Blue light, is also known as high-energy visible (HEV) light and is the most energetic part of the visible light spectrum (380 - 700 nm) with wavelengths ranging from indigo or ultramarine light 420-440 nanometers, blue light 450-495 nanometers to cyan light 480 - 520 nanometers. Blue light has lower energy than ultraviolet (UV) radiation (280–400 nm) and can reach further into the dermis, up to the depth of 1 mm. [1] Sunlight is the primary natural source of blue light. Up to 50% of the damaging oxidative stress in human skin is generated in the VIS spectrum and the other 50% by UV light [2], contributing to premature ageing, ox-inflammageing and hyperpigmentation like age spots.
Blue light from electronic devices The use of electronic devices has led to increased exposure to artificial blue light sources, however the amount of blue light emitted during the conventional use of electronic devices is by far not enough to trigger harmful skin effects. If you sit in front of a monitor uninterrupted for a week at a distance from the screen of approximately 30 cm, this would be the same as the blue light intensity of spending one minute outside on a sunny day in Hamburg Germany at around midday at midsummer. If you hold a smartphone right next to the skin, the intensity does increase, but it would still take approximately 10 hours of uninterrupted use to match the effect on the skin of just one minute of sunlight. The emissions from electronic devices are barely noticeable in comparison to natural blue light directly from the sun and are, thus negligible. However, blue light or HEV light from sunlight can be harmful for skin. Dr Ludger Kolbe Chief Scientist for Photobiology and his team at Beiersdorf AG did pioneering research regarding the harmful effects of HEVIS. [3-4] I would also like to take the opportunity to debunk an important myth at the start of this article as infrared or near infrared light does not induce damaging free radicals (even in high amounts), there is no such thing "infra-ageing" as a result or IR and in fact red light photobiomodulation supports skin rejuvenation. Read more Direct effects of blue light and HEV Light on skin Blue light and HEV light can have both beneficial and detrimental effects on the skin. The most significant direct effects are mediated through their interaction with chromophores, such as flavins, porphyrins, and opsins, which can trigger the overproduction of reactive oxygen species (ROS), reactive nitrogen species (RNS). and hyperpigmentation. Reactive oxygen and nitrogen species cause DNA damage and modulate the immune response. [1] This oxidative stress can lead to: Photo-ageing: Exposure to blue light and HEV light can induce premature skin aging, causing wrinkles, fine lines, and loss of elasticity. Hyperpigmentation: Blue light and HEV light can stimulate melanin production, leading to uneven skin tone and the development of age spots or other forms of hyperpigmentation. DNA Damage: The ROS and RNS generated by blue light and HEV light can cause DNA damage, plus potentially increase the risk of skin cancer. Inflammation: The oxidative stress triggered by blue light and HEV light can cause an inflammatory response in the skin, exacerbating conditions like acne, eczema, and psoriasis. Molecular and physiological mechanisms of direct blue light effects on the skin [1]
Indirect effects of blue light and HEV Light on skin Blue light and HEV light can also have indirect effects on the skin by disrupting the body's circadian rhythms. This occurs via both the central mechanism, which involves stimulation of light-sensing receptors located in the retina, and via the peripheral mechanism, which involves direct interaction with skin cells. By disrupting the normal circadian rhythm, blue light can negatively affect the skin's natural overnight repair and regeneration processes. [1] The circadian rhythm has been shown to affect multiple cellular and physiological processes occurring in the skin:
Molecular mechanisms of indirect effects of blue light on the skin [1]
Ideal daytime & nighttime skin care regimen When considering cosmetic interventions, a strategy of daytime protection plus defense and night-time repair may be optimal. The skin's own repair mechanisms, such as base excision repair and nucleotide excision repair, attempt to mitigate blue light induced DNA damage. [12] Daytime protection plus defense Of course prevention and/or reduction of blue light exposure from sunlight is key. Reduce the time spent on electronic devices, especially before bedtime, can help minimize the disruption of circadian rhythms and the indirect effects of blue light and HEV light on the skin. Against premature ageing and hyperpigmentation an evidence based effective approach could be the daily use of tinted broadband sunscreen preferably containing Licochalcone A (the most effective anti-oxidant reducing damaging free radical activity from both UV and blue light and moreover protects against collagenase MMP-1 expression) strengthening skin's biological defense [4-5-6-7], while iron oxides in colour pigments provide physical protection