Veronica Di Nardo1, Farah Daaboul2, Catherine E. Amey3, and Victoria Barygina4
1 Centro Studi per la Ricerca Multidisciplinare e Rigenerativa, Università degli Studi Guglielmo Marconi, Rome, Italy
2 Institute of Dermatological and Regenerative Sciences, Florence, Italy
3 Azienda Ospedaliera San Giovanni di Dio e Ruggi D’Aragona, Salerno, Italy
4 Department of Biomedical Experimental and Clinical Sciences, University of Florence, Florence, Italy
As already seen from a nutritional standpoint, optimal skin health is dependent on multiple factors. In order for the body to efficiently deliver ingested nutrients to the skin, the internal systems need to be functioning properly and not overly burdened (e.g. via leaky gut and malabsorption, excessive inflammation and oxidative stress, toxicity, etc.).
An important component of proper skin function is the quality and quantity of macro‐ and micronutrients ingested. Excess consumption of inflammatory, carbohydrate‐rich, and nutrient‐poor foods common in the Western diet promote inflammatory cascades, and can be a contributing factor in the manifestation of skin disease .
Diet and Specific Diseases
The role of diet as a causal factor in acne has been hotly debated over the years . An endocrine driver (i.e. Western diet‐mediated mTORC1 [mammalian target of rapamycin complex 1]‐hyperactivity) now provides a scientific rationale for dietary intervention in acne, another manifestation of metabolic syndrome .
Along with other prevalent diseases such as obesity, type 2 diabetes, cancer, and neurodegenerative disease, acne has been linked to insulin resistance. A comprehensive dietary approach addresses this problem and involves (i) reducing the total energy intake , (ii) reducing hyperglycemic carbohydrates, (iii) reducing insulinotropic dairy proteins , and (iv) reducing leucine‐rich meat and dairy proteins . This four‐pronged “anti‐inflammatory” diet is an effective means to attenuate the mTORC1‐signaling pathways for those consuming a typical Western diet [1, 3].
Acne severity has also been linked to changes in the gut microbiota, therefore gut health and probiotics are important considerations . In addition, resveratrol has been proven to have bactericidal activity against Propionibacterium acnes  and green tea extract has led to significant reductions in lesions [8, 9]. Another potent functional food is pomegranate extract which is antibacterial, antilipase, antikeratinocyte proliferation, and anti‐inflammatory [8, 10]. See Table 19.1 for a listing of dietary interventions.
Table 19.1 Summary of dietary interventions cited above for skin disease.
|Acne||Atopic dermatitis||Psoriasis||Rosacea||Skin aging||Vitiligo|
(see Table 19.2)
|Low‐calorie and low‐protein diet||x|
|Elimination of skim milk and whey byproducts||x|
|Balance Omega 6:Omega 3, 1:1–2:1||x||x|
|GLA – Borage oil, Evening Primrose oil||x|
|Limit foods rich in tannins||x|
|Elimination or reduction of coffee, tea, hot drinks, tobacco, alcohol, spicy foods||x|
|Elimination or reduction of alcohol||x|
|Supplementation, folic acid, Vitamin D, antioxidants||x|
|Probiotics – Gut microbiota||x||x||x||x|
|Identify food allergens and sensitivities||x|
|Nutrients useful for gut healtha||x||x|
|Test for Vitamin D deficiency||x||x||x||x|
a Nutrients useful for gut health: bone broth, fermented foods, probiotics, prebiotics, cruciferous vegetables (ICZ).
Atopic dermatitis (AD) tends to begin in early life when the epithelial barrier surface is unable to retain moisture and protect the skin from bacteria, irritants, and allergens, leading to elevated immunoglobulin (IgE) levels and allergic skin reactions.
An altered microbiota has been documented in immune‐driven inflammatory skin disorders such as AD . Breastfeeding , pre‐ and postnatal probiotic supplementation,  as well as prebiotic supplementation  in infancy has decreased AD risk and chronicity . The lack of fermented foods in the diet, useful for maintaining gut health, appears to be another risk factor in AD development .
Supplementation of g‐linolenic acid (GLA), found in borage oil and evening primrose oil, has been shown to improve epidermal differentiation associated with essential fatty acid (FA) deficiency . Vitamin D deficiency increases the risk of sensitization to food allergens and has been associated with AD severity in infants . Foods rich in quercitin (such as onions) may be helpful in alleviating allergic reactivity and improving skin barrier function . Common AD food triggers include eggs, dairy, chocolate, peanuts, nuts, soy, wheat (possible gluten sensitivity), fish, and shellfish .
