¹Windsor Clinical Research Inc., Windsor, ON, Canada
²Schulich School of Medicine and Dentistry, Western University, Windsor Campus, ON, Canada

Conflict of interest:
Jerry Tan has served as an advisor, consultant, investigator and speaker for Galderma. Maegan Miklas has no conflicts to declare.

Abstract:
Trifarotene 50 μg/g cream is a fourth generation topical retinoid with retinoic acid receptor gamma selectivity. It was recently approved by the US FDA and Health Canada for the topical treatment of facial and truncal acne for those aged 9 and older based on two identically designed phase 3 trials demonstrating superiority in lesion count reduction and global acne improvement compared to vehicle. These studies and a 1 year study also demonstrated safety and tolerability with cutaneous adverse events developing in an anticipated timeframe (1 week) for the face. These were of lesser degree and tended to develop later at the trunk. Future studies will be required to evaluate the comparative efficacy of trifarotene 50 μg/g cream against other treatments for acne.

Key Words:
acne, facial, retinoid, topical, trifarotene, truncal

Background

Topical retinoids serve as cornerstone therapy for acne with efficacy demonstrated across the spectrum of acne severity. Retinoids are classified by their common biological pathway, where the molecules themselves or their metabolites bind to a retinoid receptor: either retinoic acid receptors (RARs) or retinoid X receptors (RXRs), both of which have three subtypes: alpha, beta, and gamma.¹ Since tretinoin, subsequent generations of topical retinoids, determined by structural modifications, have sought to either increase efficacy, improve tolerability, or both.² Trifarotene (chemical name 4-[3-(3-tert-butyl-4-pyrrolidin-1-ylphenyl)-4-(2-hydroxyethoxy)phenyl]benzoic acid; C29H33NO4) is a fourth generation retinoid with higher selectivity and agonist activity for RAR gamma (RARγ), the most abundant subtype in skin.^3,4 The selectivity of trifarotene for RARγ differentiates it from the existing first- and third-generation topical retinoids, which target both RARβ and RARγ.⁴ Trifarotene is pharmacokinetically stable in keratinocytes but quickly metabolized in hepatic microsomes, indicating a favorable safety profile. In addition, it has comedolytic, anti-inflammatory, and antipigmenting properties.^4,5 In this paper, we review the efficacy, safety, and tolerability of trifarotene 50 μg/g cream, a novel topical retinoid recently approved by the US FDA and Health Canada for the topical treatment of facial and truncal acne.⁶

Clinical Trials in Acne

The efficacy, safety, and tolerability of Trifarotene 50 μg/g cream was assessed in two large identically designed randomized, double-blind, vehicle-controlled trials of 12-week duration (PERFECT 1 and PERFECT 2 ClinicalTrials.gov: NCT02566369 and NCT02556788).⁵ Subjects aged 9 years and older with moderate acne vulgaris of the face and trunk were enrolled. Evaluation of acne at the trunk was a unique feature of these trials and required appropriate delineation of truncal sites that could be amenable to self application, repeatable evaluation, and modesty as recruitment would involve males and females. A special T-shirt, with cutouts at the décolletage and upper back, was developed to outline the appropriate regions to fulfill the prior enrollment criteria.

Primary efficacy endpoints for facial acne were based on a composite of global success and absolute change in inflammatory and noninflammatory lesion counts. Secondary efficacy endpoints were for truncal acne and based on corresponding measures. Global success required achievement of clear or almost clear, and at least a 2-grade improvement from baseline of moderate or severe over the course of the 12-week studies (global grading was on a 5 category scale of none, almost clear, mild, moderate, and severe). Standard safety and tolerability assessments were undertaken.

A total of 2420 subjects were randomized 1:1 (1214 to trifarotene 50 μg/g versus 1206 to vehicle) in the two studies with a mean age of 20 years, slight predominance of females, and mainly phototypes II-III. Almost 90% of subjects were white with lesser proportions of black/African-Americans, Asians and others.

Onset of effect, such as reduction in inflammatory and noninflammatory lesions, were seen as early as week 1 for the face and week 2 for the trunk.⁵ The proportion of subjects achieving facial global success was significantly in favor of trifarotene for both studies, with a treatment difference at week 12 of 9.9% for study 1 and 16.6% for study 2 (p<0.001 for both). Reduction of facial acne lesion count was also in favor of trifarotene in inflammatory and noninflammatory lesion counts in both studies. For inflammatory counts, the difference from baseline to end of study between arms was -3.6 in study 1 and -5.5 in study 2 (p < 0.001 for both). For noninflammatory counts, the corresponding results were -7.1 and -8.5 (p < 0.001 for both).

