Skin Aging: The causes, effects, and how to slow it
Written and Reviewed by: Elysium Health
- There are internal and external factors that cause skin aging, some of which share similar mechanisms of action, such as the production of reactive oxygen species (ROS).
- Sun exposure, which is the primary external cause of skin aging, generates ROS, which impacts many cellular processes, including the maintenance of collagen, elastin, and DNA.
- Changes in thickness, elasticity, and barrier function occur in the skin, resulting in wrinkles, sagging, and dryness. Our skin also becomes more fragile and prone to bruising.
- Skin aging can be slowed with proper nutrition, topicals, supplements, and sunscreen.
- Mosaic: A clinically proven daily softgel for skin aging that strengthens and protects the skin from the inside-out. Developed with the advisement of Dr. Granstein, a world-renowned dermatologist, Mosaic’s novel formulation combines carotenoids with other synergistic phytonutrients and hyaluronic acid to create a foundation for optimal skin health–improving its resilience against stressors, increasing whole-body moisture, and reducing visible signs of aging.
- Basis: NAD+ levels have been shown to decline with age in various tissues, including the skin. Basis boosts NAD+ levels to support collagen and ceramide production, protect DNA from stressors, and target aging at the cellular level.
Let’s take a moment to appreciate our skin, the body’s largest organ, and all the ways it helps us move through the world: regulating body temperature, storing water and fat, sensing temperature and pressure, producing hormones, protecting us from harmful aspects of the environment, and more. The skin is an essential component of the nervous, immune, and endocrine systems. This three-layered organ consists of the epidermis (outer layer), dermis (middle), and hypodermis (deepest). It’s constantly renewing itself and adapting to our environment. Our skin is even home to some 1,000 species of bacteria living on the epidermis, which protect us from being colonized by invaders and participate in immune function.
Like the rest of our organs, the skin changes with age as a result of intrinsic factors and environmental, or extrinsic, factors. Connective tissue breaks down, repair and regeneration decline, and the overall functionality of our skin as a barrier to the outside world degrades. Because our skin is intricately connected to the rest of our biology, the changes to our skin are meaningful to our appearance and to our overall health. This article explores those age-related changes to skin, why they happen, and what we may be able to do about it.
Three layers deep: the structure of your skin
Together with your hair, nails, oil glands, and sweat glands, your skin makes up your integumentary system. Your skin consists of three interconnected layers working harmoniously: the epidermis, dermis, and hypodermis.
What is the epidermis?
The epidermis is the outermost layer of the skin, ranging from 0.05 mm thick on the eyelids to 1.5 mm thick on the palms and the soles of the feet. Its main function is to protect us from the environment, though it also contains pigment that gives our skin color and helps to transfer substances out of the body. The epidermis itself has five layers that work together to regenerate this outer surface of the skin: the basal cell layer or stratum germinativum (innermost), squamous cell layer, stratum granulosum, stratum lucidum, and stratum corneum (outermost layer).
The major cell type present in the epidermis is the keratinocyte. New keratinocytes are generated in the basal cell layer and move their way up to the surface, changing shape and function as they mature, and ultimately die, forming the outermost layer of our skin: 10 to 30 layers of dead keratinocytes. These cells turn over completely every 28 to 30 days in young people and 45 to 50 days in elderly adults. Another important biological event that begins in the epidermis is the production of vitamin D3 when our skin comes into contact with sunshine.
What is the dermis?
The dermis is the middle layer of the skin and also the thickest layer at 1.5 mm to 4 mm thick. It consists of two layers—the reticular dermis and papillary dermis—and is held together mostly by collagen with the support of elastin. Within the dermis are essential cells and structures, including blood vessels, lymph vessels, hair follicles, sweat glands, sebaceous (oil) glands, nerve endings, connective tissue, and fat cells. These components of the dermis participate in many of the functions of the skin, including sensing pain, temperature, and pressure; sweating; keeping the skin moist; flexibility and protection from injury; regulating body temperature; and protecting from infection or invasive organisms.
What is the hypodermis?
The hypodermis is also known as the subcutis or subcutaneous fat layer, and as the name suggests it consists mainly of fat (adipocytes), as well as collagen and elastin. Since body fat varies from person to person, the thickness of the hypodermis is also variable. Other cells and structures present in the hypodermis include blood vessels, lymphatic vessels, nerves, sweat glands, and macrophages (white blood cells). This layer acts as a shock absorber, a store of fat for energy reserves, insulation for the body, and plays a role in immune function. It also connects the skin to the muscle and bones in your body.
