A Review of the Effects of Lifestyle Factors on Skin Aging

Abstract

Skin aging reflects both intrinsic biological processes and cumulative lifestyle behaviors. While lifestyle medicine pillars are well established in cardiometabolic disease prevention, their relevance to dermatologic aging is increasingly supported by evidence. This narrative review synthesized human observational studies, randomized trials, and preclinical models examining the effects of nutrition, physical activity, psychological stress, sleep, substance use, and social connection on skin aging. Outcomes included visible aging phenotypes, barrier function, dermal structure, inflammatory signaling, oxidative stress, mitochondrial function, and cellular senescence. Plant-predominant, antioxidant-rich diets were associated with fewer wrinkles, improved hydration, and reduced atrophy. High-sugar and high-salt diets accelerated senescence and extracellular matrix damage in preclinical models. Regular exercise promoted dermal thickness, collagen synthesis, and reduced inflammatory signaling. Chronic stress and poor sleep impaired barrier recovery, reduced collagen-related gene expression, and accelerated visible aging. Tobacco, heavy alcohol, and stimulant use were strongly linked to premature aging through oxidative stress, inflammation, and microvascular injury. Social isolation was associated with elevated systemic inflammation, suggesting indirect relevance to skin aging. Lifestyle behaviors are consistently associated with skin aging physiology and appearance. Longitudinal and interventional studies are needed to clarify causality and guide dermatologic practice.

“Most studies describe associations rather than causation, but the consistency across the pillars of lifestyle medicine suggests that lifestyle-based strategies may help promote healthier, more resilient skin across the lifespan.”

Introduction

Lifestyle medicine is a specialty that focuses on evidence-based lifestyle interventions to treat and prevent chronic diseases. The pillars of lifestyle medicine include a whole-food plant-predominant diet, regular exercise, stress management, avoidance of risky substances, restorative sleep, and social connection. Although often discussed in relation to cardiovascular and metabolic disease, this framework is equally relevant to dermatology. The skin is the body’s largest organ and can function as a visible measure of overall well-being. Skin aging represents the combined effects of intrinsic biology and lifestyle-driven factors accumulated across the lifespan. This review covers the published literature on how lifestyle factors influence skin aging with a focus on the six pillars of lifestyle medicine.

The aim of this review is to review current evidence regarding the influence of modifiable lifestyle behaviors on cutaneous aging through the lens of lifestyle medicine. This review examines published human and preclinical data related to nutrition, physical activity, psychological stress, substance use, sleep, and social connection, with attention to mechanistic pathways and clinical endpoints where available. By integrating these findings, we aim to clarify the extent to which lifestyle behaviors may modify aging phenotypes and to identify areas where further investigation is needed to inform preventive and therapeutic strategies in dermatologic practice.

Nutrition, Diet, and Skin Aging

Nutrition is increasingly recognized as a factor that may influence skin aging. Early research highlighted both the challenges of defining an optimal diet for healthy skin and the need to clarify the precise role of nutrition in the aging process. ¹ More recent clinical reviews suggest that a whole-food, plant-based (WFPB) diet, also known as a whole-food, plant-predominant dietary pattern, may be associated with a more youthful appearing skin.^2,3

A WFPB dietary pattern may enhance intrinsic antioxidant defenses by providing essential vitamins, and protecting cellular integrity. ² This dietary pattern may also limit exposure to carcinogens and advanced glycation–related “gerontotoxins” that accelerate tissue injury. Emerging evidence suggests that WFPB diets may preserve telomere length.^2,3

Preclinical models provide additional insights into dietary influences on skin aging. In an 8-week rat study, high-salt intake accelerated skin aging through oxidative stress and the activation of senescence-associated pathways, including increased expression of SASP proteins. ⁴ Diets high in sugar have been shown to have similar detrimental effects by promoting advanced glycation end products (AGEs) that disrupt collagen and elastin function in a mouse model. ⁵ By contrast, phytochemical-enriched diets demonstrated protective effects; for example, long-term intake of glucoraphanin-enriched kale by mice reduced senescence scores and activated antioxidant pathways including Nrf2 and TβRII/Smad signaling. ⁶