The proportion of subjects achieving truncal global success was also significantly in favor of trifarotene for both studies with a treatment difference at week 12 of 10.7% for study 1 and 12.7% for study 2 (p<0.001 for both). Truncal acne lesion count reduction was also in favor of trifarotene in inflammatory and noninflammatory lesion counts in both studies. For inflammatory counts, the difference from baseline to end of study between arms was -2.6 in study 1 and -5.7 in study 2 (p<0.001 for both). For noninflammatory counts, the corresponding results were -4.1 and -5.1 (p<0.001 for both).

Cutaneous tolerability assessments showed greater levels of erythema, scaling, dryness, and stinging/burning compared to vehicle, which tended to peak at week 1 for the face and week 2 for the trunk. Mean levels for these parameters were mild or less for the face and trunk.

Overall, truncal mean scores for intolerability were less compared with the face. The proportion discontinuing treatment due to adverse events in the trifarotene arms was 1.5%.

In a 52-week open-label study involving 453 patients with moderate acne on the face and trunk, 13% experienced cutaneous adverse events related to trifarotene 50 μg/g cream.⁷ The majority of these adverse effects developed in the first 3 months of treatment, were mainly of mild severity and reported as itching (4.6%), irritation (4.2%), and sunburn (1.8%). Severe related adverse events occurred in three different patients and were reported as irritation, pruritus, and erythema. Local intolerability scores (related to erythema, dryness, scaling, stinging/burning) trended higher for facial compared to truncal sites of application. Maximum scores for facial involvement tended to be within the first week compared to trunk, which occurred more frequently in weeks 2-4. Overall, 2.9% of subjects discontinued due to related emergent adverse events. Global success at end of study was 65% for facial and 67% for truncal acne.

Conclusion

In two large randomized vehicle-controlled 12-week trials and in a 52-week open label study of moderate-to-severe acne at the face and trunk in subjects aged 9 years and older, trifarotene 50 μg/g cream demonstrated efficacy, safety, and cutaneous tolerability. As expected with topical retinoids, cutaneous adverse events developed with trifarotene use in an anticipated time for the face. At the trunk, these adverse reactions were of a lesser degree and tended to develop later. Future studies will be required to evaluate the comparative efficacy of this novel agent against current topical incumbents in the treatment of acne.

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¹McGovern Medical School at The University of Texas Health Sciences Center at Houston, Houston, TX, USA
²Baylor College of Medicine, Houston, TX, USA
³Katta Dermatology, Bellaire, TX, USA
⁴Rice University, Houston, TX, USA

Conflict of interest:
Rajani Katta is the author of a book for the general public on diet and dermatology and has been an advisory board member for Vichy Laboratories. Ariadna Perez Sanchez and Evelyne Tantry have no conflicts to declare for this work.

Abstract:
There is growing awareness of the complex link between nutrition and skin. In the last few decades, our understanding of this link has grown significantly with research findings from multiple laboratory, animal, and human studies. From the impact of diet on clinical features of aging skin, to documentation of the biochemical and histologic changes that occur, our understanding of this link continues to expand and evolve. In this paper, we review the research on the impact of diet on skin aging. A number of long-term observational population studies have documented that healthier diets are linked to fewer signs of skin aging. Animal and laboratory studies have elucidated the biochemical processes that play a large role in the development of these clinical findings. A number of studies have also reported on the role of specific dietary compounds in impacting these processes, whether by combating or potentiating these forces. This body of research serves as guidance in recommending nutritional strategies that can combat the skin aging forces of oxidation, inflammation, and glycation.

Key Words:
antioxidants, anti-wrinkle diet, glycation, inflammation, nutrition, oxidation, skin aging

Introduction

The clinical features of skin aging are well documented and a common question in clinical practice is whether dietary choices have any impact on these features. Based on research ranging from long-term human population to intervention studies, laboratory investigations, and animal studies, a diverse body of data links diet to skin aging.

This research provides significant guidance when discussing nutritional strategies that can promote healthy skin aging. Skin aging is particularly impacted by the processes of oxidation, inflammation and glycation. For each, dietary choices can play a large role in modifying these forces. Specifically, certain dietary patterns, foods, nutrients, and compounds have the ability to either potentiate or combat these processes.

