Collagen Supplements: Joint Health Claims vs. the Actual Research

The Claims, Listed Plainly

Collagen is now a billion-dollar category, and the marketing has gotten sloppy enough that a single tub might carry four separate claims that come from four separate bodies of research, some of which do not apply to the product in the tub. Before evaluating anything, the claims need to be separated, because they have wildly different levels of support.

Here is what collagen supplements are actually sold on:

Notice how rarely the population in column two matches the person buying the product. That mismatch is the central issue in this category. A 62-year-old with radiographic knee osteoarthritis and a 27-year-old whose knees ache after a heavy squat session are not the same customer, and the evidence that applies to the first one does not automatically transfer to the second.

Does It Even Survive Digestion?

The oldest objection to collagen supplements is that eating a protein cannot possibly deliver that protein to a specific tissue, any more than eating a heart builds heart muscle. Your gut breaks proteins into amino acids and small peptides, and those get used wherever the body decides. That objection is mostly correct and slightly incomplete, and the incomplete part is where the entire scientific case for collagen lives.

Two findings complicate the simple story. The first is Oesser and colleagues (1999), who fed mice carbon-14 labeled gelatin hydrolysate and tracked where the radioactivity went. Roughly 95% was absorbed within 12 hours, and radioactivity accumulated in cartilage at levels above what a control dose of labeled proline produced. This study is quoted constantly in marketing copy as proof that collagen goes to your joints.

It does not show that. A radiolabel tracks carbon atoms, and carbon atoms from a digested protein can end up in cartilage after being fully broken down and reassembled from scratch. Radioactivity in cartilage is consistent with intact peptides arriving there, and it is equally consistent with ordinary amino acid recycling. The study is suggestive, and it is not evidence of targeted delivery.

The second finding is stronger. Iwai and colleagues (2005) analyzed human plasma after volunteers drank collagen hydrolysate and found that hydroxyproline-containing peptides appear in the bloodstream as peptides, not only as free amino acids. Prolyl-hydroxyproline, usually written Pro-Hyp, accounted for roughly half of the collagen-derived peptides in plasma. Concentrations peak one to two hours after ingestion and fall by half around the four-hour mark. Subsequent work has replicated this and identified related dipeptides such as hydroxyprolyl-glycine.

This matters because hydroxyproline is a fingerprint. It appears almost exclusively in collagen, so a hydroxyproline-containing dipeptide in the blood came from collagen and got there without being fully dismantled. In cell culture, Pro-Hyp stimulates the growth of specific fibroblast populations. So the plausible mechanism for collagen supplements is signaling, not construction: small collagen-specific peptides circulate and act as a message to connective tissue cells that collagen turnover is happening.

Why the "Building Blocks" Story Is Weak

The most common pitch is that collagen supplies the raw materials your body needs to rebuild cartilage. Run the arithmetic on that and it falls apart quickly.

Collagen makes up roughly 30% of total protein in the human body. For an 80 kg adult, that is somewhere in the range of three to four kilograms of collagen. A 10 gram daily scoop is about a quarter of one percent of that pool. Meanwhile you are already eating 120 to 200 grams of protein a day if you lift seriously, and your body synthesizes collagen out of ordinary dietary amino acids. Glycine, proline, and lysine are not scarce nutrients in a Western diet.

There is a narrow version of the raw-materials argument that holds up: glycine is conditionally essential, meaning endogenous synthesis may not fully cover requirements under high turnover, and collagen is about a third glycine by residue count. That is a defensible point. It is a much smaller point than "feeds your joints," and it argues for glycine, not for a branded joint formula.

Take the raw-materials framing seriously and you get a prediction: any protein source supplying adequate glycine and proline should work as well. Nobody sells that, and nobody has tested it, because the commercial case depends on collagen being special. The signaling mechanism is a better argument and the one the actual researchers use. Keep that in mind when a label leans on the building-block metaphor, because it usually indicates the copywriter did not read the papers being cited.

The Athlete Trials, and What EFSA Did to Them

Two studies carry almost the entire weight of the claim that collagen helps healthy, active people with joint discomfort. Both deserve a close look, because they are cited far more often than they are read.