Human studies have also examined the effects of diet on skin aging. In a randomized controlled pilot study, subjects consumed 20% of their daily energy intake from either almonds or a calorie-matched snack for 16 weeks. Researchers found that daily almond consumption improved skin lipid composition and reduced wrinkle severity, supporting the role of whole-food sources rich in antioxidants and healthy fats in skin quality. ⁷ Another study of 4025 women (40-74 years) assessed nutrient intakes and skin aging. In this study, higher linoleic acid intakes were associated with a lower likelihood of senile dryness and skin atrophy. Researchers also found that higher intakes of fat and carbohydrates increased the likelihood of a wrinkled appearance and skin atrophy. ⁸ In a separate study of 2753 elderly Danish women, a red meat and snack–dominant dietary pattern was associated with more facial wrinkles, whereas a fruit-dominant dietary pattern was associated with fewer wrinkles. ⁹

These human studies help reinforce the role of nutrition in skin health. Specifically, these studies suggest that antioxidant-rich, plant-predominant diets may be associated with reduced skin aging.^3,10 Overall, the evidence positions diet as a modifiable lifestyle factor with measurable influence on skin aging.

Exercise and Skin Aging

Physical activity refers to any bodily movement produced by skeletal muscles that results in energy expenditure and is a broad category encompassing all forms of movement. Exercise is a subcategory of physical activity defined as structured, planned movement of large skeletal muscle groups undertaken specifically to maintain or improve physical fitness. These terms are related but not interchangeable and are distinguished throughout this section. Exercise has emerged as a promising strategy to counteract skin aging. Its benefits for cardiovascular, metabolic, and musculoskeletal health are well established, and accumulating evidence shows that exercise may also improve dermal structure, mitochondrial function, and skin barrier integrity.^11-14 This growing body of work positions exercise as a lifestyle intervention that may have direct dermatologic benefits.

One mouse study examined whether an exercise-regulated myokine, CXCL10, helps control collagen production in the skin. Researchers used an in-vitro contraction model where C2C12 muscle cells were electrically stimulated to mimic exercise, collected the conditioned media, and applied it to primary mouse dermal fibroblasts. Compared with non-stimulated media, “exercise-conditioned” media significantly increased fibroblast collagen gene expression and collagen secretion. Because CXCL10 levels drop in muscle after contraction, the team tested its role and found that blocking its receptor (CXCR3) increased collagen, while adding back recombinant CXCL10 partially reversed exercise-conditioned collagen induction. They also showed that a single bout of treadmill running in mice increased skin collagen expression in vivo. Taken together, the findings suggest that exercise-induced reductions in the myokine CXCL10 may be one pathway by which exercise boosts dermal collagen synthesis. ¹¹

In another animal study, researchers examined whether exercise could slow skin aging using SAMP8 mice, which are a well-established model of accelerated aging. These mice naturally develop early skin thinning, inflammation, and collagen loss, which makes them useful for testing anti-aging interventions. In this study, age-matched SAMR1 mice served as the normal-aging control group. The SAMP8 mice were assigned to one of 3 conditions for 8 weeks. The groups were no exercise, aerobic treadmill running, or resistance ladder climbing. High IL-18 and IL-18R drive inflammation and aging, while high IL-18BP blocks IL-18 and protects the skin. Sedentary SAMP8 mice showed elevated IL-18 and IL-18R and reduced IL-18BP, which is consistent with the heightened inflammatory signaling seen in aged skin. However, both aerobic and resistance exercise lowered the inflammatory signals (IL-18 and IL-18R), reduced how strongly IL-18 and its receptor were activated and expressed in the skin, and increased the natural blocker of IL-18 (IL-18BP). Overall, these findings suggest that exercise may delay age-related skin changes in this fast-aging model by down-regulating the pro-inflammatory IL-18/IL-18R pathway. ¹²

One translational study in humans and mice studied whether endurance exercise can directly slow skin aging and the receptors at play. Researchers first compared physically active adults with sedentary age-matched controls. They found that exercisers had a thinner stratum corneum and less thinning of the stratum spinosum in older age. Exercisers also had both higher mitochondrial DNA (mtDNA) content and mitochondrial gene expression in skin and buccal cells. In a 12-week cycling program for sedentary older adults, they then showed that aerobic training reduced stratum corneum thickness, increased dermal collagen, and boosted skin mtDNA. The study also included parallel in vitro and mouse experiments demonstrating that exercise activates skeletal-muscle AMPK, which increases IL-15 release. IL-15 then boosts mitochondrial function in dermal fibroblasts, and low-dose daily IL-15 injections partially mimicked the skin-rejuvenating effects of exercise. ¹³