It is well documented that certain populations differ in the rate of development of skin aging. Multiple large scale studies have reported that in those with healthier dietary patterns, fewer fine lines and wrinkles are seen,^1,2 while other population studies have documented fewer pigmentary changes³ and less skin atrophy and dryness.⁴ In one study of over 500 non-diabetic subjects, it was found that as blood glucose levels increased, perceived age increased.⁵

In researching the role of nutrition, researchers have focused on different avenues of study. Population studies, human interventional studies (both long-term and short-term), animal studies, and laboratory studies have all been used to investigate the role of dietary patterns, foods, nutrients, and/or dietary compounds. Population research now focuses on the study of dietary patterns,⁶ due to the complexity of long-term dietary effects. Human interventional studies have detailed both the beneficial and harmful effects of specific foods, nutrients, or compounds. Animal and laboratory studies have provided data on the biochemical and histologic effects of dietary compounds. Taken together, this body of research supports a strong, complex relationship between diet and skin aging. Importantly, this research identifies a number of areas where dietary modification may promote an improvement in the parameters of skin aging.

The Pathophysiology of Skin Aging

Skin aging is a highly complex process. Our current understanding of this process, while not complete, has indicated that the intricate and intertwined processes of oxidation, inflammation, and glycation play major roles. Each of these is highly impacted by diet.

Ultraviolet radiation (UVR) is the major contributor to extrinsic skin aging, and the impact of UVR on the skin has been well described. UVR is responsible for multiple direct effects on the skin, as well as numerous downstream effects. UVR may produce direct DNA damage via induction of DNA photoproducts.⁷ It also results in oxidative stress, with a resultant increase in free radical production, especially reactive oxygen species (ROS).⁸ These cause additional DNA damage⁹ as well as damage to both structural (collagen and elastin) and enzymatic proteins. Effects on lipids include peroxidation of cell membrane lipids.¹⁰

Metabolic processes, pollution, smoking, and other factors also contribute to oxidative stress. Due to constant exposure, the body’s defense mechanisms are designed to withstand the damaging effects of free radicals. Endogenous enzyme systems include superoxide dismutase, glutathione peroxidase, catalase, and others. The epidermis and dermis also contain antioxidant defenses, including vitamin C, vitamin E, carotenoids, selenium, and others.^11,12 While these are important components of the body’s endogenous defense systems, they require constant replenishment from dietary sources. and others. The epidermis and dermis also contain antioxidant defenses, including vitamin C, vitamin E, carotenoids, selenium, and others.^11,12 While these are important components of the body’s endogenous defense systems, they require constant replenishment from dietary sources.

Photooxidative stress also activates several inflammatory pathways and contributes to chronic inflammation, which impacts the clinical and molecular features of aging^13,14 as well as the promotion of skin tumorigenesis.¹⁵ Activation of these pathways ultimately acts to increase the expression of several matrix metalloproteinases (MMPs).^13,14,16

MMPs encompass a number of different enzymes, including collagenases. Along with elastases, these act to remodel the extracellular matrix (ECM), with resulting fragmentation of the collagen and elastin fibers that provide structural support and elasticity to the skin. UVR also results in the reduced expression of tissue inhibitor of MMPs (TIMPs), which ordinarily would act to inhibit ECM destruction.¹⁷

Several other inflammatory pathways are activated by oxidative stress, including pathways which promote the release of a number of inflammatory cytokines and prostaglandins. The induction of pro-inflammatory genes leads to the release of inflammatory mediators from keratinocytes, fibroblasts, white blood cells, and others, including interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-alpha. These further contribute to the effects of chronic inflammation.

Glycation is another factor that accelerates aging of the skin. Glycation is distinct from photoaging, but is closely intertwined. Glycation refers to the non-enzymatic process whereby sugar molecules covalently bond to proteins, lipids, or nucleic acids. The resulting products are known as advanced glycation end products (AGEs) or glycotoxins. AGEs are a heterogeneous group of molecules, with the prevalent AGE in the human body, including the skin, being carboxymethyl lysine (CML).

