You've noticed the changes. Perhaps it started with a softening along the jawline, a sense that your face is sitting differently than it used to. Maybe you've already started taking collagen—dutifully adding it to your morning coffee or smoothie, hoping to turn back the clock. And yet, despite months of consistent supplementation, the results feel... underwhelming. Here's why that might be—and what you can do about it.

The Collagen Myth We Need to Unlearn
The dominant story we've been told about facial ageing is one of loss. Collagen disappears, the narrative goes, so we must replace it. This framing has driven an entire industry of fillers, supplements, and topical products promising to 'restore' what time has taken away. But this story is incomplete—and in many cases, biologically misleading.
What's actually happening beneath your skin is far more complex. It's not simply that you're losing collagen—it's that your collagen is being actively broken down while the systems responsible for rebuilding it are simultaneously impaired. Think of it like trying to fill a bathtub while someone has pulled the plug. You can keep adding water, but until you address the drain, you'll never get ahead.
This is the fundamental limitation of collagen supplementation alone. Those peptides you're taking can provide valuable building blocks—amino acids like glycine, proline, and hydroxyproline that serve as raw materials for new collagen. Research does show they can modestly stimulate the fibroblasts (the cells that manufacture collagen) and improve dermal density. But here's the catch: if your internal environment is hostile to collagen, what you build will be rapidly dismantled.

The Real Culprit: Oxidative Stress
At a cellular level, skin ageing is fundamentally an oxidative process. Your dermal fibroblasts—those precious collagen-producing cells—are exquisitely sensitive to what scientists call reactive oxygen species, or ROS. These are essentially unstable molecules that accumulate from sun exposure, pollution, metabolic stress, and chronic inflammation.
Here's the crucial distinction - these free radicals don't just 'use up' your collagen. They activate enzymes called matrix metalloproteinases—MMPs for short—that actively dismantle your collagen fibres. Your collagen network isn't passively fading away. It's being enzymatically cleaved, cut apart from the inside while new synthesis is simultaneously impaired because your fibroblasts are exhausted and your mitochondria are struggling.
The result? Skin that appears thinner, less elastic, and structurally unstable—even when total collagen content hasn't yet dramatically fallen. This is why you can look in the mirror and see changes that seem disproportionate to what the numbers might suggest.
Without controlling this biochemical environment, collagen becomes disposable infrastructure. You're not starved of building blocks—you're operating in a hostile oxidative environment that continuously erodes what you build.

Astaxanthin: The Antioxidant Your Skin Has Been Waiting For
If oxidative stress is the silent enemy of collagen, then targeted antioxidant support becomes not a luxury, but a necessity. This is where astaxanthin enters the conversation—and it deserves far more attention than it typically receives.
Astaxanthin is a carotenoid—the pigment that gives salmon and flamingos their distinctive pink colour. But what makes it remarkable for skin isn't its colour; it's its unique molecular architecture. Unlike vitamin C, which is water-soluble and stays in watery compartments, or vitamin E, which remains within fat-soluble spaces, astaxanthin can span both. It positions itself across cell membranes, protecting them from damage on both sides.
For your skin, this matters enormously. The integrity of your cell membranes—in keratinocytes, in fibroblasts, in the mitochondria within those cells—determines resilience, hydration, and barrier function. Astaxanthin protects these structures from lipid peroxidation, the process by which fats in your cell membranes become rancid and dysfunctional.
Human studies have demonstrated that astaxanthin supplementation reduces markers of oxidative stress, improves skin elasticity, decreases wrinkle depth, and enhances moisture retention. But perhaps most importantly for our purposes, it down-regulates those collagen-destroying MMP enzymes while preserving collagen fibre organisation. It also protects mitochondrial DNA within fibroblasts from oxidative injury—and this matters because when mitochondria become inefficient, fibroblasts shift toward a senescent, inflammatory state rather than actively producing quality collagen.
Astaxanthin's ability to neutralise singlet oxygen—one of the most damaging ROS generated by UV exposure—is substantially greater than that of beta-carotene or vitamin E, making it particularly relevant in sun-related skin ageing and structural dermal degradation.