against blue light (like zinc oxide and titanium dioxide). Against hyperpigmentation there are (tinted) sunscreens which on top contain the most potent human tyrosinase inhibitor found in dermatological skin care called Thiamidol® [8-9] and one of the 3 ingredients in the "new Kligman Trio" (NT) [18] and Glycyrrhetinic Acid which supports skin's DNA repair and skin pigmentation [10] and inhibits hyaluronidase activity (HYAL1). Most regular sun filters used in sunscreen don't offer any protection against blue light, however according to the website of BASF the chemical UV filters Tinosorb® A2B and Tinosorb® M can reduce the exposure to blue light. [11] Scattering and absorption of blue light [5] The penetration depth of visible light is influenced by the reflection, scattering, and absorption mediated not only by the skin’s physical barrier but also by the VL chromophores in the skin and Fitzpatrick skin or photo-type (FST). The primary VL-scatter and absorption molecules in the skin include hemoglobin, melanin, bilirubin, carotene, lipids, and other structures, including cell nuclei and filamentous proteins like keratin and collagen. Melanin and keratins are the primary VL absorbers and scatterers in the epidermis, while hemoglobin is the dominant absorber, and collagen is the major VL scatter in the dermis. Melanin's absorption spectrum ranges from 200 to 900 nm, with the peak absorption varying based on melanin moiety. This means that individuals with darker skin types, which have higher melanin content, are more prone to hyperpigmentation from blue light or VIS due to the greater absorption and scattering of VIS in their skin on top of the previously mentioned higher levels of tyrosinase–DCT complexes leading to increased melanogenesis, leading to both transient and long-lasting pigmentation [13], dependent upon the total dose and exacerbation of melasma especially in individuals with FSTs III to VI. Blue light tanning Recent data demonstrate synergistic effects between VL and UV-A on erythema and pigmentation. VL-induced pigmentation is more potent and more sustained than UVA1-induced pigmentation in darker skin tones.Typically, three mechanisms are involved in the responsive reaction of melanocytes to VL, with increased melanin content: immediate pigment darkening (IPD), persistent pigment darkening (PPD), and delayed tanning (DT). [15] Read more. VL can also exacerbate post inflammatory hyperpigmentation (study with FST IV and V). [16] Blue light therapy While the detrimental effects of blue light and HEV light on the skin have been well-documented, these wavelengths have also shown promise in the treatment of certain skin conditions. In controlled clinical settings, blue light has been used to: Treat Acne: Blue light can reduce the growth of Propionibacterium acnes, the bacteria responsible for acne, and has an anti-inflammatory effect. Manage Psoriasis and Atopic Dermatitis: Blue light has been found to have an anti-inflammatory and antiproliferative effect, making it potentially beneficial for the treatment of these chronic inflammatory skin diseases. Reduce Itch: Some studies have suggested that blue light may help alleviate the severity of itching in certain skin conditions. Vitiligo: Blue light therapy via LEDs can stimulate repigmentation in patients with vitiligo with minimal adverse events, however larger studies are needed. [17] The optimal protocols for blue light therapy are still being developed, and the long-term safety of this treatment modality requires further investigation and should not be initiated without HCP recommendation and monitoring. Overall, the research suggests that prolonged or excessive exposure to high-energy blue light, can have negative long-term effects on skin structure, function, and appearance in all phototypes. As our understanding of the individual variations in skin's response to blue light exposure deepens, the development of personalised or tailored effective solutions become increasingly more tangible. Always consult a qualified healthcare professional or dermatologist to determine what the most suitable approach is for your particular skin condition and rejuvenation goals. Take care! Anne-Marie References
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Mitochondria are the "powerhouses" or "lungs" of our cells and bioenergetic semi-autonomous organelles with their own genomes and genetic systems. [1] They are responsible for generating the energy that fuels a wide range of cellular processes in the skin, including cell signaling, pigmentation, wound healing, barrier integrity [2], metabolism and quality control. [3] Mitochondria exist in each cell of the body. Their primary role is cellular respiration; a process converting the energy in nutrients (like glucose) into a usable form of energy called ATP or Adenosine Triphosphate. Mitochondria are particularly abundant in the skin, reflecting the skin's high metabolic demand. When the functionality of mitochondria is impaired or declines, it impacts skin's vitality, health and beauty. Mitochondrial dysfunction is 1 of the 12 hallmarks of skin ageing.