Glycation is an important factor in atherosclerosis,¹⁸ renal disease,¹⁹ diabetic complications, and other conditions. It plays an important role in skin aging as well. The accumulation of AGEs within the skin results in typical structural and functional changes that are colloquially known as sugar sag.²⁰

AGEs have a large impact on the collagen and elastin fibers that maintain the structural framework of the skin and provide resilience and elasticity. Glycation results in intermolecular collagen cross-linking, resulting in increased stiffness and vulnerability to mechanical stimuli.²¹ In addition, cross-linked collagen cannot be repaired as well. Collagen is highly susceptible to glycation, in part due to its long half-life, and may undergo up to a 50% increase in glycation over a lifetime.²² Glycation is closely related to oxidation and inflammation as well. Glycation increases reactive oxygen species (ROS), further accelerating oxidative damage. Additionally, AGEs may bind to specialized cellular surface receptors called receptor for AGEs (RAGEs). When activated, RAGE triggers several cellular signaling pathways.²³ These further promote inflammation and altered cytokine expression.

Nutritional Strategies to Target Key Processes in Skin Aging

Research has demonstrated that dietary components have the ability to impact each of these skin aging processes. The skin is commonly referred to as the largest organ of the body, and as such plays a substantial role in its defense. The skin barrier and its concomitant complex immune defenses play a significant role in protection against UVR, physical impact, temperature variations, irritants, allergens, microbes, and other factors. In fact, it can be said that our skin is under siege every minute of every day. Because of these constant threats, the skin barrier has many intricate built-in defense and repair mechanisms.

Dietary factors have the ability to either support these mechanisms or impair them. In other words, certain dietary patterns, foods, nutrients, and compounds have the potential to either accelerate or combat skin aging.

Oxidation

Antioxidants (AOs) are a key feature of the body’s defense against free radicals. They may act to neutralize ROS or may upregulate genes encoding for enzymes that neutralize ROS. The cutaneous impact of dietary AOs has been demonstrated in multiple studies. Several animal studies, for example, have documented that oral AOs including vitamin C,²⁴ vitamin E,²⁴ beta-carotene,²⁵ selenium,²⁶ and others play important roles in skin photoprotection.²⁷

Human interventional studies have documented these benefits as well. In one randomized controlled trial, daily tomato paste ingestion for 10 weeks resulted in improved minimal erythema doses,²⁸ while another study documented histologic improvement.²⁹ Other human intervention studies have reported benefits from dietary AOs including green tea polyphenols, cocoa flavanols, pomegranate, and others.³⁰ As detailed in an extensive review, the documented clinical, histologic, and biochemical benefits of dietary AOs have included reductions in erythema, DNA damage, markers of inflammation, extracellular matrix damage, and others.³⁰

While single nutrients (such as vitamins, minerals, and phytonutrients) may serve as AOs, a key point is that one food may provide multiple AOs. One research study evaluated the total AO capacity of over 3100 foods and found that the categories of “spices and herbs” and “herbal/traditional plant medicine” contained the most AO-rich products analyzed in the study.³¹ Berries, fruits, and vegetables also included many common foods and beverages with medium-to-high AO values.³¹

While dietary AOs may be beneficial, high-dose AO supplements have not shown benefit. In fact, some have demonstrated harm, as outlined in a later section.

Inflammation

Many research studies have delineated the role of diet in modifying the inflammatory process. For example, some phytochemicals may specifically interrupt the inflammatory pathway that activates nuclear factor-kappa beta (NF-KB), including turmeric, cloves, ginger, garlic, and others.³² This pathway impacts MMPs and collagen remodeling, and in fact researchers were able to demonstrate that compounds from garlic in a mouse model inhibited UVB-induced wrinkle formation. This was accomplished via the modulation of NF-KB, with a resulting decrease of MMPs and collagen fiber destruction.³³

Multiple studies have described the impact of dietary patterns, foods, nutrients, and compounds on inflammatory biomarkers. One review article³⁴ specifically examined research on dietary patterns affecting high sensitivity C-reactive protein (hsCRP), a marker of inflammation with demonstrated predictive value for coronary heart disease.³⁵ Multiple dietary patterns had some evidence of impact, including the Dietary Approaches to Stop Hypertension (DASH) and similar diets.³⁴

The effects of specific foods and nutrients were described in one summary analysis in which researchers looked at over 1900 studies. These evaluated the effects of foods and nutrients on six major biomarkers of inflammation. If a nutrient increased levels of IL-1B, IL-6, TNF-alpha, or CRP, or decreased levels of IL-4 or IL-10, it was considered pro-inflammatory.³⁶ Using these results, researchers developed a dietary inflammatory index that highlights anti-inflammatory foods. Some of the strongest effects were seen with foods including turmeric, green/black tea, ginger, garlic, and onion, as well as with macronutrients and micronutrients including fiber, magnesium, vitamin D, and omega-3 fatty acids.³⁶ Highly anti-inflammatory phytonutrients included flavones, isoflavones, beta-carotene, and flavonols.