Clark et al. (2008): the Penn State athlete study

Clark and colleagues (2008), published in Current Medical Research and Opinion, recruited 147 varsity and club athletes at Penn State and randomized them to 10 g of liquid collagen hydrolysate or a xanthan gum placebo for 24 weeks. The paper reports that six parameters improved significantly versus placebo, including joint pain at rest as assessed by the examining physician and joint pain while walking as reported by participants. This was the first 24-week trial to report a joint pain benefit in athletes, and it is still the study most often pointed to.

Now the part that almost never gets mentioned. In 2011, Gelita AG applied to the European Commission for permission to make a joint health claim on collagen hydrolysate. The application went to the European Food Safety Authority panel on dietetic products, which had access to the full dossier including this trial. The panel's assessment noted that the study evaluated 15 separate parameters related to joint pain and discomfort, and that no endpoint remained statistically significant once the significance threshold was adjusted for multiple comparisons.

"On the basis of the data presented, a cause and effect relationship has not been established between the consumption of collagen hydrolysate and the claimed effect." Scientific Opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies, 2011.

This is a textbook multiple comparisons problem. Test fifteen endpoints at the conventional 5% threshold and you expect somewhere close to one false positive by chance alone, and the number of nominally significant results climbs further when the endpoints are correlated with each other, which pain measures always are. Reporting six of fifteen as wins without adjustment is not fraud, and it is not a result you should build a purchase decision on. EFSA also concluded that the animal and in vitro work did not predict an effect on joint maintenance in humans, and the joint health claim was refused.

Zdzieblik et al. (2017): activity-related knee discomfort

Zdzieblik and colleagues (2017), in Applied Physiology, Nutrition, and Metabolism, ran a cleaner study. They randomized 180 physically active adults aged 18 to 30 who had exercise-related knee pain but no diagnosed joint disease to 5 g of a specific collagen peptide preparation or placebo for 12 weeks. The primary endpoint was change in pain during or after activity on a visual analog scale, and the collagen group improved significantly more than placebo, p = 0.024.

A pre-specified primary endpoint is a meaningful upgrade over Clark's fifteen-parameter shotgun. Three caveats belong alongside it. The p-value of 0.024 is not a comfortable margin. The preparation tested was a specific branded ingredient from a manufacturer that co-funded the work and employs or has employed several authors across this literature. And it remains, nearly a decade on, without a well-powered independent replication in a healthy training population. A finding that only ever appears in trials the manufacturer paid for is a finding at an early stage, regardless of how many times it gets cited.

Osteoarthritis: Where the Evidence Is Real

Set the athlete question aside and the picture improves considerably. Osteoarthritis has been studied far more, with more trials, larger samples, and validated instruments, and the pooled result is consistently positive.

The strongest single analysis is Liang and colleagues (2024) in Osteoarthritis and Cartilage, a trial sequential meta-analysis of 25 randomized controlled trials covering 2,856 patients. Collagen derivatives produced a standardized mean difference of -0.35 for pain (95% CI -0.48 to -0.22, graded moderate certainty) and -0.31 for function (95% CI -0.41 to -0.22, graded high certainty). Safety was clean, with no increase in withdrawals or adverse events versus control. Trial sequential analysis, which is a formal check on whether the accumulated sample is large enough to stop asking, indicated the evidence base has sufficient power for a firm conclusion.

That is a genuinely good result by supplement standards. Most things in this category never accumulate 25 trials, and fewer still get a high-certainty GRADE rating on any outcome. A 2023 meta-analysis restricted to knee osteoarthritis reported a somewhat larger analgesic effect at SMD -0.58 (95% CI -0.98 to -0.18, p = 0.004, moderate quality evidence), with wider confidence intervals reflecting fewer included studies.

An earlier and more granular meta-analysis, García-Coronado and colleagues (2019) in International Orthopaedics, is worth reading because it breaks the WOMAC index into its components. Total WOMAC improved by 8.00 points versus control, and pain on a 100 mm visual analog scale improved by 16.57 mm. But among the WOMAC subscores, only stiffness reached significance, at 0.41 points. The pain and physical function subscores did not differ significantly from control.

So the same intervention improves a composite score and a standalone pain scale while failing to move the pain subscore of the composite. That is what an effect looks like when it sits near the edge of detectability. It is not a reason to dismiss the finding. It is a reason to stop describing it as dramatic.