The skin is particularly susceptible to mitochondrial stress due to its constant exposure to environmental insults, such as UV radiation, pollution, and other oxidative stressors. These factors can damage mitochondrial DNA, leading to increased production of reactive oxygen species (ROS) and disrupting the delicate balance of cellular processes. [4] In aged post-mitotic cells, heavily lipofuscin-loaded lysosomes perform poorly, resulting in the enhanced accumulation of defective mitochondria, which in turn produce more reactive oxygen species causing additional damage (the mitochondrial-lysosomal axis theory). [5] Optimal mitochondrial function is indispensable for sustaining the specialized functions of each cell type, like keratinocyte differentiation, fibroblast ECM production, melanocytes melanin production and distribution, immune cell surveillance, sebocytes and adipocytes. [6] Mitochondrial dysfunction is both directly and indirectly linked to chronological ageing and photo-ageing. [7] As mitochondrial function declines, the skin's ability to regenerate and repair itself is decreased. [2=1] This results in visible signs of aging, such as wrinkles, loss of elasticity, dryness, uneven pigmentation, melasma, age spots, lipomas, impaired wound healing. [2-4-5-8-9] Mitochondrial dysfunction also has been implicated in skin conditions like acne, eczema, lupus, psoriasis, vitiligo, atopic dermatitis and even skin cancer. [10] Ageing is associated with changes in mitochondrial morphology, including [6]
Good mitochondrial function or metabolism: [7]
Dysfunctional Mitochondria: [7]
Mitochondrial proteins Mitochondria contain >1,100 different proteins (MitoCoP) that often assemble into complexes and supercomplexes such as respiratory complexes and preprotein translocases. The chaperones Heat Shock Proteins HSP60-HSP10 are the most abundant mitochondrial proteins. [3] Small heat shock proteins form a chaperone system that operates in the mitochondrial intermembrane space. Depletion of small heat shock proteins leads to mitochondrial swelling and reduced respiration. [14] Mitochondrial hyperpigmentation Emerging research has shed light on the intricate relationship between mitochondrial dysfunction and the development of hyperpigmentation, a condition characterized by the overproduction and uneven distribution of melanin in the skin. One of the key mechanisms underlying this connection is the role of mitochondria in the regulation of melanogenesis, the process by which melanin is synthesized. Mitochondria are involved in the production of various cofactors and signaling molecules that are essential for the activity of tyrosinase, the rate-limiting enzyme in melanin synthesis. [15] When mitochondrial function is impaired, it can lead to an imbalance in the production and distribution of these cofactors and signaling molecules, ultimately resulting in the overproduction and uneven deposition of melanin in the skin. [15] This can manifest itself as age spots, melasma, and other forms of hyperpigmentation. The link between mitochondrial dysfunction and hyperpigmentation has been further supported by studies on genetic disorders that involve mitochondrial dysfunction, such as mitochondrial DNA depletion syndrome. In these conditions, patients often exhibit a range of pigmentary skin changes, including patchy hyper- and hypopigmentation, as well as reticular pigmentation. [16] Mitochondrial crosstalk and exosomes Mitochondria can crosstalk and move beyond cell boundaries. [17] Mitochondria-derived material might be transferred to neighboring cells in the form of cell-free mitochondria or included in extracellular vesicles [18-19]. This process supports cellular repair and contributes to vital mitochondrial functions. Besides restoring stressed cells and damaged tissues due to mitochondrial dysfunction, intercellular mitochondrial transfer also occurs under physiological and pathological conditions. [20] The transfer of active mitochondria from mesenchymal stem cells (MSCs) has been identified as a repair mechanism for rejuvenating damaged skin fibroblasts. [21] MITOCHONDRIAL SUPPORT Q10 or Coenzyme Q10 (CoQ10) Q10 is part of the mitochondrial respiration