It was never about more collagen.What interested us was which signals the body actually picks up.
Dr. Thomas SchroeterFounder

Loss of collagen as we age: Causes, symptoms and effective regeneration methods

What happens to your body's collagen as you age?

Ageing skin
From around 25, the body makes a little less collagen every year.
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    Introduction

    Collagen is a vital protein that plays a crucial role in maintaining the strength and elasticity of our skin. It is a fibrous protein that makes up a significant portion of our connective tissues and contributes to the overall structure and integrity of our skin. As we age, the synthesis of collagen decreases, leading to a loss of skin elasticity, thinning of the epidermis, and an increased susceptibility to damage. In this article, we look at why ageing skin loses collagen and at the approaches described in the dermatology literature. 

    Laughing woman with curly hair, close-up of mouth and cheek
    As we age, skin makes less collagen; it loses elasticity, and its outermost layer becomes thinner.

    The Importance of Collagen in Skin Health

    Collagen is the most abundant protein in the human body, accounting for approximately one-third of all proteins. It is primarily found in tendons, muscles, bones, skin, ligaments, and other fibrous tissues. Within the skin, collagen provides strength and support, ensuring that the skin remains firm, supple, and resistant to damage. It forms a dense network that gives the skin its structural integrity. It also plays a critical role in the renewal of skin cells and the replacement of damaged and dead cells.

    There are various types of collagen, with types I, II, and III being the most prevalent in the body. For the firmness and elasticity of the skin, types I and III are the decisive ones. Each type of collagen has unique roles and structures, contributing to the overall function and health of our skin. The body's own collagen production tapers off gradually from the middle of the third decade of life. That is a normal process, and the collagen content of the skin declines along with it. This is where visible skin ageing begins.

    Abstract acrylic painting with yellow, red and blue cell-like bubbles of paint
    Older skin holds less collagen, partly because its connective-tissue cells make less of the precursor of type I collagen.

    Mechanisms of Collagen Loss in Aging Skin

    Cellular Fibroblast Aging

    One of the underlying mechanisms of collagen loss in aging skin is cellular fibroblast aging. Fibroblasts are responsible for the synthesis of collagen in the skin. With age, the skin's connective-tissue cells (fibroblasts) make less type I procollagen, a precursor of collagen. This is one reason why older skin contains less collagen. This reduced collagen synthesis contributes to the overall decrease in collagen levels observed in aging skin.

    Reduced Mechanical Stimulation

    In addition to cellular fibroblast aging, reduced mechanical stimulation in aging skin also contributes to collagen loss. With age, skin cells are less closely attached to the collagen fibres. These findings suggest a lower level of mechanical stimulation on the cells in aged skin, leading to a reduction in collagen synthesis.

    Photodamage and Collagen Synthesis

    While the mechanisms underlying collagen loss in photodamaged skin and chronologically aged skin share similarities, there are also distinct factors at play. Photodamaged skin, which has been exposed to excessive ultraviolet (UV) radiation, exhibits fragmented collagen in the dermis, inhibiting collagen synthesis. Damaged collagen fails to provide the necessary mechanical tension on fibroblasts, impairing their ability to synthesize collagen efficiently. The presence of collagen fragmentation in chronologically aged skin is also observed, but the extent to which this contributes to overall collagen reduction is still not fully understood.

    Upregulation of Collagen-Degrading Enzymes

    Collagen loss in aging skin is further aggravated by the upregulation of collagen-degrading matrix metalloproteinases (MMPs). UV radiation from the sun stimulates the production of MMPs in the skin, leading to collagen fragmentation in photodamaged skin. Over time, repeated exposure to UV radiation can induce chronic upregulation of MMPs, gradually degrading collagen in chronologically aged skin. This gradual rise in collagen-degrading enzymes has been described for aged skin. 

    Wrinkled older hands with a signet ring resting on the handle of a walking stick
    As collagen declines, skin loses its ability to spring back: it sags, wrinkles deepen and the epidermis thins.