Small, Significant, and Possibly Meaningless

Statistical significance answers whether an effect is likely to be real. It says nothing about whether the effect is large enough for a human to notice. Clinical research handles this with the minimal clinically important difference, the smallest change a patient can actually perceive as an improvement. Comparing the collagen numbers to those thresholds is the single most clarifying exercise in this entire topic.

Every number lands in the same neighborhood: real, small, and hovering around the threshold where a patient would report noticing anything. For context, that is roughly the territory occupied by glucosamine and chondroitin, and it sits below what a course of NSAIDs or a structured exercise program delivers for knee osteoarthritis.

Type I vs Undenatured Type II

This is where most consumers get separated from their money, because two products sold in the same aisle under the same word operate on mechanisms that are mutually exclusive.

Hydrolyzed type I collagen is what you buy in a tub. It comes from bovine hide or fish skin, it is enzymatically chopped into peptides of roughly 2 to 5 kilodaltons, and it is dosed in grams. The proposed mechanism is the Pro-Hyp signaling story described earlier. Type I is the collagen of skin, tendon, ligament, and bone, and it constitutes about 90% of the collagen in your body.

Undenatured type II collagen, sold almost entirely as the branded ingredient UC-II, is a completely different proposition. Type II is the collagen of articular cartilage. The dose is 40 milligrams per day, which is roughly 250 times smaller than a hydrolysate serving, and the manufacturing goal is to keep the triple helix intact rather than break it apart. The mechanism proposed is oral tolerance: intact type II epitopes reach gut-associated lymphoid tissue, are sampled by immune cells in Peyer's patches, and drive the development of regulatory T cells that recognize type II collagen. Those T cells then circulate, encounter type II collagen in joint tissue, and release anti-inflammatory mediators locally. This is a well-established immunological concept that originated in the rheumatoid arthritis literature.

The pivotal human trial is Lugo and colleagues (2016) in Nutrition Journal, which randomized 191 adults with knee osteoarthritis to UC-II at 40 mg, glucosamine hydrochloride plus chondroitin sulfate, or placebo for 180 days. UC-II produced a significantly greater reduction in total WOMAC than both placebo and the glucosamine-chondroitin arm, with within-group reductions of roughly 40% in pain, stiffness, and physical function from baseline. The study was funded by the ingredient's owner and involved company-affiliated authors, which is the standard caveat in this field.

Tendons, Ligaments, and Vitamin C

The tendon literature is the most scientifically interesting part of the collagen story and the least mature.

Shaw and colleagues (2017) in The American Journal of Clinical Nutrition ran a randomized, double-blind crossover in eight healthy men who took 5 g or 15 g of vitamin C-enriched gelatin or placebo, waited an hour, then did six minutes of rope skipping, repeating the pattern three times a day for three days. The 15 g dose doubled circulating amino-terminal propeptide of type I collagen, a blood marker of collagen synthesis. Blood from the supplemented subjects also improved mechanical properties in an engineered ligament model.

Two design choices in that study became the practical protocol everyone repeats. The one-hour lead time exists because plasma glycine, proline, and hydroxyproline peak around an hour after ingestion, which is when you want them available during loading. The vitamin C is there because prolyl hydroxylase and lysyl hydroxylase, the enzymes that stabilize new collagen's triple helix, both require ascorbate as a cofactor. Skip the vitamin C and you are supplying substrate to an enzyme running short on what it needs.

The honest limits: n = 8, a blood marker rather than a tendon, and three days rather than a training block. Subsequent systematic reviews of longer trials report increases in tendon cross-sectional area and stiffness when 15 to 30 g per day is combined with resistance training, but they grade the certainty of evidence as low to very low because sample sizes are small and outcomes are inconsistent across studies. Almost nothing has been measured that a lifter would name as the goal, such as injury incidence, days lost, or return to full training.

For existing tendon problems, Praet and colleagues (2019) in Nutrients ran a crossover pilot in 20 patients with chronic mid-portion Achilles tendinopathy, pairing a branded collagen peptide with a twice-daily calf strengthening program. At three months, the group starting on collagen improved VISA-A scores by 12.6 points versus 5.3 for the group starting on placebo. The authors framed it as collagen possibly accelerating the benefit of a well-structured loading program, which is the correct framing. Twenty patients in a pilot is a signal to investigate, not a treatment recommendation.

The Skin Data, and Why It Matters Here

Skin is a joint article's business for one reason: the skin literature is where somebody finally ran the analysis that the joint literature still needs.