Psoriasis, an autoimmune disorder of the skin, is further exacerbated by metabolic syndrome, alcoholism , folate deficiency (with elevated homocysteine) [23, 24], and Vitamin D deficiency . Improvement of symptoms has been reported via an anti‐inflammatory diet, reduction of overall protein , weight loss, and alcohol reduction. Ingestion of the correct balance of Omega 6 to Omega 3 FAs  and supplemental folate  and vitamin D , if deficient, are necessary. The dietary intake of wheat (another proinflammatory food) should be considered , with many patients reporting improvement on a gluten‐free diet . The disease severity has also been improved with the integration of turmeric (curcumin) both orally and topically [31, 32].
Rosacea, sometimes called adult acne, is a chronic skin condition that causes persistent redness in the central region of the face. Consumption of coffee, tea, hot drinks, tobacco, alcoholic beverages, and spicy food is seen to trigger flushing and rosacea outbreaks. Studies have also demonstrated intestinal dysbiosis via the presence of small intestinal bacterial overgrowth (SIBO)  and helicobacter pylori infection  as having a potential pathogenic role in rosacea, thus making gut health a priority. The anti‐inflammatory dietary guidelines could therefore be considered in order to address inflammation via the gut–skin axis. Since skin immunity impairment may be a causal factor, testing for Vitamin D deficiency is recommended [35, 36].
Skin Aging and Photoprotection
Diet has been shown to have a correlation with skin aging. Less actinic skin damage (wrinkling) has been observed in those consuming more vegetables, legumes, olive oil, and fish, whereas more actinic damage is seen with a higher intake of meat, dairy, butter, margarine, and sugar products . In general, antioxidants are effective in reducing the free radical damage of collagen and elastin and in preventing premature aging .
Antioxidants provide photoprotection and are derived primarily through nutrition. The risk of sunburn can be decreased by ingesting foods rich in carotenoids, tocopherols, vitamin C, and Omega 3 oils at least 8–10 weeks before sun exposure [39, 40]. Pomegranate juice has also been demonstrated to protect against UVA‐ and UVB‐induced cell damage in SKU‐1064 human skin fibroblasts  making pomegranate juice extract an effective photochemoprotective agent [42, 43]. Other protective foods and supplements include Cacao extract [44, 45], astaxanthin [46, 47], resveratrol , turmeric , and green tea [50, 51]; surprisingly, one study reported significant improvement in facial wrinkles in photoaged skin by consuming 3600 mg (a small dose) of aloe vera gel for 90 days .
Vitiligo is an autoimmune disease leading to patchy skin depigmentation, with immune dysfunction and oxidative stress as the key mechanisms driving the destruction of melanocytes [53, 54]. Being linked to autoimmune thyroid disease [55, 56], it is often comorbid with celiac disease [54, 57, 58] and symptom improvement on a gluten‐free diet has been noted . An anti‐inflammatory diet rich in antioxidants with additional supplementation shows promise to help manage immunomodulatory activity [53, 60]. The inclusion of onions in the diet, containing quercetin and thiols which exert potent antioxidant activity, is also beneficial . Aggravating foods tend to be those rich in tannins such as mango, cashew, pistachio, cassava, areca nut, red chilies, cherries, raspberries, cranberries, blackberries, and tea . In a study of 5000 vitiligo cases, whereas genetic predisposition was less important, malnutrition, and junk food consumption, as well as infections and antibiotic use immediately prior to skin depigmentation, were significant factors in children , emphasizing the importance of appropriate nutrition and gut health as preventative measures in the young.
Inflammation and Functional Foods
There are many food sources rich in antioxidant constituents proven to modulate inflammation that can be incorporated into the diet. Common spices including turmeric, red pepper, cloves, ginger, cumin, anise, fennel, basil, rosemary, garlic, and pomegranate can block the NFĸB activation of inflammatory cytokines . Other well‐documented inflammation‐modulating foods, beverages, and supplements include green tea, aloe vera gel, and resveratrol. Examples of powerful carotenoid antioxidants are green leafy vegetables which contain lutein and zeaxanthin, and lycopene found in tomatoes. Cruciferous vegetables not only contain sulforaphane, but also indolocarbazole (ICZ) which boosts immune function and improves the gut microbiota balance .