One 16-week randomized trial in 56 sedentary middle-aged Japanese women compared twice-weekly supervised aerobic training vs resistance training and measured cheek skin elasticity, dermal ultrasound, and ECM-related gene expression in fibroblasts cultured with participants’ plasma before and after training. Both exercise types improved skin elasticity and reduced low echogenic pixels in the upper dermis, but only resistance training increased dermal thickness and more strongly boosted ECM genes such as biglycan. Blood profiling of over 1480 circulating factors showed that resistance training lowered several inflammatory mediators (including CCL28, N,N-dimethylglycine, and CXCL4) that suppressed biglycan and other ECM genes in vitro, while CXCL8 was positively linked to biglycan expression. These results suggest that while both aerobic and resistance exercise can rejuvenate dermal structure, resistance training may be especially important for reversing age-related dermal thinning by reducing specific inflammatory signals and enhancing dermal matrix production. ¹⁴

Overall studies suggest that exercise may mitigate age-related changes in skin structure, improve vascular supply, and support dermal proteoglycan profiles central to extracellular matrix integrity.^11-14

Stress and Skin Aging

Chronic stress is increasingly recognized as a contributor to skin aging. Long-term psychological stress may accelerate aging by disrupting normal gene regulation through epigenetic changes, which can weaken the skin’s ability to repair and maintain itself. ¹⁵ This influence may extend beyond transient changes and contributes to long-term deterioration in skin resilience.

Duarte et al (2024) explain that psychological stress can directly affect the skin and speed up aging. According to this research, the skin has its own stress-response system that produces cortisol, catecholamines, neuropeptides, and other signals. When these pathways stay activated for long periods, they are linked to DNA damage, telomere shortening, weakened mitochondria, more senescent cells, inflammation, and reduced autophagy. ¹⁶ Stress hormones can also shift the skin’s microbiota. Glucocorticoids lower antimicrobial defenses, and catecholamines and Substance P can encourage certain bacteria to grow or become more aggressive. ¹⁶ Oxytocin may counter some of these effects, but its role in skin and the microbiome is still not well understood. Overall, stress-related signals appear to promote several aging processes in the skin, both by acting on skin cells themselves and by altering the skin’s microbial balance. ¹⁶

In a survey-based study, researchers examined 403 women aged 18-34 in China and Japan. They also collected data from 60 dermatologists and 60 psychologists to understand the relationship between psychological stress and early signs of skin aging. Nearly half of the young women reported mild to extremely severe stress, and those in the higher-stress group were more likely to notice features consistent with early aging. The features they noted were roughness, dullness, dryness, decreased firmness and elasticity, yellow/sallow tone, and greater skin reactivity. When asked which signs they personally associate with stress, young women most often identified dark eye circles, dull skin, and a perceived slow metabolic rate. Generally, healthcare professionals noted that stress commonly accompanies acne, dry skin, rashes, wrinkles, fluctuating skin type, sagging, poor elasticity, and rough texture. Both dermatologists and psychologists frequently recommended improving sleep, practicing meditation, increasing physical activity, taking time away from work, and reconnecting with supportive relationships as part of stress management. ¹⁷

Another clinical study examined how psychological stress affects skin-barrier function by comparing women going through marital separation with age-matched women who described themselves as “happy.” Researchers measured transepidermal water loss before and after tape stripping to assess barrier strength and recovery. They found that both groups had similar baseline barrier strength, but the high-stress group showed significantly slower barrier recovery at 3 and 24 hours. This suggests that psychological stress may delay the skin’s ability to repair itself after disruption. ¹⁸

A clinical study followed 27 medical, dental, and pharmacy students to examine how psychological stress during final exams affects skin-barrier function. Researchers measured perceived stress and then assessed barrier recovery after tape stripping at a low-stress baseline, during exam week, and again during a later low-stress period. They found that although baseline TEWL and barrier integrity were unchanged, students showed significantly slower barrier recovery at 3, 6, and 24 hours during the high-stress period. When stress levels returned to normal, barrier recovery also normalized. This suggests that psychological stress may temporarily impair the skin’s ability to repair itself. ¹⁹

A 2025 exploratory study compared women with mild and moderate chronic stress and found that the moderate-stress group had lower antioxidant capacity, higher TEWL, and noticeably rougher skin with more fine lines. In lab experiments, cortisol and epinephrine caused DNA damage, reduced collagen-related and hyaluronic-acid genes, and slowed wound healing. Cortisol also reduced filaggrin and loricrin in reconstructed epidermis, showing that chronic stress hormones can weaken the skin barrier and accelerate visible aging. ²⁰