A 2025 systematic review and meta-analysis in The American Journal of Medicine pooled 23 randomized controlled trials covering 1,474 participants. Across all 23 trials, collagen supplementation significantly improved skin hydration, elasticity, and wrinkles, which is the headline two previous meta-analyses had also reported. Then the authors did something the earlier reviews had not: they stratified the trials by funding source.

The trials funded by industry showed the benefit. The trials without industry funding showed no effect on hydration, elasticity, or wrinkles. The authors concluded that funding source and study quality alter the overall picture enough that no clinical benefit can be considered confirmed.

That result should change how you read every other collagen claim. It does not prove the joint findings are similarly inflated, and drawing that conclusion would be its own overreach. What it establishes is that in the closest adjacent literature, using the same ingredient suppliers and frequently the same investigators, the entire apparent effect disappeared once the sponsor's money was removed from the analysis. Until someone runs the same stratification on the osteoarthritis trials, the possibility sits unresolved over the whole field.

The Funding Problem

Very little of this literature is independent, and the concentration is unusual even by supplement standards. The branded ingredients that appear in the pivotal trials come from a short list of manufacturers, and those manufacturers fund the studies, employ or collaborate with the investigators, and in some cases hold patents on the compounds being tested.

A concrete example of why this matters. Zdzieblik and colleagues (2015) published in the British Journal of Nutrition a trial in which older sarcopenic men doing resistance training for 12 weeks gained a mean of 4.2 kg of fat-free mass and lost 5.4 kg of fat mass on 15 g per day of collagen peptides, substantially outperforming placebo. Those numbers are extraordinary. A published critical commentary in the same journal pointed out that the 4.2 kg fat-free mass gain is unrivalled by any protein supplementation study in older resistance-training men, exceeds what has been reported in trials combining resistance training with testosterone administration, and that the roughly 1.3 kg between-group difference is between 2.7 and 5.6 times larger than the effect sizes found in meta-analyses of protein supplementation.

In September 2025, a decade after publication, the journal issued a corrigendum disclosing that part of the study costs had been paid by the collagen manufacturer and that one author is a co-inventor on a patent application covering the active substance. The original paper had omitted both. The corrigendum does not retract the findings and no misconduct was alleged, but a reader in 2016 through 2025 evaluating that paper was working without information that would have changed how skeptically they read it.

Does Collagen Count as Protein?

Nutritionally, collagen is a poor protein by every metric that predicts muscle protein synthesis.

This is confirmed directly rather than inferred from the amino acid profile. Oikawa and colleagues (2020) compared whey protein with collagen peptides in healthy older women and found that whey stimulated both acute and longer-term muscle protein synthesis while collagen did not, with and without resistance exercise. Collagen has been tested against the outcome that matters and it failed.

The practical consequence is an accounting problem. Add 15 g of collagen to a food tracker and it registers as 15 g of protein toward your daily target, even though close to none of it contributes to the muscle-building portion of that target. Someone eating 180 g of protein a day can absorb that error without consequence. Someone at 110 g on a cut who counts a collagen scoop toward the total is functionally eating 95 g of usable protein while believing they hit 110. See how much protein you actually need per day for the targets this eats into.

The Honest Verdict

Sorting the claims by how much weight each one bears:

Knee osteoarthritis: worth trying. Twenty-five trials, 2,856 patients, a small but robustly pooled benefit for pain and function, high-certainty grading on function, and a clean safety record. The effect is small enough that it should sit behind exercise therapy and weight management in your priority order, and collagen is cheap, safe, and better supported than most things sold for joints. Ten grams a day of a hydrolysate, or 40 mg of a genuinely undenatured type II, for at least 12 weeks before judging.

Tendon support alongside loading: defensible, unproven. The mechanism is coherent, the acute marker data is real, the longer-term trials are small and low certainty, and nothing has been measured that answers the question a lifter is asking. Fifteen grams plus vitamin C an hour pre-session is a low-cost bet with a plausible upside and no meaningful downside. Do not expect it to substitute for a rehab program.

Ordinary training aches in healthy lifters: weak. Two manufacturer-funded trials, one of which a regulator reanalyzed and rejected, and no independent replication in nearly a decade. If your knees hurt after squats, the highest-yield interventions are load management, technique, sleep, and addressing whatever tissue is actually irritated. See managing training injuries for the sequence that generally works.

