’t have access to the cited review of direct empirical evidence for oral supplementation, but taking it at face value that there’s a clear statistical signal of benefit when pooling the available trials involving 291 people total, I think that’s the level of evidence where we should be looking for unambiguous mechanistic support. I also want to distinguish between one of many redundant interventions that are good for people who aren’t trying very hard to be healthy, and an irreplaceable input. I tried to evaluate the mechanistic argument here by following the references, and independently checking whether the magnitudes work out (since “Gemini calculated” is not a source I can check).
Šimek et al. (2023) used 13C-labeled hyaluronic acid (HA) in mice and confirmed that Bacteroides species break HA into oligosaccharides under 3 kDa, some of which are absorbed. Kimura et al. (2016) found HA-derived disaccharides and tetrasaccharides in rat skin after oral dosing. So there are big enough fragments passing through to serve some sort of signaling function. But the same tracer study measured systemic bioavailability at ~0.2%.
This reminded me of how sometimes people recommend eating glutathione to raise your glutathione levels. It works, but in an attenuated way that makes it a fractional Gettier case, like eating muscles to get strong. The way glutathione gives you glutathione is not because it passes into the system intact (very little if any does), but because glutathione is made of the ingredients for glutathione: cysteine, glycine, and glutamate. Your body breaks it down into its ingredients during digestion, and the ingredients supply substrate for assembling glutathione in cells as needed. But only two of those ingredients are frequently scarce, to different extents depending on your diet, and supplemental glutathione is expensive, so you’re paying a lot of extra money for glutamate, and a nonoptimal ratio of supplemental cysteine to glycine; in my case I eat enough meat that I’m better off just supplementing glycine when I’m well, and adding NAC and extra glycine when I’m sick.
The ingredient explanation doesn’t seem to support a benefit to oral supplementation here. The body contains about 15 grams of HA and turns over roughly 5 grams per day, synthesized endogenously from UDP-sugar precursors derived from ordinary glucose metabolism. At 200 mg orally per day and 0.2% bioavailability, you’re adding ~0.4 mg systemically against 5,000 mg of daily endogenous production from ingredients that are abundant in most diets.
Here’s a steelman. Much like the proline peptides in collagen, orally ingested HA hits the gut first, so maybe it’s specifically beneficial as a signal in the gut.
Šimek et al. concluded that the mechanism of action is “the result of the systematic regulatory function of hyaluronan or its metabolites rather than the direct effects of hyaluronan” at distant sites. The fragments that aren’t absorbed get fermented into short-chain fatty acids. Multiple studies cited in the post confirm prebiotic effects: shifts in Bacteroides populations, increased short-chain fatty acid (SCFA) production.
Is the measured benefit to oral supplementation mainly signaling or prebiotic? If it’s signaling, then there’s a case specifically for oral supplementation of HA. But if the benefit is primarily via SCFA production and microbiome modulation, then oral HA is one prebiotic among many. You can eat full-fat dairy aged enough to taste a little like barf, Hershey’s chocolate that’s been enzymatically lipolyzed to similar effect, soluble fiber, or resistant starch, or drink a little vinegar, and get substantially overlapping SCFAs delivered to the same places. Since different people have problems with different foods for different reasons, and not all short-chain fatty acids are exactly the same, the substitution between these is imperfect and it’s conceivable that oral HA might be the best solution to some problem for someone somewhere.
ETA: Looks like healthy guts make a ton of HA endogenously, so even at the gut, oral supplementation’s likely to be redundant unless you have an immature or severely damaged gut.
You can ask the chatbot of your trust to run either in thinking/pro mode or deep research to calculate the number yourself. While it would be preferable if there would be a better source for the numbers.
Šimek et al. (2023) says in it’s abstract “The poor bioavailability (~0.2 %) of oral hyaluronan indicates that the mechanism of action is the result of the systematic regulatory function of hyaluronan or its metabolites rather than the direct effects of hyaluronan at distal sites of action (skin, joints).”
I do say “As a result, native hyaluronan has little to no systemic bioavailability”, which I think is in line with the summary of Šimek. “systematic regulatory function of hyaluronan or its metabolites” would be the CD44 receptor dynamic I wrote about. Šimek does not argue that the effect is likely because of microbiome changes.
Do you think Šimek makes a mistake in how he reasons about his data, or do you think I don’t really base my argument for the things roughly working like Šimek argues them to work?
Maybe, supply and signal is inaccurate in that the supply is not meaningful and it’s all signal. That would be an update to my argument but it doesn’t change anything about the core benefits of supplementing it.