The Gut Microbiome

The gut-skin axis is an area of intense research, due to the impact of the gut microbiome on inflammation and skin barrier function,^37-39 as well as features of skin aging.^40,41 While more research is needed to delineate these impacts, the gut microbiome is considered an important factor in inflammation. Diet serves as the foundation for healthy gut flora, particularly a focus on fiber-rich foods, which beneficially support the growth of good gut microbes.^42-44 Fermented and cultured foods, with beneficial live microbes, may also play a role,⁴⁵ while prebiotic and probiotic supplementation research is ongoing to determine potential efficacy as well as dosing strategies.

Foods that Impact MMPS

Collagenase and elastase play important roles in ECM remodeling, thereby contributing to loss of skin elasticity, wrinkling, and sagging. Some foods and nutrients are able to block the activity of collagenase, such as green tea, white tea, and pomegranate,⁴⁶ while inhibition of elastases was also seen with ginger⁴⁷ and spices such as turmeric, cinnamon, and nutmeg.⁴⁸ Foods with anti-inflammatory capabilities, by blocking inflammatory pathways, may also ultimately result in lower levels of MMPs, as with curcumin,⁴⁹ omega-3 fatty acids,⁵⁰ and garlic.³³

Glycation

The accumulation of AGEs within the body arises from two main sources. The first is via endogenous production in the presence of hyperglycemia. The second is via the ingestion of foods that contain preformed AGEs, also known as dietary AGEs.

Therefore, nutritional strategies to limit AGE-induced tissue damage focus on three main areas. The first is a focus on patterns, foods, and compounds that limit hyperglycemia. The second is a focus on foods and compounds that limit the biochemical processes of glycation. The third is limited ingestion of dietary AGEs. Additional strategies, as outlined previously, include a diet rich in antioxidants and anti-inflammatory foods, as these processes are closely intertwined with glycation.

Limiting Hyperglycemia

Improving glycemic control is a key strategy in limiting AGE production. In one experimental study, improved glycemic control in human volunteers over a 4-month period resulted in significantly decreased new collagen glycation.⁵⁰ In fact, a key tenet of an anti-wrinkle diet is diabetes prevention. A full review of dietary strategies to limit hyperglycemia is beyond the scope of this review, and readers are referred to comprehensive reviews on this subject.⁵¹

Strategies supported by research include a low glycemic load diet, which focuses on low glycemic index foods as well as portion sizes.^52,53 Food groups and components with demonstrated benefits include fiber, monounsaturated fatty acids, fruits, vegetables, and others.⁵¹ Eating order (with protein consumed earlier)⁵⁴ and vinegar consumption with a meal⁵⁵ have also demonstrated benefits. Specific foods that have shown promise include garlic, onions,⁵⁶ nuts,⁵⁷ turmeric,⁵⁸ cinnamon,⁴⁸ fenugreek,⁵⁹ and a number of other spices.⁶⁰

Foods and Compounds that Limit Glycation

A number of dietary compounds have demonstrated the ability to inhibit AGE biosynthesis.⁶¹ Some limit glycation via their antioxidant properties, while others act via other mechanisms, such as trapping reactive intermediate compounds.^61-63

In laboratory studies, anti-glycation properties have been demonstrated by foods such as cinnamon,⁶⁴ garlic,⁶⁵ rosemary,⁶⁶ yerba mate,⁶⁷ and tomato paste⁶⁸. One laboratory study evaluating multiple foods demonstrated significant anti-glycation activity by ginger, cumin, cinnamon, black pepper, and green tea.⁶⁹ Phytonutrients exhibiting beneficial effects include the flavonoids luteolin, quercetin, and rutin,⁷⁰ as well as the phenolic acids ferulic acid, chlorogenic acid, vanillic acid, and others⁷¹. In animal studies, curcumin has inhibited collagen cross-linking,⁷² while green tea extracts have reduced AGE formation⁷³ and inhibited collagen cross-linking⁷⁴.