Bone broth is a nutrient‐dense traditional food that promotes healthy skin, nails, and hair. Rich in minerals, proline, glycine, and glutamine, it also contains the essential nutrients required for the maintenance and repair of the intestinal mucosa , thereby nutritionally enhancing the functionality of the gut–skin axis.
Anti‐inflammatory Diet for Skin Disease
Given that there is an inflammatory component in the manifestation of skin disorders, an anti‐inflammatory dietary protocol is indicated as part of the overall nutritional consideration. Apart from addressing insulin resistance, dietary intake of FAs needs to maintain the correct Omega 6 to Omega 3 balance. The typical Western diet ranges from 10 : 1 to 20 : 1, versus a 3 : 1 to 1 : 1 healthy FA ratio found in non‐Western diets. Food and gluten sensitivity should be assessed on a patient‐by‐patient basis, with the elimination of foods proven to be problematic (e.g. gluten sensitivity and/or other food allergens). The guidelines in Table 19.2 contain a balanced mix of all essential macro‐ and micronutrients via a prevalence of nutrient‐dense foods and an abundance of vegetables and fruits, primarily with a low GI (glycemic index), and the Table 19.3 summarizes nutraceutical use cited in this chapter for each specific skin disease.
Table 19.2 Anti‐inflammatory dietary parameters.
|Caloric intake||Reduced. Elimination of highly processed carbohydrates, sugar and “junk food”|
|Vegetables and fruit||High and varied consumption, including nutrient‐dense “functional foods” and those with a lower glycemic index|
|Meat and dairy||Reduction or elimination (especially skim milk and whey products)|
|Beneficial Oils||Balance Omega 6 to Omega 3 ratio (1 : 1–2 : 1)|
|Examples of anti‐inflammatory diets||Paleo diet  (moderate or limited animal protein) Elimination of legumes, grains, dairy, sugar|
Vegan diet  (balanced plant‐based diet)
Table 19.3 Functional foods used in skin disease studies.
|Astaxanthin||Photoprotection||Skin aging [46, 49]|
Gene regulation and UVB damage
|Photoprotection, skin aging [44, 45]|
|Curcumin (Tumeric)||Antioxidant, anti‐inflammatory, anti‐proliferative, anti‐microbial||Psoriasis |
|Photoprotective||Skin aging |
|GLA (g‐linolenic acid found in borage oil and evening primrose oil)||Improvement of epidermal differentiation||Atopic dermatitis |
|Green Tea||Lesion reduction||Acne [8, 9]|
|Photoprotection, antioxidant||Skin aging [50, 51]|
|Folate||Potential protectant from ultraviolet‐induced photosensitization reactions||Psoriasis |
|Omega 6 to Omega 3 balance||Anti‐inflammatory||Psoriasis |
|Pomegranate extract||Anti‐inflammatory, antibacterial, antilipase, antikeratinocyte proliferation||Acne [8, 10]|
|Photoprotection||Skin aging [41, 43]|
|Quercitin||Anti‐inflammatory, alleviate allergic reactivity, improve skin barrier function||Atopic dermatitis |
|Resveratrol||Bactericide||Propionibacterium acne |
|Vitamin D||Skin innate immunity (immuomodulatory), anti‐inflammatory||Psoriasis [28, 35]|
|Atopic Dermatitis |
|Rosacea [35, 36]|
Nutrition and Oxidative Stress
As previously noted, the skin is a unique and complex organ of the human body. It has a shield function protecting our organism from constant environmental, mechanical, and chemical threats as well as pathogen infiltration, dehydration, and ultraviolet radiation. To allow this, a proper redox (reductive–oxidative) balance between oxidants and reductants should be maintained in the skin. The shift of redox balance to more oxidative conditions is called “oxidative stress,” and the deficiency of oxidants is defined as “reductive stress”; both states are involved in aging and numerous dermatologic pathologies . The principles of the redox system in the skin and the role of nutrition in its maintenance will be discussed below.
Formation and Role of Oxidative Species in Human Skin
The most potent oxidants in the human body are reactive oxygen species (ROS) and reactive nitrogen species (RNS) that include free radicals and non‐radical reactive molecules derived from molecular oxygen (O2). ROS and RNS are constantly produced in physiological conditions and play a crucial role in cell metabolism. Low levels of ROS act as signaling molecules of intracellular pathways in the maintenance of physiological functions including proper cellular differentiation, tissue regeneration, and adaptation to environmental changes [68, 69]. Excessive ROS/RNS production leads to the damage of proteins, lipids, and DNA with formation of stable detectable products of oxidation such as protein carbonyls and 3‐nitrotyrosine, malondialdehyde (MDA) and 4‐hydroxy‐2‐nonenal (HNE), and 8‐hydroxyguanine and 8‐nitroguanine, respectively .