Taken together, the evidence across these studies indicates that chronic psychological stress exerts a measurable and consistent impact on skin aging. Stress-related hormonal and neurochemical signals impair barrier repair, reduce antioxidant capacity, suppress collagen-related and hyaluronic acid gene expression, and promote hallmarks of cellular aging including DNA damage, senescence, and mitochondrial dysfunction. The skin’s own stress-response system amplifies these effects, and disruption of the skin microbiota further compounds barrier vulnerability. These findings highlight stress management as a clinically relevant pillar of skin health and suggest that interventions targeting chronic stress, including sleep optimization, mindfulness, physical activity, and social support, may help preserve skin resilience and slow the visible progression of cutaneous aging.

Sleep and Skin Aging

Sleep quality may also influence how the skin ages. Poor sleep can raise cortisol levels, slow repair processes, and weaken the skin barrier.

In a controlled study of 60 healthy women, participants were classified as either poor-quality sleepers (PSQI > 5; ≤5 hours of sleep) or good sleepers (PSQI ≤ 5; 7-9 hours). Skin aging was assessed using SCINEXA™, a validated clinical tool. Poor sleepers showed higher intrinsic aging scores, more transepidermal water loss, slower barrier recovery after tape stripping, and less repair of UV-induced erythema. Good sleepers recovered faster and also reported better satisfaction with their appearance. ²¹ These findings suggest that good-quality sleep may help maintain barrier function and support healthier-looking skin.

In a separate cross-sectional study of 219 healthy women aged 18-38 years, those with a regular late bedtime (>11 p.m.) showed lower skin hydration, higher transepidermal water loss and sebum, and reduced elasticity, firmness, and greater wrinkle formation compared with women who went to bed before 11 p.m. These differences occurred despite both groups averaging more than 7 hours of sleep per night. Late bedtime was also linked to reduced bacterial α-diversity and an altered microbiome, characterized by higher Pseudomonas and lower levels of Streptococcus, Neisseria, Stenotrophomonas, Acinetobacter, and Haemophilus. Together, these findings suggest that later sleep timing may negatively affect both skin physiology and microbial composition. ²² Similarly, in a prospective cohort study, 32 Korean women in their 40s were studied under a protocol of 6 nights of 8 hours of sleep followed by 6 nights of 4 hours of sleep (restricted sleep). Skin hydration, texture, gloss, elasticity, and wrinkles were evaluated. The results showed a decline in hydration after one night of sleep restriction. Additionally, texture deteriorated by day 4, with elasticity most affected. ²³

These studies suggest that restorative sleep may have protective effects on skin quality and appearance. Studies suggest that poor or insufficient sleep may impair barrier recovery and worsen both visible and perceived signs of aging. Restorative sleep may enhance reparative processes and may be important in maintaining a healthy skin barrier. These studies suggest that restorative sleep supports both objective measures of skin physiology and subjective assessments of attractiveness. Although more research is needed, incorporating healthy sleep habits (7-9 hours of quality sleep) into lifestyle-based recommendations may offer an evidence-based approach to healthy skin maintenance.^21-23

Substance Abuse and Skin Aging

Risky substances, including cigarette smoking, heavy alcohol use, and certain illicit drugs, are recognized contributors to accelerated skin aging. These exposures generate oxidative stress, promote inflammation, disrupt dermal extracellular matrix turnover, impair microvascular supply, and trigger premature cellular senescence. Evidence comes from diverse methodologies, ranging from multinational epidemiologic surveys to controlled laboratory studies, and consistently shows an association between substance use and aging-related skin changes.^24-27

Epidemiologic data consistently implicate cigarette smoking and alcohol use in accelerating facial aging. In a multinational survey of 3267 women, both smoking and heavy alcohol intake were independently associated with more severe visible signs of aging. Smoking was linked to greater severity of forehead, crow’s feet, and glabellar lines; under-eye puffiness and tear-trough hollowing; deeper nasolabial folds and oral commissures; more pronounced perioral lines; and reduced lip fullness, but not midface volume loss or visible cheek vessels. Heavy alcohol use (≥8 drinks per week) was associated with increased upper facial lines, under-eye puffiness, oral commissures, midface volume loss, and visible blood vessels. ²⁴

Another cross-sectional study of 301 adults in Brazil found that smoking, particularly heavy smoking, was strongly associated with facial wrinkling. Higher tobacco load was linked to a greater likelihood and severity of wrinkles, even after adjusting for age, sun exposure, and other confounders. ²⁵