Muscle, body composition, strength: no. Contradicted by direct muscle protein synthesis measurement. The one trial that reported large body composition changes has since had a funding and patent disclosure added and has been publicly criticized for reporting numbers that exceed what testosterone plus training produces.

Skin: unresolved and trending negative. Significant in the pooled analysis, null in the independently funded subset.

Collagen is not a scam, and it is not the joint solution the category sells. It is a cheap, safe, well-tolerated supplement with a small, real effect in osteoarthritis, an interesting and immature tendon story, and a marketing layer that has run several hundred meters ahead of the data. For a broader look at dosing, food sources, and the skin evidence in more depth, our collagen peptides guide covers the practical side.

Recurring Errors

Assuming osteoarthritis evidence applies to healthy joints

Nearly all the good collagen joint data comes from people with diagnosed, degenerative joint disease. Damaged tissue with active remodeling and an inflammatory component is a different biological situation from a healthy 30-year-old's knee that aches after volume squats. Improvement in the first population predicts nothing reliable about the second, and the marketing crosses that gap without comment.

Buying a milligram dose of a hydrolyzed product

Forty milligrams only makes sense for undenatured type II working through oral tolerance. If the label says hydrolyzed and the dose is in milligrams, neither mechanism applies at that dose, and the product is citing evidence that belongs to a different molecule in a different structural state.

Treating "clinically studied ingredient" as a quality signal

It usually means the manufacturer funded a study on their own ingredient. That is how ingredient marketing works and it is not inherently discrediting. It also is not the independent validation the phrase is engineered to imply.

Counting collagen toward your protein target

Zero tryptophan, low leucine, DIAAS near zero, and a direct trial showing no muscle protein synthesis response. It counts on a nutrition label and it does not count for the purpose you are tracking protein for.

Taking it without loading the tissue

Every plausible mechanism for tendon and cartilage benefit runs through mechanical stimulus. The supplement supplies substrate or signal to a remodeling process; loading is what starts that process. Collagen on rest days with no loading program attached is the passive half of a protocol.

Quitting after four weeks

Connective tissue turns over on a timescale of months. The osteoarthritis trials mostly ran 12 to 24 weeks and the Lugo trial ran 180 days. Four weeks tells you nothing about whether it works and roughly matches the window in which placebo effects on self-reported pain are strongest.

Expecting a supplement to outperform the thing it is being added to

Exercise therapy produces larger effects on osteoarthritis pain than collagen does. Loading produces tendon adaptation that collagen at best amplifies. The pattern that shows up across the whole category, and across supplements generally, is covered in how to spot bad fitness advice.

Frequently Asked Questions

Does collagen actually help joint pain?

In diagnosed knee osteoarthritis, the pooled evidence says yes with a small effect. The 2024 trial sequential meta-analysis in Osteoarthritis and Cartilage, covering 25 trials and 2,856 patients, found a standardized mean difference of -0.35 for pain and -0.31 for function. In healthy people with ordinary training aches, the evidence is much thinner. The two most-cited athlete trials were manufacturer-funded, and when EFSA reanalyzed the larger one with a correction for multiple comparisons, no endpoint remained significant.

How much collagen should I take for joints?

It depends on which product, because the two categories run on incompatible logic. Hydrolyzed type I peptides are dosed at 5 to 15 g per day, and the joint trials mostly used 10 g. Undenatured type II is dosed at 40 mg per day, roughly 250 times smaller, because the claim is immunological rather than nutritional. A large dose of undenatured type II makes no sense, and 40 mg of a hydrolysate makes no sense either. Match the dose to the mechanism the product claims.

Does collagen count toward my daily protein intake?

It counts on a label and it does not count for building muscle. Collagen contains no tryptophan and only about 2 to 3% leucine against whey's 10%, giving it a DIAAS near zero as a standalone protein. Oikawa and colleagues (2020) found collagen peptides failed to raise muscle protein synthesis in older women. At 180 g of protein a day, a collagen scoop is harmless. At 110 g on a cut, counting it toward the target quietly lowers your real intake.

What is the difference between type I and type II collagen supplements?