In living cells O2 can be reduced by one or two electrons with the formation of, respectively, superoxide (O2•−) or hydrogen peroxide (H2O2). The main site of non‐enzymatic production of O2•− is the electron transport chain of mitochondria; whereas NADPH (nicotinamide adenine dinucleotide phosphate) oxidases, located in cellular membranes, together with xanthine oxidase and nitric oxide synthase, are the main enzymatic sources of O2•−. Two‐electron reduction of O2 is performed by a number of flavoprotein oxidases, such as glycolate oxidase and monoamine oxidase. H2O2 can be also formed by spontaneous or enzymatic dismutation of O2•−; the latter is performed by a family of superoxide dismutases (SODs) located throughout the cell. In the presence of transition metals such as iron (Fe2+) and copper (Cu2+), both O2•− and H2O2 can be further reduced to an extremely reactive hydroxyl radical (HO•). In contrast H2O2 can be enzymatically reduced to water by catalases and gluthathion peroxidases. Further, O2•− can react in almost diffusion‐limited rates with •NO (nitric oxide) synthesized by enzyme •NO synthase (NOS) resulting in formation of highly reactive damaging RNS – nitroperoxide (ONOO−) .
Finally, the most significant method of ROS formation in the skin (and eyes) is molecular oxygen activation by solar UV radiation and visible light. Two types of solar UV light reach the skin: UVA (320–400 nm, 95–98%) and UVB (290–320 nm, 2–5%) . UVB penetrates into epidermal cells, while UVA penetrates all epidermis reaching the dermis. Both UVA and UVB cause excessive ROS production in the skin which, besides direct DNA damage, lead
s to the activation of various inflammatory molecular pathways, triggering photodamage of the skin. For instance, UVR‐triggered ROS activate the activator protein‐1 (AP‐1), which through specific molecular pathways blocks a procollagen synthesis reducing collagen levels, stimulates matrix metalloproteinases (MMPs) that degrade collagen, and activates NFkB, a major activator of the inflammatory response. Resulting cytokines or interleukins production forms a positive feedback loop that stimulates the further ROS production in the skin. Finally, ROS trigger a “fibroblast collapse”  resulting in increased production of elastase by fibroblasts that degrades elastin, reducing its levels. Impressively, it is thought that up to 80–90% of skin aging is due to photoaging. Such extrinsic aging can be decelerated by avoiding the sun, applying UV‐protection creams, and by constant replenishment of skin antioxidants with diet and topical application.
Antioxidant System in Human Skin
Antioxidants, or reductants, are a group of enzymes (such as superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GTPx], thioredoxin, peroxiredoxin [PRX], glutathione transferase [GST] and others) and non‐enzymatic molecules that can reduce oxidants preventing their attack on DNA, lipids, and proteins. Nonenzymatic molecules, also called low molecular weight antioxidants (LMWAs), include endogenous (biosynthesized) and exogenous (dietary‐derived). LMWA can be lipid‐ or water‐soluble and the relation to water defines their localization in cellular membranes or in fluids (cytoplasm, blood, etc.) .
Human skin is very rich in both enzymatic and nonenzymatic antioxidants that are gradiently distributed in the skin, with the highest concentration in the epidermis with respect to dermis. Thus, the epidermis has a greater abundance of the antioxidant enzymes such as SOD, CAT, and GTPx and of biosynthesized antioxidants (glutathione and uric acid) with respect to the dermal layer.
Three unique antioxidant nodes present in human skin increase its protection from deleterious sun radiation: melanin, melatonin, and vitamin D synthesis machineries. Melanin performs the most exceptional protection of the skin from incoming UV radiation. Two forms of melanin, eumelanin and pheomelanin, are produced by melanocytes in the basal layer of the epidermis and transported by melanosomes to keratinocytes. Here melanin is positioned superficially to cell nuclei in order to protect DNA from UV radiation. Melanin, being an exceptional chromophore, absorbs UVB and UVA and to a lesser extent visible light and dissipates more than 99.9% of the absorbed UV energy as heat remaining unchanged .