The intrinsic and extrinsic factors responsible for skin aging
These three layers of your skin form a complex and elegant boundary organ exposed to the world around us that plays an essential role in our health. With age, a combination of intrinsic and environmental factors causes changes to our skin that impact its appearance and function. Intrinsic and environmental causes are different but overlapping; the same components of the skin may naturally degrade with age while also being exacerbated by environmental factors, especially the sun.
Intrinsic causes of skin aging
Intrinsic causes are part of chronological aging and the decline in function that accompanies it. Regardless of sun exposure, we can all more or less expect the appearance of our skin to change: thinner and more translucent, with wrinkles, sagging, pigmentation, and dryness. The functionality changes, too, becoming more likely to be bruised, more prone to skin disorders and cancer, less effective at regulating heat, and less efficient at healing wounds. There are several underlying causes.
GeneticsYour genes play a role in skin aging, as some genes are upregulated and others downregulated during chronological aging. How this relates to one’s individual genome has yet to be clarified.
Reactive oxygen speciesReactive oxygen species (ROS) play a role in intrinsic and extrinsic aging. They are the byproducts of normal cellular activity, but they increase with age. What makes ROS dangerous is that they consist of atoms or molecules with an unpaired electron, making them reactive and unstable—prone to stealing electrons from other molecules. In skin aging, ROS cause damage to many cellular components, including proteins, lipids, and DNA, leading to cellular dysfunction. ROS also lead to the overexpression of matrix metalloproteinases (MMPs), which degrade collagen and inhibit their synthesis.
Cellular senescenceCellular senescence is one of the hallmarks of aging—and it’s a driving force of skin aging, too. Triggered by common cellular stressors, cells cease to divide but remain metabolically active. As senescent cells accumulate, they can secrete problematic molecules which impact neighboring cells and tissues—and even those elsewhere in the body. In particular, senescent keratinocytes and fibroblasts impact the integrity and function of the skin.
Thinning of the epidermisIn the innermost layer of the epidermis, basal cells don’t proliferate as well with age, leading to a thinning of the epidermis and less contact between the epidermis and the dermis. As a result, less nutrition makes its way into the epidermis.
Changes to collagen and elastinA natural part of aging includes reduced production and degraded quality of collagen, the major structural protein in the skin. Elastin, one of the other primary components of the structure of skin, also degrades with age. This leads to a loss in strength and resiliency of our skin. Learn more about collagen and skin aging here.
Moisture retentionSkin aging is associated with a loss in skin moisture, including greater transepidermal water loss, a measure of the water that escapes from the stratum corneum and a measure of the integrity of the skin, as well as a decrease in the skin’s hyaluronic acid (HA). HA is a major component of the extracellular matrix of the skin and a humectant, capable of binding over 1,000 times its weight in water, that plays a critical role in maintaining skin hydration. By age 60, we have half as much HA in the epidermis (outer layer of the skin) compared to our 20s, contributing to decreased volume, hydration, plumpness, and impaired barrier function in the skin. Sebaceous glands also become smaller with age, producing less sebum, or oil, which helps to moisturize and protect the skin—contributing to dryer skin with age.
Hormonal changesHormonal changes occur with age, in particular among women during and after menopause. The decrease in estrogen is associated with multiple aspects of skin aging, including dryness and decreased thickness, firmness, and elasticity.
Reduced blood flow and vasculatureThe size of blood vessels in the skin decreases with age, although the changes to vasculature are much more pronounced in photoaged skin.
Loss of fatChronological aging is accompanied by a general shift from subcutaneous fat to visceral deposits, which contributes to changes in appearance—sagging, wrinkles, sunken cheeks, thinning skin—as well as to metabolic disorders.
Extrinsic causes of skin aging
Extrinsic aging to the skin is primarily caused by exposure to ultraviolet radiation from the sun—also known as photoaging. Other contributing factors are exposure to air pollutants, nutrition, sleep quality, and toxins. Another word you might hear for this category of extrinsic or environmental causes of skin aging is the exposome.
Ultraviolet light: the primary driver of extrinsic skin aging
UV light is a form of radiation that comes from the sun—and man-made sources like tanning beds and nail polish drying devices. UV from the sun is the primary cause of extrinsic skin aging. Understanding how UV is different from other forms of light gives us insight into its harmful effects.