Glutathione: The Master 
While astaxanthin works at the membrane level, glutathione operates upstream and systemically. It's often called the 'master antioxidant,' and this isn't marketing hyperbole—it's biochemical fact.
Glutathione doesn't just neutralise free radicals directly; it regenerates other antioxidants, including vitamin C and vitamin E, keeping your entire antioxidant network functional. In skin, adequate glutathione levels protect fibroblasts from oxidative stress-induced cell death and suppress inflammatory signalling pathways that drive collagen breakdown.
Here's where hormones enter the picture. Estrogen naturally upregulates antioxidant enzymes and supports collagen synthesis. As women approach and move through perimenopause and menopause, declining estrogen unmasks a pre-existing oxidative vulnerability. Glutathione levels, already challenged by chronic stress and toxin exposure, become even more critical to maintain.
Supporting glutathione status—whether through precursors like N-acetyl cysteine, through liposomal delivery systems, or through strategies that reduce its consumption—becomes a foundational intervention, not an optional add-on. This is especially true if you're noticing that your skin's resilience has shifted notably in your forties or fifties.

The Lipid Layer - Your Skin's Forgotten Barrier
There's another casualty of oxidative ageing that rarely makes it into the collagen conversation: your skin's lipid layer.
The outermost layer of your skin—the stratum corneum—contains a matrix of lipids composed primarily of ceramides, cholesterol, and free fatty acids. This isn't just waterproofing; it's a signalling interface that determines how your skin communicates with the environment and how well it holds onto moisture.
Oxidative stress and chronic inflammation alter this lipid composition and promote lipid peroxidation, weakening barrier integrity and increasing water loss through the skin. This creates a vicious cycle: barrier dysfunction increases inflammatory signalling, which further accelerates collagen degradation in the dermis below. Diets low in essential fatty acids, excessive sun exposure, insulin resistance, and systemic inflammation all contribute to this breakdown.
From this perspective, skin sagging isn't just a dermal issue—it's a reflection of impaired lipid biology and chronic inflammatory tone throughout your system.

SPMs: Resolving Inflammation
When we talk about inflammation and skin ageing, it's important to understand that the goal isn't simply to suppress inflammation—it's to resolve it. These are different processes, and the distinction matters.
Specialised pro-resolving mediators, or SPMs, are signalling molecules derived from omega-3 fatty acids that actively guide inflammation toward resolution. They don't just dampen the inflammatory response; they orchestrate cleanup, tissue repair, and return to homeostasis. Think of them as the difference between hitting the pause button on inflammation versus actually completing the inflammatory cycle and moving on.
Chronic, low-grade inflammation—the kind that accumulates with age, stress, poor diet, and hormonal shifts—creates an environment where inflammation never fully resolves. It smoulders beneath the surface, continuously activating those collagen-destroying enzymes and keeping fibroblasts in a defensive, non-productive state.
SPM supplementation offers a way to support proper inflammatory resolution, shifting the tissue environment away from chronic degradation and toward repair. When combined with antioxidant support and collagen substrates, this creates a terrain that actually allows structural preservation rather than endless rebuilding.

Reframing the Approach - From Repair to Preservation
This brings us to a fundamental reframe of how we should think about skin ageing. Slowing collagen loss isn't about chasing volume after the fact—it's about preserving structural integrity by controlling oxidative load, supporting mitochondrial health, stabilising the lipid barrier, and maintaining anti-inflammatory signalling.
Collagen supplementation can absolutely be valuable, but only when layered onto a terrain that allows collagen to persist. Antioxidants like astaxanthin and glutathione aren't 'cosmetic supplements'—they are structural protectants. SPMs aren't anti-inflammatory drugs—they are resolution facilitators. Essential fatty acids aren't just heart-healthy fats—they are barrier builders.
When you understand this, you stop asking 'How do I replace what I've lost?' and start asking 'How do I protect what I still have?'