Given that it takes the Bacteroides salyersiae and friends, to break down the hyaluronan before it can become available and hyaluronan supplementation leads to an increase of those bacteria, I think it’s plausible that mice that haven’t seen any hyaluronan in their diet don’t immediately have enough breakdown in the five days that Kimura supplemented them. Mice also aren’t evolved to be hunters, so might reasonably differ from humans
It seems to me the other way around, some unhealthy guts make hyaluronan and they need to be pretty unhealthy to get to levels approaching the clinical supplements level of 120mg-240mg.
The bacteria that produce hyaluronan themselves seem to be pathogens like Streptococci and Pasteurella multocida that encapsulate themselves in it and use it as a protective shield and to stick somewhere. If you have a lot of hyaluronan in the gut, bacteria like Bacteroides salyersiae that break down hyaluronan grow in number and also produce more of the enzyme that breaks down the protective shield of those pathogens and thus reduces their viability in the gut. I think it’s plausible that you actually need hyaluronan to get those bacteria to break to produce a lot of the enzyme that break down hyaluronan.
Even if you say “it’s the microbiome” that still leaves the question open of how the microbiome would affect the skin and joints. It could be by reducing pathologic bacteria’s and those pathologic bacteria produce skin and joint problems. It could also be because of a signaling dynamic.
There are around 150 to 400 different species in one’s human gut with around 3,600 to 4,600 for the whole population. There’s a lot of complexity and different prebiotics and probiotics likely do have different effects.
Blocking endogenous HA receptor binding in mice impairs gut development and barrier function (Riehl et al. 2015) within about 5 days, so we know that signal is generated routinely. Immunostaining of healthy human jejunum also shows intense HA in the lamina propria with no staining in the epithelial layer, so healthy guts do produce substantial HA endogenously. That doesn’t tell us whether it’s produced steadily or mainly during episodic damage and repair, or whether epithelial HA produces different effects, or whether supplement levels send an important extra signal.
The Bacteroides as pathogen shield argument is new and interesting. I’d expect hyaluronidase producing bacteria to roughly equilibrate to available HA over time, whether from endogenous production, episodic repair, or diet. Do you have specific reasons to think supplementing HA would change the ratio rather than just the levels?
Hmmm, here is what my AI says (prompted simply “where in food is hyaluronan and what happens if you do not consume enough of it”). Translated and simplified, because I asked in Slovak.
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You need to distinguish between which food contains hyaluronan, and which food helps your body produce it.
Food that contains hyaluronan:
bone soup (need to cook for 6 − 48 hours)
offal
chicken skin
Food that helps your body produce hyaluronan:
soy products, e.g. tofu (via phytoestrogens, supports hyaluronan production)
leafy greens, e.g. spinach, kale (via magnesium, supports hyaluronan production)
sweet potatoes and root vegetables (magnesium)
almonds, nuts (magnesium)
citrus fruits (via naringenin, blocks hyaluronan dstruction)
*
I specifically confirmed that aspic, chicken stomachs, and chicken liver contain hyaluronan.
Then again, when I closed the incognito window, and opened a new one, and asked the same question again, the AI was suddenly much more skeptical about it, so...
Bone soup certainly is one of the best sources, I still have to write another post on bone soup. I’m skeptical of the 6-48 hours. That timeframe optimizes magnesium, potassium and calcium yields but it has the chance to break down the hyaluronan in ways that mean that you get shorter spike and not the 24-48 hours of effect that you get from the bacteria in your stomach doing the work of breaking it down.
I’m planning to go for 90 minutes first boil + 60 minutes second boil in a pressure cooker myself.
Skin (whether from chicken or other animals) is certainly another valid source. Skin does have elastin breakdown products that bone soup doesn’t have. I haven’t made up my mind of the merits of wanting to consume those, but I would note that ChatGPT calls them “usually pro-inflammatory”.
Having good magnesium levels is certainly helpful for a lot of bodily progresses. I think there’s a common belief that among people who supplement a lot that many people suffer from magnesium deficiency than have too much magnesium.
soy products, e.g. tofu (via phytoestrogens, supports hyaluronan production)
Trying to understand the merits of tofu and phytoestrogens is probably worth it’s own post, but not one I’m particularly interested in writing at the moment.
I would not translate “blocks hyaluronan destruction” into “helps with hyaluronan production”. I think a healthy body does break down hyaluronan and recreates it and if you hamper that by reducing the breakdown you probably get more problems then benefits.