The sun gives off electromagnetic radiation in multiple wavelengths, only a small fraction of which can be detected by the human eye—that’s visible light. You can see the different wavelength components of sunlight (at least the visible range) as color bands in a rainbow, which forms when sunlight passes through water droplets in the air, causing the different wavelengths of light to bend to different degrees and separate. UV has a wavelength that’s shorter, and higher in frequency, than visible light; the meaning of ultraviolet (from Latin “ultra,” meaning “beyond”) is “beyond violet” because it has a higher frequency than violet. All electromagnetic radiation interacts with atoms and molecules to cause changes. In the case of our eyes and visible light, it’s vision. It’s less advantageous and more harmful in the case of our skin and UV.
UV consists of UVA, UVB, and UVC components, each corresponding to a particular wavelength. UVC has the shortest wavelength (100–280 nm) and highest energy among UV rays. UVA has the longest wavelength (315–400 nm) and least energetic photons. UVB falls in-between. UV rays from the sun that reach us when we’re outside for a run or having a picnic are about 95% UVA and 5% UVB. We can ignore UVC in this conversation because its absorbed by the ozone layer and atmosphere and doesn’t reach the Earth’s surface. UV rays can also reflect off surfaces like water and sand, resulting in increased UV exposure.
Because of their different wavelengths and energetic properties, UVA and UVB interact with our skin differently, contributing to skin aging in unique and overlapping ways. UVA makes its way into the dermis, or middle layer of skin, while UVB is absorbed by the epidermis. These two types of UV cause several problems at the level of cells and tissues that prematurely age our skin.
Reactive oxygen speciesJust as ROS play a role in intrinsic skin aging, they are a primary driver of photoaging. UVA generates reactive oxygen species, which as we mentioned previously cause damage to many cellular components, including proteins, lipids, and DNA. The creation of UV-induced ROS sets in motion several cellular processes that cause harm to the skin and promote aging: Excessive ROS activate the NF-kB pathway, which plays a role in inflammation; this increases levels of tumor necrosis factor alpha (TNF-α), a regulator of the inflammatory response; the end product is an increase in matrix metalloproteinases (MMPs), which degrade the extracellular matrix, degrade collagen, and prematurely age the skin. Skin pigment offers protection against aspects of this process, with darker skin being more resistant to MMP increases and even DNA damage.
Collagen degradationIt’s worth emphasizing collagen degradation on its own because it’s the most abundant protein in the body and is used to make connective tissue—an element of skin, bone, muscles, tendons, and cartilage. UV radiation causes MMPs and other proteolytic enzymes to break down collagen and get in the way of collagen synthesis. The body attempts to repair itself after this series of events, but over time damage accumulates. The result can be a rough and wrinkled appearance. Learn more about collagen and skin aging here.
Solar elastosisUV causes the overexpression of elastin, a stretchy protein that contributes to the elasticity of the skin. The result is elastosis: deposits of shortened elastin that gives the skin a thickened and yellow appearance.
DNA damageUVB is absorbed directly by DNA and causes mutations that can eventually result in skin cancer.
SunburnAcute UV damage causes sunburn, or solar erythema, which damages proteins and DNA, and induces complex inflammatory and immune responses. Sunburns increase photoaging and the risks of skin cancers.
Immune suppressionUV-induced inflammation and damage can weaken the immune system in the skin as well as the whole body, resulting over time in a weakened ability to fend off certain skin cancers.
HyperkeratosisWhile aging tends to thin the skin, UV exposure can actually cause the epidermis to thicken by damaging keratinocytes, disrupting their normal cell cycle, and later causing them to proliferate. This is called hyperkeratosis.
Reduced vasculatureThe size of blood vessels in the skin decreases with age, as mentioned previously, but they are much more pronounced in photoaged skin. In skin exposed to UV over time, there’s also an increase in the number of blood vessels and the area they cover.
While not originating from the sun, indoor tanning involves intentional exposure to UV radiation that may be up to 10 times more powerful than sunlight, adding to the burden of photoaging as well as the risk of skin cancer. And it turns out that UV is not the only type of light that contributes to aging, although it is the primary culprit: Research suggests that visible light and infrared light also contribute to skin aging.
Don’t I need sunshine for vitamin D?