A Practical Framework
So what does this mean practically? It means building a multi-layered strategy that addresses each of the underlying drivers:
First, provide the building blocks. Quality collagen peptides remain valuable—they offer amino acid substrates and may signal fibroblasts to increase activity. But think of this as necessary, not sufficient.
Second, protect the terrain. Astaxanthin for membrane protection and MMP inhibition; glutathione support for systemic redox balance and fibroblast preservation. These shift the balance away from degradation and toward maintenance.
Third, resolve inflammation. SPMs to guide chronic, smouldering inflammation toward completion, freeing fibroblasts to do repair work rather than defensive signalling.
Fourth, support the barrier. Adequate essential fatty acids—from diet and supplementation as needed—to maintain lipid integrity in the stratum corneum and reduce the inflammatory cascade that follows barrier dysfunction.
Fifth, address the hormonal context. If you're perimenopausal or postmenopausal, recognise that your antioxidant requirements have shifted. Estrogen was doing work that now needs to be supported through other means.

The Bigger Picture
From a functional perspective, facial ageing in women is a visible manifestation of systemic redox imbalance, inflammatory burden, and hormonal transition. Jowling and sagging reflect a failure of collagen architecture, not simply a deficit of collagen itself.
When we address the underlying drivers—oxidative stress, mitochondrial decline, lipid peroxidation, and chronic inflammation—we're no longer just trying to make the face look younger. We're altering the biological trajectory of skin ageing itself, preserving resilience rather than endlessly repairing damage after it has already occurred.
Your skin is telling you something about what's happening inside. The question isn't just 'How do I look better?'—it's 'What is my skin revealing about my deeper health?' When you approach it this way, the interventions you choose become about more than aesthetics. They become about supporting the whole system that your skin depends on.
And that shift in perspective—from surface repair to systemic preservation—is where real, lasting change begins.