In a laboratory study specifically evaluating the anti-glycation potential of polyphenols in herbs and spices, the most potent spices were cloves, allspice, and cinnamon, while potent herbs included sage, marjoram, tarragon, and rosemary.⁷⁵ The researchers noted that level of inhibition correlated with total phenolic content. Similar findings were seen in a study evaluating spices used in European cuisine, with strong activity by star anise, cinnamon, allspice, cloves, and oregano.⁷⁶

Strategies to Reduce Dietary AGEs

Dietary strategies to limit ingestion of preformed AGEs focus on three main areas. These include the type of food, cooking method, and use of ingredients that modify AGE production.

Meat products, high in fat and protein, contain some of the highest levels of dietary AGEs, and are particularly prone to developing new AGEs during cooking.⁷⁷ High-fat cheeses are also relatively high in AGEs. In contrast, carbohydrate-rich fruits, vegetables, and whole grains contain low levels.

Cooking methods have a marked impact on AGE production. Dry heat methods such as grilling, roasting, and frying can increase AGE levels by 10 to 100 times.⁷⁷ Reduction strategies include moist cooking methods such as steaming and boiling, as well as cooking for lower temperatures and for shorter times. It is noteworthy that even with cooking, foods such as fruits, vegetables, and whole grains remain relatively low in AGEs. The exception is for carbohydrate-rich foods that are also high in fat, such as biscuits.

An additional strategy is the use of ingredients such as lemon juice and vinegar prior to cooking, as these reduce the amount of AGEs ultimately produced.⁷⁷

The Role of Nutrient Supplementation

A common question in patient care centers on the use of dietary supplements, more specifically, given the link between dietary compounds and the biochemical processes that impact skin aging, is if there is a benefit to consuming supplementation either in addition to, or in place of, dietary consumption?

While a review of supplements is beyond the scope of this article, a few points must be emphasized. At this time, there is very limited evidence for benefit of nutrient supplementation beyond the treatment of deficiency states. Indeed, there is significant evidence of potential harm from some supplements.

The primary role of supplementation has always been, and continues to be, in the treatment of deficiency. Although research from deficient-state conditions is often used to justify supplementation in general, evidence is lacking for this approach.

As one example, biotin deficiency leading to hair loss may be improved with supplementation, but has not shown efficacy in hair loss overall.^78,79

In the case of AOs, supplements have not shown benefit and in some cases have shown harm. AO supplements were the subject of much research, given promising observational human studies of dietary intake as well as laboratory and animal studies. Unfortunately, multiple trials of high-dose (as opposed to dietary dose) vitamins C and E, beta-carotene, and selenium, indicated that they were not effective in non-melanoma skin cancer (NMSC) prevention.²⁷ In fact, some may even become pro-oxidant at high doses, as in a study of women exhibiting higher rates of skin cancer after use of a supplement containing vitamins C and E, beta-carotene, selenium, and zinc (with median follow-up of 7.5 years).⁸⁰ This emphasizes the point that nutrients must be at the right dose in order to provide benefits. In the case of AOs, the ideal dose appears to be physiologic doses, such as that supplied via whole foods.

This issue of short-term tolerability not necessarily equaling long-term safety is an important point to remember as researchers continue to study promising supplements. Nicotinamide has shown benefit in a sharply defined population, with a 23% reduction in new NMSC in those at high risk, and has been well-tolerated over a 1-year period.⁸¹ The herb Polypodium leucotomos has demonstrated photoprotective abilities in short-term studies, but also lacks long-term data.^82,83

In the case of other supplements, evidence is simply lacking. One review summarized published trials of collagen supplementation used for skin conditions ranging from aging skin, to wound healing, to cellulite.⁸⁴ In total, the authors found only 11 studies, some funded by the manufacturer and some lacking placebo, utilizing at least three different types of collagen at widely differing doses and duration.

Conclusion

A number of research studies have documented the link between diet and skin aging. These results may be used to develop dietary recommendations that combat the forces of oxidation, inflammation, and glycation. For those wishing to promote healthy skin aging, a diet that incorporates these strategies is recommended, with a focus on foods that are naturally rich in antioxidants, are anti-inflammatory, limit hyperglycemia, and inhibit glycation. When counseling patients, it is important to emphasize that a number of eating patterns focusing on these underlying principles (Table 1) may achieve this goal. Table 2 provides more details on dietary strategies that combat these aging processes.

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