chain and essential for cellular energy production. About 95% of our cellular energy is generated with support of Q10, which is produced by the human body itself. During skin ageing, both the cellular energy production and levels of Q10 are declined. Q10 is a powerful anti-oxidant [22], thus protecting cells from oxidative stress and damage and has proven to be able to "rescue" senescent cells by decreasing elevated senescent markers like p21 levels and β-Galactosidases positive cell numbers (in-vitro). Q10 is bio-active, increasing collagen type I and elastin production. [23=8] Q10 can be supplemented via nutrition, however also via topical application and is considered an evidence based active ingredient in skin care products. Ubiquinol (reduced form) shows higher bioavailability compared to ubiquinone (oxidized form). [23] Glutathione Glutathione is formed in cell's cytoplasm from glutamic acid, cysteine and glycine. It is present in 2 forms: reduced (GSH) and oxidized (GSSG). Reduced GSH is an active anti-oxidant, while the presence of inactive GSSG is increased under oxidative stress. The ratio between GSH and GSSH is considered a measure of oxidative stress. Glutathione participates in redox reactions, acts as co-factor of many anti-oxidant enzymes and is the most important non-enzymatic anti-oxidant, essential for synthesis of proteins and DNA. Low Glutathione results in accelerated ageing and inflammatory skin diseases. Mitochondrial glutathione (mGSH) is the main line of defense for the maintenance of the appropriate mitochondrial redox environment to avoid or repair oxidative modifications leading to mitochondrial dysfunction and cell death. [24] Glutathione can be increased via supplementation via precursors cysteine or N-acetylcysteine (not recommended for pregnant women) or the reduced form of Glutathione itself, or increased via topical active ingredients like Licochalcone A. [25] Nicotinamide NR nicotinamide ribosome which is the precursor of NMN nicotinamide mononucleotide which is the precursor of NAD+ nicotinamide adenine dinucleotide all could have a protective effect on mitochondria. Nicotinamide adenine dinucleotide is present in living organisms as ions NAD+ and NADP+ and in reduced forms NADH and NADPH. NADH is a cofactor of processes inside mitochondria:
Resveratrol Although systemically Resveratrol promotes mitochondrial biogenesis. [27] Other data shows that UVA (14 J/cm(2)) along with resveratrol causes massive oxidative stress in mitochondria. As a consequence of oxidative stress, the mitochondrial membrane potential decreases which results in opening of the mitochondrial pores ultimately leading to apoptosis in human keratinocytes. [28] Red light therapy By incorporating red light therapy into your skin care routine, you can help to counteract the damaging effects of mitochondrial dysfunction and support the skin's natural renewal processes. Next to the use of sunscreens (especially when containing Licochalcone A), CoQ10, anti-oxidants and Nicotinamide, emerging treatments like mitochondrial transfer and therapies focused on improving mitochondrial quality control processes are being investigated as potential solutions for preventing and addressing mitochondrial dysfunction in the skin. As we continue to explore the 12 hallmarks of ageing skin, I am confident that we will gain valuable insights and develop breakthrough innovations that will improve skin quality, health, beauty and vitality. Always consult a qualified healthcare professional or dermatologist to determine what the most suitable approach is for your particular skin condition and rejuvenation goals. Take care! Anne-Marie References
Many people associate a tan with health, beauty and an active lifestyle. Although a moderate dose of solar radiation is indispensable for our health, unfortunately, there is no such thing as a real "healthy tan" or "healthy sun-kissed glow" as it is always a visible sign of skin damage. Tanning is a response by the skin to exposure to ultraviolet (UV) radiation (and HEV or Blue Light), either from natural sunlight or artificial sources like tanning beds which leads to photo-ageing, pigmentary disorders (like age spots or hyperpigmentation) and immunosuppression, hence skin cancer. When skin is exposed to sunlight: UV rays and high energy visible light (HEV) or also called Blue Light (the most energetic region of HEV), it produces more melanin, a pigment that darkens the skin as a (partial) protective mechanism to prevent further damage. The amount of artificial blue light emitted during the conventional use of electronic devices is not enough to trigger harmful skin effects. (Click here to read more)
