The clinical dose is 10g/day. Most products give you 2.5g.

Hydrolysed collagen (collagen peptides) is collagen that has been broken down by enzymatic hydrolysis into shorter amino acid chains (2–5 kDa). Whole collagen protein molecules are too large to be absorbed intact through the gut wall. Hydrolysis produces peptides small enough to enter the bloodstream, reach the dermis, and stimulate fibroblast activity. Every clinical trial showing skin elasticity benefits — including all 11 RCTs reviewed by Choi et al. 2019 — used hydrolysed collagen, not whole protein. The form distinction is the most important variable when comparing products.

The minimum effective dose for skin elasticity is 2.5g per day, established in Proksch et al. 2014. Most clinical trials used 2.5–10g daily. For athlete joint discomfort, Clark et al. 2008 used 10g daily over 24 weeks. There is no strong evidence that doses above 10g produce proportionally greater benefits. A standard daily serving of 10g covers the full studied range and is the clearest target. Most products in Australia provide 5g or less per serve — below the threshold used in the majority of RCTs.

Proksch et al. (2014) showed statistically significant improvements in skin elasticity at 4 weeks, with more pronounced changes at 8 weeks. Choi et al. (2019) reviewed RCTs ranging from 4 to 24 weeks and found consistent results across that window. The Clark et al. (2008) joint study ran 24 weeks. A fair trial of collagen supplementation for skin outcomes is 8–12 weeks of consistent daily use at the correct dose. For joint outcomes, allow 3–6 months. Collagen is not a fast-acting supplement — effects are tissue-level biology accumulated over time.

Type I is the predominant collagen in skin, tendons, and bone — the most relevant type for skin supplementation. It is the type that declines most with age and UV exposure. Bovine and marine hydrolysed supplements are predominantly Type I. Type II is the primary structural protein in cartilage, specifically relevant for joints — it is taken in a different form (undenatured UC-II) at much lower doses (40mg). Type III collagen is found alongside Type I in skin and connective tissue at lower concentrations. Most "collagen for skin" products contain Type I; products marketed for joints typically contain Type II.

Both are primarily Type I collagen when hydrolysed. Marine collagen has a slightly smaller average peptide size, which some researchers suggest may improve absorption — and it is the preferred choice for those avoiding bovine products. However, most high-quality RCTs, including Proksch et al. 2014 and several studies in Choi et al. 2019, used bovine-sourced hydrolysed collagen. Head-to-head comparisons between marine and bovine at equivalent doses are limited. Neither source has demonstrated decisive clinical superiority for skin outcomes.

Dietary collagen from bone broth, skin-on fish, and organ meats provides amino acids — particularly glycine and proline — that support collagen synthesis. However, no controlled trial has demonstrated equivalent outcomes from dietary sources versus hydrolysed peptide supplementation at clinical doses. The bioavailability advantage of hydrolysed peptides (pre-broken into 2–5 kDa chains) is what the RCT evidence is built on. Whole food collagen follows a different absorption pathway. Both approaches support collagen biology, but the dose control that supplementation allows is what allows clinical comparison.

No. Collagen is an animal protein — plants structurally cannot produce it. Products marketed as "plant-based collagen" contain collagen-support nutrients: vitamin C (a required cofactor for collagen synthesis), zinc, copper, and silica. These are genuine cofactors for your body's own collagen synthesis, and they are worth taking. However, they are not collagen and have not been tested against the skin outcomes measured in the RCT literature reviewed by Choi et al. 2019. If you avoid animal products, a clearly labelled collagen-support supplement with proven cofactors is the honest alternative.

UV radiation activates matrix metalloproteinases — enzymes that break down dermal collagen fibres — and is the primary environmental driver of photoageing. The first-principles approach is behavioural and dietary: avoid peak UV hours (10am–2pm AEST) when UVA intensity is highest, and support your skin's natural defences through diet. Astaxanthin (a carotenoid from krill and algae) has the strongest evidence for dietary photoprotection, with multiple RCTs showing measurable reduction in UV-induced skin damage. Lycopene, beta-carotene, and EGCG from green tea also demonstrate measurable photoprotective activity in human trials. Collagen supplementation works best alongside this approach.