In human skin, melanin competes for the absorption of UVB light with another potent chromophore, 7‐dehydrocholesterol (7‐DHC), accumulated in basal cell and spinous keratinocyte layers probably as a side‐reaction product from the cholesterol‐forming system. Keratinocytes are the only cell type known today that possess the enzymatic machinery able to synthetize vitamin D (1,25‐dihydroxyvitamin D3) from 7‐DHC under UVB radiation. It was found that over 90% of the vitamin D production in most individuals occurs due to exposure of the skin to sunlight; and less than 10% from dietary sources. Thus, whole‐body exposure to UVB radiation of the minimal erythema dose for 15–20 minutes is able to induce the production of up to 250 μg vitamin D (10 000 IU). According to Dr. Michael Holick 10 minutes of summer sun on the hands and face is sufficient to generate 10 μg of vitamin D, which is considered to be the daily requirement . Importantly, application of sunscreen with a sun protection factor (SPF) of 8 reduces production of vitamin D in skin by more than 95% . Both 7‐DHC and Vitamin D perform direct and indirect antioxidant activities. They have been shown to inhibited iron‐dependent liposomal lipid peroxidation . Vitamin D prevents human keratinocytes from the cyclobutane pyrimidine dimers (products of DNA oxidation) formation following UVB irradiation. Finally, vitamin D can regulate the rennin‐angiotensin II system and inhibit the NFkB molecular pathway leading in both cases to a reduction of ROS production .
Melatoninergic antioxidative system (MAS) comprises melatonin synthetized by keratinocytes and their metabolites, e.g. 6‐hydroxymelatonin (6‐OHM) and N1‐acetyl‐N2‐formyl‐5‐methoxykynuramine (AFMK), that are even more potent ROS scavengers than melatonin itself. At high concentrations (1 mmol) melatonin acts as a direct free‐radical scavenger and UVB light photosensitizer whereas at lower concentrations (100 nmol) it can stimulate the activity for main antioxidant enzymes: Mn‐SOD, Zn/Cu‐SOD and GTPx .
Other endogenous chromophores of the skin are able to absorb in selected spectrums. Urocanic acid, synthesized by keratinocytes, effectively absorbs in same spectral region as DNA. Uric acid, a product of xanthine oxidation by xanthine oxidase, with absorption maximum at 293 nm, is present in all skin layers and effectively absorbs UVB radiation. Hemoglobin present in the vessels of the dermis and one of its break‐down products, bilirubin, present in the whole skin, absorb visible light .
Along with the endogenous, these diet‐derived antioxidants play a crucial role for skin redox balance maintenance. Vitamin C is the most abundant hydrophilic free‐radical scavenger in the human skin  assumed from vegetables (peppers, broccoli etc.) and fruits (kiwi, berries, papaya, etc.), and to some extent from animal sources (liver, lamb brain, etc.). Aside from its direct ROS scavenging function, Vitamin C has a prominent role as a primary replenisher of vitamin E and other molecular antioxidants in the human organism. This is why great amounts of Vitamin C are needed in the skin where its concentration can vary from 6 to 63 mg VitC/100 g Wet Weight for the epidermis and from 3 to 13 mg VitC/100 g Wet Weight for the dermis . Liposoluble antioxidants such as Vitamin E, assumed with vegetable oils, nuts, and green leafy vegetables, and carotenoids (β‐carotene, lycopene, lutein, zeaxanthin, and their isomers found in yellow and red vegetables and fruits, and in egg yolk and liver) protect the cellular membrane structures from oxidative stress damage and from propagation of lipid the peroxidation chain reaction. Diverse carotenoids and polyphenols (resveratrol, genistein, silymarin, etc.) depending on their structure can absorb different bandwidths of light from UV (most flavonoids) to visible light 400–500 nm (flavonoids chalcones, most carotenoids) . Plant polyphenols assumed from vegetables, fruits, and red wine exhibit a remarkably diverse range of biophysicochemical properties that make them rather unique and intriguing natural antioxidants. Besides UV protection, polyphenols are able to scavenge directly both radical and nonradical reactive species, serving also as chain‐breaking antioxidants .
Finally, the skin, among few organs of the human body (blood [erythrocytes], eye lens, semen), has a specific transporter, which provides tissue‐specific absorption of a unique antioxidant molecule L‐ergothioneine, that due to its structure doesn’t need to be recharged (reduced) after its reductive activity. L‐ergothioneine is synthesized by fungi and mycobacteria, captured by plants, and comes to the human organism mostly from mushrooms, kidney, liver, black and red beans, and oat bran .