    Consequences of Collagen Loss in Aging Skin

    The reduction of collagen synthesis and the subsequent loss of collagen in aging skin have significant consequences for skin health and appearance. Some of the key effects of collagen loss include:

    Loss of Skin Elasticity: Collagen provides the skin with its elasticity, allowing it to stretch and bounce back. When collagen levels decrease, the skin loses its ability to retain its shape, leading to sagging and wrinkles.

    Thinning of the Epidermis: Collagen is essential for maintaining the thickness of the epidermis, the outermost layer of the skin. As collagen levels decline, the epidermis becomes thinner, making the skin more fragile and prone to damage.

    Increased Formation of Wrinkles: The decrease in collagen synthesis and the breakdown of existing collagen contribute to the formation of wrinkles. Fine lines and deep wrinkles become more prominent as the skin loses its structural support.

    Vulnerability to Damage: Collagen loss compromises the skin's ability to withstand external stressors and injuries. The skin becomes more susceptible to damage from environmental factors, such as UV radiation and pollution.

    Impaired Skin Cell Renewal: Collagen plays a crucial role in the renewal of skin cells. As collagen levels decline, the process of cell turnover slows down, leading to a dull and uneven complexion. 

    Ball-and-stick model of a small ring-shaped molecule on a black background
    At the molecular level, oxidative stress, UV-induced DNA damage and chronic inflammation are among the drivers of skin ageing.

    Understanding the Molecular Mechanisms of Skin Aging

    The aging process of the skin is influenced by various molecular mechanisms, both intrinsic and extrinsic. These mechanisms contribute to the progressive deterioration of the skin's structure and function. Some of the prominent models and advancements in molecular mechanism studies related to skin aging include:

    Oxidative Stress

    Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) and the body's antioxidant defense system, plays a significant role in skin aging. ROS, generated from different sources within the body, contribute to dermal changes associated with aging. The production of ROS can be influenced by internal factors, such as mitochondrial dysfunction, as well as external factors like UV radiation. The accumulation of ROS leads to DNA damage, protein degradation, and inflammation, all of which contribute to skin aging.

    DNA Damage

    Exposure to UV radiation can cause DNA damage in skin cells, disrupting the function of genes involved in skin stem cell homeostasis. The accumulation of DNA damage and mutations can accelerate the aging process and increase the risk of skin cancer. Repair mechanisms, such as nucleotide excision repair, play a vital role in maintaining DNA integrity and preventing premature aging caused by UV exposure.

    Telomere Shortening

    Telomeres are repetitive DNA sequences that cap the ends of chromosomes and protect them from degradation and recombination. Telomeres shorten with each cell division, eventually leading to cellular senescence. The enzyme telomerase helps maintain telomere length, preventing premature telomere shortening and supporting healthy cell regeneration. UV exposure and other external factors can accelerate telomere shortening and disrupt the balance between cell proliferation and senescence.

    Inflammaging

    Inflammaging refers to chronic inflammation that occurs as a result of aging. It contributes to the onset and progression of age-related diseases, including skin aging. UV radiation can induce inflammation in the skin, leading to damage and the release of pro-inflammatory molecules. This chronic inflammation further accelerates the aging process and exacerbates the loss of collagen and other extracellular matrix components.

    Intrinsic Aging

    Intrinsic aging is an unavoidable physiological process that occurs internally as we age. It is characterized by a gradual decline in the production of collagen and other skin components. Intrinsic aging primarily affects the basal layer of the skin, where the reproduction of cells decreases, resulting in a thinner epidermis and reduced nutrition exchange. Cellular senescence and the accumulation of damaged proteins and lipids contribute to the overall deterioration of skin health.

    Extrinsic Aging

    Extrinsic aging is influenced by external factors, such as UV radiation, pollution, smoking, and poor nutrition. UV radiation, in particular, plays a significant role in extrinsic aging by causing collagen breakdown and impairing the skin's ability to regenerate. The thickening of the epidermis, the formation of solar elastolysis, and the impairment of blood vessels are some of the visible effects of extrinsic aging on the skin. 