MELANIN Melanin is only produced by cells called melanocytes, mostly distributed in the epidermal-dermal junction. Melanocytes contain specialized organelles called melanosomes to store and produce melanin. Melanosomes are transferred from the melanocytes to the neighboring keratinocytes, which are the most abundant cells in the epidermis. One melanin-forming melanocyte surrounded by 36 keratinocytes and a Langerhans cell is called the melano-epidermal unit. [1.2] Melanocytes use the amino acid tyrosine to produce melanin and protect epidermal keratinocytes and dermal fibroblasts from the damaging effects of solar radiation.. [13] The are two melanin pigment classes:
Differences in skin pigmentation do not result from differences in the number of melanocytes in the skin, as one might assume, but from differences in the melanogenic activity (melano-competence), the type of melanin produced in melanosomes (the ratio between eumelanin and pheomelanin differs per Fitzpatrick phototype) and the size, number and packaging of melanosomes, with melanin content of melanosomes ranging from 17.9% to 72.3%. [7] The amount of melanin is never enough for adequate photoprotection, and a "base tan" does not prevent sunburn. Particularly darker phototypes are more sensitive for the damaging effects of Blue Light. Both eumelanin and pheomelanin production are promoted by UV radiation and Blue Light and therefore sunscreens offering a combination of both UV (A + B) protection and Blue Light defense are recommended for all phototypes. TANNING PROCESS The skin's tanning process occurs in four distinct phases: [3]
ROLE OF UVA, UVB AND BLUE LIGHT One of the most important acute effects of UVR is DNA photodamage. UVA and UVB show different properties regarding their biological effects on the skin. [7] Shorter wavelengths (nm) correspond to higher energy. Infrared does not induce oxidative stress. Read more UVA radiation (320-400 nm) penetrates deeper into the skin and can induce indirect DNA damage by the generation of reactive oxygen species (ROS), leading to premature skin aging. UVA, in contrast to UVB is not filtered by window glass, is able to penetrate deeper into the skin and reach the dermis. They are present constantly, with relatively equal intensity, during all daylight hours throughout the year. It has been estimated that 50% of exposure to UVA occurs in the shade. UVA rays are less intense than UVB, but there are 30 to 50 times more of them. To produce the same erythemal response, approximately 1000 times more UVA dose is needed compared with UVB. [7] The bulbs used in tanning beds emit mostly UVA. UVB radiation (280-320 nm) is less prevalent than UVA, primarily affects the outermost layers of the skin, causing direct DNA damage (more potent than UVA) and triggers inflammatory responses that lead to increased melanin production. UVB radiation fluctuates throughout the day, are at their strongest at noon. and are more cytotoxic and mutagenic than UVA. The action spectrum for UV-induced tanning and erythema are almost identical, but UVA is more efficient in inducing tanning whereas UVB is more efficient in inducing erythema (redness). Dark skin is twice as effective compared to light skin in inhibiting UVB radiation penetration. [7] UVB helps the skin to produce Vitamin D. Blue light (400-500 nm) visible light accounts for 50% of sunlight [11] and can contribute to immediate, delayed, continuous and long-lasting pigmentation by activating melanocyte-specific photoreceptors and increasing melanin synthesis, particularly in individuals with darker (melano-competent) skin types [9], cause DNA damage [10] and generate damaging reactive oxygen species in both the epidermis and the