As with endogenous antioxidants, the concentration of diet‐derived antioxidants is much higher in the epidermis then in the dermis, reaching its maximum concentration in the most outer layer of the skin, the stratum corneum. Interestingly, some antioxidants such as uric acid, carotenoids, and tocopherol can be secreted on skin surface by sweat or/and sebaceous glands and perform the additional protection of skin from the solar radiation . It should be noted that all skin antioxidants work in synergy  thus the integration of, for example, Vitamin C, should be associated with correct nutrition that permits the assumption of other antioxidants.
The Antioxidant Diet
Although the major part of exogenous antioxidants arrives from fruits and vegetables, other foods are also essential for human diet and the relation between protein, lipid, and carbohydrate quality and oxidative stress has been a point of interest for many researchers. Controversial data exists about the association between protein quality and oxidative stress. A recent study conducted by A.M. de Carvalho et al. (2017) showed the direct association between protein and arginine from meat intake and MDA levels in a general population of San Paolo, Brazil, independently of lifestyle . Instead, the association was not significant for total protein and protein from vegetable intake. Authors proposed that the excess of arginine, which is a precursor of •NO, can stimulate the oxidative stress. The trial study of Azadbakht et al. (2007) brought different results: postmenopausal women affected by metabolic syndrome were randomly assigned to three isoenergetic DASH diets differing only by protein sources: meat for the control diet and soy nuts and soy proteins for the other two patterns . A significant reduction of MDA was observed in all groups but it was greater after consuming soya products. The authors suggested that, firstly, the DASH diet, rich in fruit, vegetables, whole grains, and low‐fat dairy products and low in saturated fat, total fat, cholesterol, refined grains, and sweets can be a dietary strategy to improve redox status; secondly, that MDA reduction after soy consumption is mediated by antioxidant phytochemical compounds and not by any difference in protein quality. Both studies can however point to a common conclusion that not only the selected nutrient, but the whole dietary pattern, can play a role in redox status amelioration.
The association between carbohydrates and oxidative stress has been poorly explored; however, the latest data indicate greater antioxidant and anti‐inflammatory properties of ancient varieties of wheat (species remained unchanged for last 100 years) with respect to modern varieties. Thus emmer, einkorn, spelt, khorasan, and other italian wheat species showed higher content of dietary antioxidants such as polyphenols and carotenoids and such minerals as Se2+, Mg2+, and Zn2+ needed for antioxidant enzymes . For simple carbohydrates a number of studies showed a possible correlation between glycemic index and lipid peroxidation (MDA and isoprostanes) levels, while glycemic load was positively associated only with MDA levels. In fact, high serum glucose levels through formation of advanced glycation proteins interfere with molecular and cellular functioning and promote the release of damaging side products, such as H2O2 .
A number of studies have evaluated that the quality and not quantity of fat can be linked to oxidative stress condition. Thus monounsaturated fatty acids (MUFA) seem to improve lipid and protein oxidation, whereas saturated fatty acids (SFA) have a negative effect on these parameters. It was hypothesized that dietary trans fatty acids (TFA) derived from industrial hydrogenation induce oxidative stress. Instead, natural TFA such as vaccenic acid didn’t show any effect on redox status .
Finally, dairy products contain a range of both lipophilic and hydrophilic antioxidants: proteins (especially casein), peptides, antioxidant enzymes (i.e. SOD, CAT, and GTPx), conjugated linoleic acid (CLA), coenzyme Q10, lactoferrin, vitamins (C, E, A, and D3), carotenoids, some minerals, and some trace elements. These antioxidants are present in varying proportions depending on the dairy product type (i.e. milks, yogurts, fermented milks, and cheeses) and processing (i.e. mechanical, thermal, and fermentative). Overall, antioxidant capacity of dairy products is close to that of grain‐based foods and vegetable or fruit juices. Among dairy products, cheeses present the highest antioxidant capacity due to their higher protein content. Interestingly, the antioxidant capacity of milk increases during digestion by up to two to five times because of released antioxidant peptides. Raw fat‐rich milks have higher antioxidant capacity than less fat‐rich milk, because of lipophilic antioxidants. Probiotic yogurts and fermented milks have higher antioxidant capacity than conventional yogurt and milk because proteolysis by probiotics releases antioxidant peptides. Among probiotics, Lactobacillus casei/acidophilus leads to the highest antioxidant capacity .