You definitely need a sufficient amount of vitamin D, which is essential for healthy bone metabolism; it also supports immune health, muscle function, and brain cell activity. Roughly 42% of adults in the U.S. have a vitamin D deficiency. And yes, UVB contributes to the synthesis of vitamin D3 when it interacts with a protein called 7-DHC in the epidermis. Experts generally conclude that getting an “incidental” amount of sunshine here and there that doesn’t cause a tan or a sunburn is acceptable—and may be enough to generate sufficient vitamin D depending on your location and the time of year—but the risks of sun-seeking outweigh the benefits. Vitamin D supplements are an easy and safe solution for maintaining levels of D throughout the year.
Other forms of extrinsic skin aging
Photoaging is the most significant environmental cause of skin aging, and arguably the easiest to protect against with sunscreen and clothing. But there are several other factors that drive skin aging.
Air pollutionMany parts of the world and urban areas have significant pollution: particulate matter, polycyclic aromatic hydrocarbons (chemicals from coal and gas), oxides, volatile organic compounds (VOCs), and ground-level ozone. These all contribute to skin aging by disrupting the skin barrier, causing inflammation, and generating ROS.Smoking. Smoking is harmful to virtually every aspect of health, skin included. Smoking is associated with facial wrinkling, facial pigmentation, changes to hue and radiance, and increased tissue laxity.
NutritionThe quality of your diet certainly plays a role in overall aging, and it appears to play a role in skin aging, too. Eating too much sugar has been associated with more advanced glycation end products (AGEs) in the skin, which cause wrinkles.
SleepIf you’ve ever looked in the mirror after a night of bad sleep, you know about the impact of inadequate rest on your skin. Studies support this, finding that sleep loss is associated with looking less healthy, less attractive, more wrinkled, as well as other signs of aging.
How to combat skin aging
We all experience intrinsic skin aging to varying degrees. With extrinsic aging, we have more power to intervene and preserve the appearance and function of our skin—much like we can do with our biological age. Since photoaging is the primary environmental driver, interventions that protect you from UV exposure are the easiest wins. Other ways to slow or counteract extrinsic skin aging include diet, topicals, and energy-based devices.
Follow a skin-friendly nutrition plan.
There’s a growing “food is medicine” movement taking shape in the U.S. in response to what many doctors and scientists consider a nutrition crisis. That’s because diets rich in vegetables, nuts, and quality proteins play a core role in maintaining optimal health, while poor diets are associated with a variety of chronic diseases. For your skin, nutrition is also essential—though more long-term studies are needed to establish specific protocols.
Avoid excess sugarAs mentioned previously, studies have implicated sugar and the accumulation of advanced glycation end products (AGEs) in the skin with wrinkles and sagging.
Check your cooking methodsSome cooking methods also produce more AGEs than others, including grilling, frying, and roasting.
Get your vegetablesOne study found that a diet high in vegetables, legumes, and olive oil may be protective against skin wrinkling over time from the sun.
Load up on carotenoidsCarotenoids are pigments in fruits, flowers, and roots that give them their vivid colors. They’re also highly efficient antioxidants that provide plants with photoprotection. They’re critical for our skin health, too. Carotenoids are found in our skin, where they protect against ROS-induced oxidative stress and degradation of collagen and elastin. For dietary carotenoids to be absorbed intestinally, they must be released from the food matrix. Food processing and cooking help release carotenoids embedded in their food matrix and increase intestinal absorption. Because they do not need to be released from the plant matrix, carotenoid supplements are more efficiently absorbed than carotenoids in food. Learn more about the skin benefits of carotenoid here.
Use vitamin C and retinol.
One way to take care of your skin is with topicals—and the science is good on two of them in particular: vitamin C and retinol. Clinical studies have found that topical vitamin C, an antioxidant that fights reactive oxygen species, can improve wrinkles, skin texture, and appearance. Retinol is a derivative of vitamin A that’s also available widely in topical form. Studies show that retinol can increase collagen in the skin and decrease MMPs, improving skin texture and pigmentation, increasing epidermal thickness, decreasing wrinkling, and generally mitigating the impact of photoaging.
Try laser resurfacing.
Carbon dioxide laser resurfacing is a technique that uses heat from a laser to resurface photodamaged skin. It works by thickening collagen fibers and generating new collagen and fibroblasts in the period following the treatment. Several studies have shown the procedure to be effective.