dermis. [12] The effects may last longer than those induced by UVA and UVB radiation. Blue Light can penetrate even deeper than UVA and reach the hypodermis. Blue light therapy is used to target acne causing bacteria and inflammation, however the risks might outweigh the benefits especially in darker phototypes and it might worsen acne marks. EPIDERMIS AND DERMIS Both dermal fibroblasts and epidermal keratinocytes play a crucial role in regulating skin pigmentation and tanning response. [13 15] In comparison to epidermal tanning, dermal tanning is less visible, however more immediate. Dermal fibroblasts secrete various paracrine factors that regulate melanocyte function, survival, and melanin production. Factors like hepatocyte growth factor (HGF), nerve growth factor (NGF), stem cell factor (SCF), and basic fibroblast growth factor (bFGF) stimulate melanogenesis and pigmentation [14 15] Fibroblast senescence and altered secretory profiles in conditions like melasma contribute to abnormal pigmentation by stimulating melanogenesis. [15] Epidermal keratinocytes produce factors like α-melanocyte stimulating hormone (α-MSH) and Wnt1 that activate melanogenic pathways in melanocytes, leading to increased melanin synthesis and transfer to keratinocytes. [15 16]. Keratinocyte-derived exosomes can enhance melanin production by melanocytes. [16] Differences in autophagic activity between various keratinocytes also influences pigmentation. [15] MicroRNAs MicroRNAs are small, non-coding RNA molecules that regulate gene expression by binding to messenger RNA (mRNA) and typically suppressing protein production, for example collagen. They are classified as epigenetic modulators. Several miRNAs have been identified as differentially expressed in aged skin compared to young skin, including: - miR-383, miR-145, miR-34a (upregulated in sun-exposed aged skin) - miR-6879, miR-3648, miR-663b (downregulated in sun-exposed aged skin) [17] Enjoy the sun, however protect your (and your children's) skin from a photo-damaging tan to remain skin health and beauty. Sunless self-tanning products containing dihydroxyacetone (DHA) or Erythrulose provide a safe alternative to achieve a "sun-kissed" glow. You can use after-sun skin care which helps to rehydrate, reduce damage of "sun-stressed" skin and support it's repair. Always consult a qualified healthcare professional or dermatologist to determine what the most suitable approach is for your particular skin condition and rejuvenation goals. Take care! Anne-Marie References
In skin biology, senescence is a process by which a cell ages and permanently stops dividing but does not die. This is why they are also referred to as "zombie cells". Age-related accumulation of senescent cells is caused by of increased levels of senescence-inducing stressors and/or reduced elimination of senescent cells. Under normal physiological conditions, senescent cells play an important role maintaining cellular homeostasis and inhibiting proliferation of abnormal cells. However, over time, large numbers of zombie cells can build up in the skin and contribute to the overall reduction in skin's regenerative properties, impacting both its beauty and health.
There are 2 forms of cell senescence: Acute senescence: Senescent cells are produced in response to acute stressors to facilitate for example tissue repair, wound healing. They are cleared by our immune system. Chronic senescence: A not programmed process as response to prolonged stress or damage and these senescent cells are not cleared by our immune system, leading to the accumulation of zombie cells impacting our skin health and beauty. It has been suggested that inflammageing is mainly related to senescent cells and their associated SASP (Senescence Associated Secretory Phenotype) which increase in the body with age and contribute to inflammageing. Senescent cells cause inflammageing and inflammageing causes cell senescence. [1] Senescence can be triggered by a number of stress signals to the cell [1]:
Mechanisms of skin cell senescence:
The presence of senescent cells accelerates the ageing process due to their communication with nearby cells through various molecules: [18]