Type I is the collagen of skin, tendon, ligament, and bone, roughly 90% of the collagen in your body. Type II is the collagen of articular cartilage. Type I supplements are hydrolyzed into peptides and dosed in grams, on the theory that peptides such as prolyl-hydroxyproline signal connective tissue cells. Undenatured type II is kept structurally intact and dosed in milligrams, because its mechanism is oral tolerance via gut immune tissue. Hydrolyzing type II destroys the structure that mechanism needs, so a hydrolyzed type II product cannot borrow the UC-II evidence.

Is collagen good for tendons?

The mechanistic case is more interesting than the outcome data. Shaw and colleagues (2017) showed 15 g of vitamin C-enriched gelatin an hour before short bursts of loading doubled a blood marker of collagen synthesis, and recent reviews report increases in tendon cross-sectional area and stiffness with 15 to 30 g per day plus resistance training. Those reviews grade certainty as low to very low, and almost nothing has been measured that a lifter cares about, such as injury rate. Vitamin C matters because it is a required cofactor for the enzymes that stabilize new collagen.

Why do collagen studies keep getting criticized for funding?

Because the pattern is unusually clean. A 2025 meta-analysis in The American Journal of Medicine pooled 23 trials of collagen for skin aging and found significant improvements in hydration, elasticity, and wrinkles overall. Split by funding source, the industry-funded trials still showed benefit and the independent ones showed none. That does not prove the joint literature has the same problem, but it draws from the same ingredients and sponsors, and nobody has run the equivalent analysis on the joint trials yet.

References

• Clark KL, Sebastianelli W, Flechsenhar KR, et al. 24-week study on the use of collagen hydrolysate as a dietary supplement in athletes with activity-related joint pain. Curr Med Res Opin. 2008;24(5):1485-1496.
• EFSA Panel on Dietetic Products, Nutrition and Allergies. Scientific Opinion on the substantiation of a health claim related to collagen hydrolysate and maintenance of joints pursuant to Article 13(5) of Regulation (EC) No 1924/2006. EFSA Journal. 2011;9(7):2291.
• Zdzieblik D, Oesser S, Gollhofer A, König D. Improvement of activity-related knee joint discomfort following supplementation of specific collagen peptides. Appl Physiol Nutr Metab. 2017;42(6):588-595.
• Liang C, Chen H, Chen H, et al. Efficacy and safety of collagen derivatives for osteoarthritis: a trial sequential meta-analysis. Osteoarthritis Cartilage. 2024;32(5):531-541.
• García-Coronado JM, Martínez-Olvera L, Elizondo-Omaña RE, et al. Effect of collagen supplementation on osteoarthritis symptoms: a meta-analysis of randomized placebo-controlled trials. Int Orthop. 2019;43(3):531-538.
• Analgesic efficacy of collagen peptide in knee osteoarthritis: a meta-analysis of randomized controlled trials. J Orthop Surg Res. 2023;18:694.
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• Oesser S, Adam M, Babel W, Seifert J. Oral administration of 14C labeled gelatin hydrolysate leads to an accumulation of radioactivity in cartilage of mice (C57/BL). J Nutr. 1999;129(10):1891-1895.
• Oikawa SY, Kamal MJ, Webb EK, et al. Whey protein but not collagen peptides stimulate acute and longer-term muscle protein synthesis with and without resistance exercise in healthy older women: a randomized controlled trial. Am J Clin Nutr. 2020;111(3):708-718.
• Zdzieblik D, Oesser S, Baumstark MW, Gollhofer A, König D. Collagen peptide supplementation in combination with resistance training improves body composition and increases muscle strength in elderly sarcopenic men: a randomised controlled trial. Br J Nutr. 2015;114(8):1237-1245.
• Collagen peptide supplementation in combination with resistance training improves body composition and increases muscle strength in elderly sarcopenic men: a randomised controlled trial -- CORRIGENDUM. Br J Nutr. 2025. doi:10.1017/S000711452510425X.
• Exceptional body composition changes attributed to collagen peptide supplementation and resistance training in older sarcopenic men. Br J Nutr. 2016;116(3):569-570.
• Effects of collagen supplements on skin aging: a systematic review and meta-analysis of randomized controlled trials. Am J Med. 2025. doi:10.1016/j.amjmed.2025.04.008.
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• Bagchi D, Misner B, Bagchi M, et al. Effects of orally administered undenatured type II collagen against arthritic inflammatory diseases: a mechanistic exploration. Int J Clin Pharmacol Res. 2002;22(3-4):101-110.