Avoid UV machines or take precautions.
UV light from nail polish dryers used to cure gel manicures is harmful. Researchers looked at human and mouse skin cells and found that even one 20-minute session led to ROS generation, DNA damage, mitochondrial dysfunction, and cell death—patterns similar to skin cancer patients. While the study is cause for concern, long-term research is needed to determine if using the machines leads to an increased risk of skin cancer. In the meantime, take precautions:
- Apply broad-spectrum sunscreen SPF 30 or higher before the polish goes on, or before your hands go under the light.
- Bring gloves with a UV protective factor built in that have the ends cut off—keep in mind that the tips of your fingers will still be exposed, but that your risks are reduced.
- Consider saving gel manicures for special occasions, or else alternating between traditional polish and gel manicures throughout the year.
Protect yourself from UV
Image: UV photography reveals hidden sun damage in the form of pigmentation spots. Chemical sunscreen, which absorbs UV, appears black in this type of photography.
Most importantly: protect yourself from the sun
Enjoy the great outdoors, but limit your exposure to ultraviolet light from the sun—the biggest environmental risk factor for skin aging and skin cancer—with SPF, clothing, and breaks in the shade. To support you in your relationship with the sun, we debunk five common myths and offer some advice from Richard Granstein, M.D., an esteemed Elysium Scientific Advisory Board member since 2016 and a leader in the field of dermatology.
Myth 1: Getting a tan is safe as long as I don’t burnTanning is actually a sign of UV damage. Exposure to UV leads to adaptive melanization of the skin, otherwise known as tanning, a physiologic response that helps protect the skin against more UV damage—but not one you want to rely on for proper skin protection.
Myth 2: I’ll know if my skin is damagedSunburn may or may not be obvious, but even normal-looking skin carries mutations caused by exposure to sun. Over time, repeated exposure leads to increased mutation load and skin cancer risk. That’s why it’s always important to use sunscreen daily.
Myth 3: Windows protect against UV damageWindows block out UVB rays, not UVA—and UV rays from the sun that reach the ground are about 95% UVA, which penetrates deeply into the inner layer of skin and causes damage to DNA. Clouds don’t offer much protection against UV damage, either.
Myth 4: I only need to apply onceHigher SPF sunscreen offers better protection from UV than lower numbers, but it doesn’t impact the longevity of the protection. Sunscreen should be applied every two to three hours.
Myth 5: It’s worth the risk for vitamin DVitamin D is essential, but many variables affect how much D we make when our skin is exposed to UVB—skin color, latitude, time of year, and more. Getting 10 minutes of sun at lunchtime in the summer a few times per week will provide a sufficient amount in many parts of the U.S., but winter is a different story. The best strategy is to get a reasonable amount of sun here and there that doesn’t cause tanning or sunburn, wear sunscreen, and maintain your levels of vitamin D with a quality supplement.
Finally, Dr. Granstein suggests wearing UVR-blocking clothing.
“UVR resistance is measured in ”UPF” (ultraviolet protection factor) similar to SPF for sunscreens. Many authorities recommend a UPF of at least 30, and clothing with a UPF 50 or greater is also available. Advantages of clothing are that items do not have to be reapplied from time to time and their effectiveness is not dependent on user skill of application.
Of course, skin that is not covered by clothing should still be protected with sunscreens. Most authorities state that a lower SPF is sufficient. However, I always recommend the higher SPF [at least 50] because most users do not apply sunscreen in the manner in which the SPF is tested. In the testing laboratory, 2 mg of sunscreen per square cm of skin is applied prior to UVR exposure. This is much more than most people apply. So, I feel that by using a higher SPF product, better protection is likely obtained when people apply a suboptimal amount of sunscreen material compared to applying a recommended lower SPF sunscreen.
Another recent issue relates to the fact that it is now known that agents in chemical sunscreens can be found in the blood after skin application. The true significance of this remains unknown although some of these agents have hormone-like activities. Thus, many people now opt for using mineral sunscreens containing zinc and/or titanium, which are not absorbed. I personally generally use mineral sunscreens.”
Richard Granstein, M.D., is the George W. Hambrick, Jr. Professor and chairman of dermatology at Weill Cornell Medicine, dermatologist-in-chief at New York Presbyterian Hospital, and an Elysium Scientific Advisory Board member.