    Slice of layered cake with cream, pistachios and a dried rosebud on a plate
    Eating too much sugar can lead to glycation end products (AGEs), which stiffen and damage collagen fibres.

    Lifestyle Habits and Collagen Loss

    Certain lifestyle habits can accelerate collagen loss and contribute to premature skin aging. It is essential to be aware of these habits and make conscious choices to protect and preserve collagen in the skin. Some lifestyle factors that can affect collagen levels include:

    Excessive Sugar Intake

    Consuming excessive amounts of sugar can lead to the formation of advanced glycation end products (AGEs). AGEs can stiffen and damage collagen fibers, compromising their stability and function. Glycation not only affects existing collagen but also inhibits the synthesis of new collagen, leading to premature aging.

    Tobacco Usage

    Smoking tobacco has been linked to collagen damage in the skin. The chemicals in tobacco smoke can directly affect the collagen layer, leading to collagen loss and the development of wrinkles. Smoking also constricts blood vessels, reducing blood flow to the skin and impairing collagen healing processes. 

    Three dabs of white cream in a row on a bare forearm against linen
    Sunscreen, clothing and shade shield your skin from UV rays, a main cause of collagen breakdown.

    What the literature describes on collagen loss

    Collagen loss is a natural part of the aging process. The dermatological literature discusses a number of approaches, described below:

    Dietary Changes

    Diet is how the building blocks reach the body in the first place. Vitamin C contributes to normal collagen formation for the normal function of skin, bones and cartilage. It is plentiful in citrus fruit and leafy greens; copper contributes to the maintenance of normal connective tissue. The amino acids glycine, proline and lysine come from the protein on your plate — meat, fish, eggs, pulses.

    Exercise and Mechanical Stimulation

    Regular exercise gets your circulation going. Resistance training such as weightlifting also puts tissue under mechanical tension. It is important to consult with a healthcare professional or a qualified trainer before starting any exercise regimen.

    Sun Protection

    Protecting the skin from harmful UV rays is crucial for maintaining collagen levels and preventing photodamage. Applying sunscreen with a high SPF, wearing protective clothing, and seeking shade during peak sun hours can help minimize collagen breakdown caused by UV radiation.

    Topical Treatments

    Dermatological studies on creams and serums containing retinol, peptides or hyaluronic acid have measured wrinkle depth and skin elasticity. These are topical cosmetics and have nothing to do with collagen taken by mouth. Consult with a dermatologist or skincare professional to find the right topical treatments for your skin type and concerns.

    Minimally Invasive Procedures

    For more significant collagen loss and skin aging concerns, minimally invasive procedures may be considered. These include treatments like microneedling, laser resurfacing, and dermal fillers. Dermatological studies of these procedures have measured skin texture and dermal volume after treatment. They are clinical procedures and have nothing to do with collagen taken by mouth. It is crucial to consult with a qualified medical professional to determine the most suitable treatment option for your specific needs. 

    Woman with closed eyes lying in bath water, one hand at her cheek
    As skin ages, its cells make less collagen.

    Conclusion

    Understanding the mechanisms of collagen loss in aging skin is essential for developing effective prevention and treatment strategies. Cellular fibroblast aging, reduced mechanical stimulation, photodamage, and upregulation of collagen-degrading enzymes all contribute to collagen loss and the subsequent deterioration of skin health. A healthy lifestyle, sun protection and the treatment options described above are the levers the dermatological literature on skin aging discusses. Consult with skincare professionals and healthcare providers to develop a personalized approach to address your specific skin concerns and goals.

    Image credits: Danie Franco, Lesly Juarez, Scott Webb, أخٌ‌في‌الله, Terry Vlisidis, K8, BATCH by Wisconsin Hemp Scientific, Coline Haslé on Unsplash

    Editorial team & review

    Review status

    Editorially approved

    This article was researched, written and edited in-house against the sources listed. It has not been reviewed by a physician. When a medical reviewer is appointed, their name, specialty and review date will appear here and in the byline.

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