Fibroblast senescence could be the main driver of the skin ageing. [3] The increased number of senescent fibroblasts results in the production of SASPs rich in pro-inflammatory cytokines, including interleukin (IL)-1, IL-6, IL-8, IL-18, matrix metalloproteinases (MMPs), and a variety of other inflammatory chemokines [2] resulting in the breakdown of collagen, loss of elasticity and wrinkle formation. [3] Autophagy in dermal fibroblasts is essential for maintaining skin balance and managing the ageing process, particularly in response to external stressors like UV radiation and particulate matter (PM), by repairing cellular machineries. [4] Insufficient autophagy leads to an exaggerated skin inflammation triggered by inflammasome activation, resulting in accelerated ageing characteristics. When exposed to UVB (in vitro), skin cell types like fibroblasts and keratinocytes show DNA damage and increased senescence markers, such as increased SASPs. [3] Dermal fibroblasts also release insulin-like growth factor (IGF)-1, essential for epidermal cell proliferation and differentiation. [5] IGF-1 signalling in senescent fibroblasts is significantly decreased [6]. Inhibition of the IGF-1 pathway decreases collagen production in the dermis, causing epidermal thinning. Additionally, mitochondrial dysfunction and increased levels of superoxide anions prompt fibroblast ageing, thereby speeding up the skin ageing process. [5] Fibroblasts isolated from photo-aged skin produce a greater amount of pro-melanogenic growth factors. [14] Ageing-associated pigmentation has also been reported to be driven by (UVA-induced) fibroblast senescence. [15-16] Keratinocyte senescence The epidermis shows less impact of senescent keratinocytes due to their quicker turnover in comparison to fibroblasts. Senescent keratinocytes experience reduced ECM production and cell adhesions [8], along with elevated MMP expression in UV-induced senescence [9], and increased SASP levels, including pro-inflammatory cytokines. [10] Airborn particulate matter (PM2.5) can penetrate a disrupted skin barrier. PM2.5-induced ROS leads to epigenetic modification: reduced DNA methyltransferase, elevated DNA demethylase expression, p16INK4a promotor hypomethylation and therewith accelerated keratinocyte senescence. [11] Keratinocytes are the main type of cells that signal the need for melanogenesis. [12] UVR-induced DNA damage in keratinocytes activates melanogenesis. [13] Melanocyte senescence Senescent melanocytes express markers of inflammageing and dysfunctional telomeres. Senescent melanocyte SASPs induce telomere dysfunction and limit the proliferation of the surrounding cells, hence, senescent melanocytes affect and impair basal keratinocyte proliferation and contribute to epidermal atrophy. [17] STRATEGIES TO COMBAT CELL SENESCENCE PREVENTION Sunscreen: Protection against UV radiation combined with blue light defense (Licochalcone A: powerful anti-oxidant, Nrf2-Activator & increasing Glutathione + Colour pigments) and prevention + repair DNA damage (Glycyrrhetinic Acid) INTERVENTION Senotherapeutics can be classified into three development strategies: [25]
Skin care ingredients: [18]
Of course a healthy life-style and diet (consider also intermittent fasting) will support both your body & skin longevity and beauty Prevention and intervention of skin cell senescence offers a promising approach to improve skin health and beauty. Always consult a qualified healthcare professional or dermatologist to determine the most suitable approach for your particular skin condition and rejuvenation goals. Take care! Anne-Marie References
Like epigenetics and exosomes, neurocosmetics represent a revolutionary approach for skin care incorporating neuroscience principles, leveraging the skin-brain connection to improve skin health and beauty. The term itself is a fusion of the words neuroscience and cosmetics. It differs from psychodermatology which like neurocosmetics connects the interaction between mind and skin, but in a different way. Some describe it as how simple sensory stimulation can improve our overall wellbeing and call it "mood beauty", however this doesn't do it justice as neurocosmetics go beyond mood boosting skincare.