References
Matrix Metalloproteinases & Oxidative Stress
Quan T, Qin Z, Xia W, Shao Y, Voorhees JJ, Fisher GJ. Matrix-degrading metalloproteinases in photoaging. J Investig Dermatol Symp Proc. 2009;14(1):20-24.
Fisher GJ, Quan T, Purohit T, et al. Collagen fragmentation promotes oxidative stress and elevates matrix metalloproteinase-1 in fibroblasts in aged human skin. Am J Pathol. 2009;174(1):101-114.
Rittié L, Fisher GJ. UV-light-induced signal cascades and skin aging. Ageing Res Rev. 2002;1(4):705-720.
Pittayapruek P, Meephansan J, Prapapan O, Komine M, Ohtsuki M. Role of matrix metalloproteinases in photoaging and photocarcinogenesis. Int J Mol Sci. 2016;17(6):868.
Feng M, Zhu S, Guo W, et al. Matrix metalloproteinases on skin photoaging. J Cosmet Dermatol. 2024;23(11):3480-3492.
Quan T, Little E, Quan H, Qin Z, Voorhees JJ, Fisher GJ. Elevated matrix metalloproteinases and collagen fragmentation in photodamaged human skin: impact of altered extracellular matrix microenvironment on dermal fibroblast function. J Invest Dermatol. 2013;133(5):1362-1366.
Poon F, Kang S, Chien AL. Mechanisms and treatments of photoaging. Photodermatol Photoimmunol Photomed. 2015;31(2):65-74.
Astaxanthin & Skin Health
Tominaga K, Hongo N, Karato M, Yamashita E. Cosmetic benefits of astaxanthin on humans subjects. Acta Biochim Pol. 2012;59(1):43-47.
Ito N, Seki S, Ueda F. The protective role of astaxanthin for UV-induced skin deterioration in healthy people—a randomized, double-blind, placebo-controlled trial. Nutrients. 2018;10(7):817.
Tominaga K, Hongo N, Fujishita M, Takahashi Y, Adachi Y. Protective effects of astaxanthin on skin deterioration. J Clin Biochem Nutr. 2017;61(1):33-39.
Zhou X, Cao Q, Orfila C, Zhao J, Zhang L. Systematic review and meta-analysis on the effects of astaxanthin on human skin ageing. Nutrients. 2021;13(9):2917.
Davinelli S, Nielsen ME, Scapagnini G. Astaxanthin in skin health, repair, and disease: a comprehensive review. Nutrients. 2018;10(4):522.
Kidd P. Astaxanthin, cell membrane nutrient with diverse clinical benefits and anti-aging potential. Altern Med Rev. 2011;16(4):355-364.
Glutathione & Antioxidant Defence
Sonthalia S, Daulatabad D, Sarkar R. Glutathione as a skin whitening agent: facts, myths, evidence and controversies. Indian J Dermatol Venereol Leprol. 2016;82(3):262-272.
Rahman I, Kode A, Biswas SK. Assay for quantitative determination of glutathione and glutathione disulfide levels using enzymatic recycling method. Nat Protoc. 2006;1(6):3159-3165.
Richie JP Jr, Nichenametla S, Neiber W, et al. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. Eur J Nutr. 2015;54(2):251-263.
Chen Y, Dong H, Thompson DC, Shertzer HG, Nebert DW, Vasiliou V. Glutathione defense mechanism in liver injury: insights from animal models. Food Chem Toxicol. 2013;60:38-44.
Hseu YC, Lo HW, Korivi M, et al. The antiaging activity of ergothioneine in UVA-irradiated human dermal fibroblasts via the inhibition of the AP-1 pathway and the activation of Nrf2-mediated antioxidant genes. Oxid Med Cell Longev. 2020;2020:2576823.
Li S, Hong M, Tan HY, Wang N, Feng Y. Insights into the role and interdependence of oxidative stress and inflammation in liver diseases. Oxid Med Cell Longev. 2016;2016:4234061.
Oral Collagen Peptide Supplementation
Proksch E, Segger D, Degwert J, Schunck M, Zague V, Oesser S. Oral supplementation of specific collagen peptides has beneficial effects on human skin physiology: a double-blind, placebo-controlled study. Skin Pharmacol Physiol. 2014;27(1):47-55.
Asserin J, Lati E, Shioya T, Prawitt J. The effect of oral collagen peptide supplementation on skin moisture and the dermal collagen network: evidence from an ex vivo model and randomized, placebo-controlled clinical trials. J Cosmet Dermatol. 2015;14(4):291-301.
Choi FD, Sung CT, Juhasz ML, Mesinkovsk NA. Oral collagen supplementation: a systematic review of dermatological applications. J Drugs Dermatol. 2019;18(1):9-16.
de Miranda RB, Weimer P, Rossi RC. Effects of hydrolyzed collagen supplementation on skin aging: a systematic review and meta-analysis. Int J Dermatol. 2021;60(12):1449-1461.