Astarita et al (2015) show that chronic methamphetamine exposure accelerates aging biology across multiple organs. In rats that self-administered methamphetamine, the authors found higher expression of senescence and inflammatory genes (p53, p21, p16, IL-6, TNF-α). These changes were seen in several tissues, including skin samples, and were linked to reactive oxygen species and NF-κB activation. Although the study did not directly assess clinical or structural skin aging, it did study the pathways involved. These findings suggest that heavy stimulant use may accelerate systemic processes that can extend to the skin, contributing to premature aging through inflammation, oxidative stress, and senescence-related changes. ²⁶

Another study analyzed how chronic methamphetamine use affects facial appearance by measuring facial asymmetry across time. Using 2D facial images from 120 meth users and a control aging database (FERET), the authors applied established geometry- and texture-based symmetry tools, including bilateral feature analysis, a global Area Mismatch metric, and SSIM-based texture comparisons. ²⁷ Across all methods, meth users showed much greater increases in facial asymmetry with age. In the study, it was measured at about 3 to 5 times higher than people aging normally. The study links these changes to well-known effects of long-term meth use, including severe dental decay (“meth mouth”), facial swelling, dark circles, soft-tissue loss, weight loss, chronic sores, and skin picking, all of which disturb facial balance and texture. ²⁷ Overall, the findings indicate that methamphetamine accelerates age-related facial distortion, producing greater and faster changes in facial geometry and skin texture than those seen in typical aging. ²⁷

In the literature, the use of risky substances is consistently associated with signs of visible aging. Specifically, tobacco, alcohol, and methamphetamine are associated with accelerated skin aging. Possible mechanisms include increased oxidative stress, vascular and immune injury, and resulting extracellular matrix degradation.^24-27

Social Connectedness and Skin Aging

Social isolation has been identified as a predictor of mortality comparable to major factors like smoking, hypertension, and lack of physical activity. ²⁸ Although there are no studies specifically looking at the effects of social connectedness on skin aging, some studies have examined the impact of social isolation on markers of inflammation. In a cross-sectional study of 4648 older adults, researchers found a significant positive association between social isolation and elevated levels of the inflammatory biomarkers interleukin-6 (IL-6) and C-reactive protein (CRP). ²⁹ This suggests that social isolation is associated with inflammatory pathways in older adults, which may influence aging processes and overall health. Although this work highlights the health impact of isolation, dermatologic endpoints were not included, leaving a gap in understanding how these pathways specifically affect the skin.

In studies on longevity, non-smoking and social support were the most significant predictors of successful aging. ³⁰ More studies are needed to better understand the impact of social support on skin aging.

Conclusion

Across the available literature, several lifestyle factors show meaningful associations with skin aging. Smoking and heavy alcohol intake have strong and consistent links, with multiple studies reporting greater wrinkle severity, volume-related changes, and other visible signs of aging among users. These clinical findings align with mechanistic data on oxidative stress, inflammation, microvascular injury, and extracellular matrix breakdown.

Nutrition also appears influential. Plant-predominant, antioxidant-rich diets are associated with fewer wrinkles, better skin hydration, and reduced atrophy in observational studies, and clinical trials suggest benefits from whole-food sources that support intrinsic antioxidant defenses and dermal structure. Preclinical work reinforces these associations by showing that high-sugar and high-salt diets accelerate senescence pathways, whereas phytochemical-rich foods may support antioxidant and repair mechanisms.

Exercise is another protective factor. Human and animal studies suggest that regular exercise may improve dermal thickness, collagen production, mitochondrial function, and inflammatory markers. Together, these factors support healthier and more resilient skin.

Sleep and psychological stress may influence skin quality and skin aging. Poor sleep quality is associated with impaired barrier recovery and reduced elasticity. Chronic stress is linked to delayed repair, reduced collagen-related gene expression, oxidative damage, and other hallmarks of aging. These findings suggest that restorative sleep and stress management may help preserve skin function.

Although social connection has not been directly studied in dermatology, population studies show that isolation is linked to higher systemic inflammation and poorer overall health, indicating a need for dermatology-specific research.

Overall, evidence supports that lifestyle behaviors can meaningfully shape the appearance and physiology of aging skin. Most studies describe associations rather than causation, but the consistency across the pillars of lifestyle medicine suggests that lifestyle-based strategies may help promote healthier, more resilient skin across the lifespan.