Kim DU, Chung HC, Choi J, Sakai Y, Lee BY. Oral intake of low-molecular-weight collagen peptide improves hydration, elasticity, and wrinkling in human skin: a randomized, double-blind, placebo-controlled study. Nutrients. 2018;10(7):826.
Reilly DM, Kynaston S, Naseem S, et al. A clinical trial shows improvement in skin collagen, hydration, elasticity, wrinkles, scalp, and hair condition following 12-week oral intake of a supplement containing hydrolysed collagen. Dermatol Res Pract. 2024;2024:8752787.
Bolke L, Schlippe G, Gerß J, Voss W. A collagen supplement improves skin hydration, elasticity, roughness, and density: results of a randomized, placebo-controlled, blind study. Nutrients. 2019;11(10):2494.
Specialised Pro-Resolving Mediators (SPMs)
Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014;510(7503):92-101.
Basil MC, Levy BD. Specialized pro-resolving mediators: endogenous regulators of infection and inflammation. Nat Rev Immunol. 2016;16(1):51-67.
Chiurchiù V, Leuti A, Dalli J, et al. Proresolving lipid mediators resolvin D1, resolvin D2, and maresin 1 are critical in modulating T cell responses. Sci Transl Med. 2016;8(353):353ra111.
Calder PC. Omega-3 fatty acids and inflammatory processes: from molecules to man. Biochem Soc Trans. 2017;45(5):1105-1115.
Jordan PM, Werz O. Specialized pro-resolving mediators: biosynthesis and biological role in bacterial infections. FEBS J. 2022;289(14):4212-4227.
Estrogen, Menopause & Skin Aging
Thornton MJ. Estrogens and aging skin. Dermatoendocrinol. 2013;5(2):264-270.
Brincat M, Versi E, Moniz CF, Magos A, de Trafford J, Studd JW. Skin collagen changes in postmenopausal women receiving different regimens of estrogen therapy. Obstet Gynecol. 1987;70(1):123-127.
Hall G, Phillips TJ. Estrogen and skin: the effects of estrogen, menopause, and hormone replacement therapy on the skin. J Am Acad Dermatol. 2005;53(4):555-568.
Lephart ED. A review of the role of estrogen in dermal aging and facial attractiveness in women. J Cosmet Dermatol. 2018;17(3):282-288.
Shu YY, Maibach HI. Estrogen and skin: therapeutic options. Am J Clin Dermatol. 2011;12(5):297-311.
Stevenson S, Thornton J. Effect of estrogens on skin aging and the potential role of SERMs. Clin Interv Aging. 2007;2(3):283-297.
Skin Lipid Barrier & Ceramides
Sahle FF, Gebre-Mariam T, Dobner B, Wohlrab J, Neubert RH. Skin diseases associated with the depletion of stratum corneum lipids and stratum corneum lipid substitution therapy. Skin Pharmacol Physiol. 2015;28(1):42-55.
Kendall AC, Pilkington SM, Murphy SA, et al. Menopause induces changes to the stratum corneum ceramide profile, which are prevented by hormone replacement therapy. Sci Rep. 2022;12(1):21715.
Mojumdar EH, Pham QD, Topgaard D, Sparr E. Skin hydration: interplay between molecular dynamics, structure and water uptake in the stratum corneum. Sci Rep. 2017;7(1):15712.
Rogers J, Harding C, Mayo A, Banks J, Rawlings A. Stratum corneum lipids: the effect of ageing and the seasons. Arch Dermatol Res. 1996;288(12):765-770.
Meckfessel MH, Brandt S. The structure, function, and importance of ceramides in skin and their use as therapeutic agents in skin-care products. J Am Acad Dermatol. 2014;71(1):177-184.
Yokota M, Yahagi S, Tokudome Y. Clinical significance of the water retention and barrier function-improving capabilities of ceramide-containing formulations: a qualitative review. J Dermatol. 2022;49(8):779-794.
Fibroblast Function & Senescence
Wlaschek M, Maity P, Makrantonaki E, Scharffetter-Kochanek K. Connective tissue and fibroblast senescence in skin aging. J Invest Dermatol. 2021;141(4S):985-992.
Gruber F, Kremslehner C, Eckhart L, Tschachler E. Cell aging and cellular senescence in skin aging—recent advances in fibroblast and keratinocyte biology. Exp Gerontol. 2020;130:110780.
Cole MA, Quan T, Voorhees JJ, Fisher GJ. Extracellular matrix regulation of fibroblast function: redefining our perspective on skin aging. J Cell Commun Signal. 2018;12(1):35-43.
Tigges J, Krutmann J, Fritsche E, et al. The hallmarks of fibroblast ageing. Mech Ageing Dev. 2014;138:26-44.
Lago JC, Puzzi MB. The effect of aging in primary human dermal fibroblasts. PLoS One. 2019;14(7):e0219165.