DEFINITION NEUROCOSMETICS Dermatologist Professor Laurent Misery back in 2002 described that neurocosmetics are products which are supposed to modulate the neuro-immuno-cutaneous-system (NICS) function at an epidermal level. Skin cells can produce neuromediators, which are mediators for transmission of information between skin, immune and the nervous system. All skin cells express specific receptors for neuromediators and by binding of the neuromediator to its receptor, modulation of cell properties and skin functions are induced like cell differentiation and proliferation (renewal), pigmentation, etc. Hence, keratinocytes, Langerhans cells, melanocytes, endothelial cells, fibroblasts and the other cells of the skin are modulated and controlled by the nerves and in return skin is able to modulate neuronal activity and growth. [1] SKIN-BRAIN CONNECTION In an article from the International Journal of Novel Research and Developments, the skin-brain connection was described as a psychobiological concept that highlights how emotions, stress, and neurotransmitters impact skin health. Indicating that the skin acts as a neuroimmunoendocrine organ, emphasizing its sensitivity to neural signals and stress responses. [4] CUTANEOUS NERVOUS SYSTEM The skin a sophisticated sensory organ that allows you to interact with your environment through touch and feel. It contains a complex network of nerves that send information about sensations like pressure, pain, itch and temperature from the skin through the spinal cord to the brain [9]. The dynamic interactions between the skin and the nervous system is influenced by factors like stress and inflammation, which can impact skin health and ageing. [7] Nerves in the skin: These nerves are like tiny messengers that tell your brain about what your skin is feeling: pressure, heat or pain. Types of nerve fibers: Some are thick and wrapped in a protective coating, which helps them send messages quickly. Others are thin and slow but are very good at sending messages about pain or temperature changes. [3] Sensory receptors: These receptors can tell if something is touching the skin lightly or if there's a lot of pressure. They can also sense if something is hot, cold, or causing pain. [3] Autonomic nervous system: Part of the cutaneous nervous system helps control things that happen in the skin automatically, like sweating to regulate body temperature. [8] Nerve cells: There are about 20 different types of neurons in our skin. [10] The contribution of epidermal keratinocytes to NICS [3]
CUTANEOUS NEURO-AGEING Neuro-ageing is defined as the changes in the nervous system which cause continuous neurodegeneration due to oxidative stress, neuroinflammation or impaired neuromodulation. As skin ages, Aβ-toxin (increased by oxidative stress) accumulates at the nerve endings innervating the tissue, causing disrupted cellular communication, particularly affecting fibroblasts’ ability to produce collagen and extracellular matrix. On top there is a decrease of nerve growth factor (NGF) production, important for the development and maintenance of nerve cells. Different factors can lead to a drop in NGF production, resulting in malfunctioning keratinocytes and reduced lipolytic activity of adipocytes, visibly impacting skin hydration and firmness. [6] Skin nerve fibres are significantly reduced in number following UV irradiation and in ageing skin [5] and therefore neuro-protectors or targetting neurodegeneration can reduce stress manifestations and promote healthy cellular communication for optimal skin function. [3] Although not much is known regarding skin specific or topical neuroprotectors (most research was focussed on the brain), probably potent anti-oxidants, by significantly reducing oxidative stress from UV and blue light and anti-inflammatory ingredients may inhibit skin neuro-ageing and can be neuroprotective especially when combined with sunscreen and strengthening of the skin barrier. NEUROCOSMETIC VARIETY OF ACTIONS
THE FUTURE OF NEUROCOSMETICS The neurocosmetics market is booming, with a projected value of USD 2.69 billion by 2030. [11] The future of neurocosmetics holds promise for innovative ingredients and concepts that harness new neuroscientific insights to revolutionize skin care and sunscreen formulations, to cater to both physical and emotional aspects of skin health and beauty. Take care! Anne-Marie References
Skin complaints related to visual display terminals (VDTs) such as smartphones, tablets, and computers are on the rise. Visually it's a rosacea-like dermatitis (erythema, oedema, papules or pustules), and can be accompanied by itch, pain and smarting (1). Some only have subjective symptoms and no visible skin problems.
It was thought that this skin condition might be caused by prolonged and repeated exposure to blue light emitted by electronic devices. The term "blue light" refers to the high-energy visible (HEV) light spectrum, which is present in the blue region of the visible light spectrum. As we are spending more and more time with or in front of screens from computers, tablets, or smartphones, there are increasing concerns about the harmful impact of blue light on skin. When referring to these light sources, we talk about artificial blue light. Dr Ludger Kolbe (Chief Scientist Photobiology) tested the radiation onto the skin emitted by different smartphones and tablets from various distances. Findings: the amount of blue light emitted during the conventional use of electronic devices is by far not enough to trigger harmful skin effects. If you sit in front of a monitor uninterrupted for a week at a distance from the screen of approximately 30 cm, this would be the same as the blue light intensity of spending one minute outside on a sunny day in Hamburg Germany at around midday at midsummer. If you hold a smartphone right next to the skin, the intensity does increase, but it would still take approximately 10 hours of uninterrupted use to match the effect on the skin of just one minute of sunlight as described. The emissions from electronic devices are barely noticeable in comparison to natural blue light directly from the sun and are, thus, negligible. The same does not apply for natural HEVIS, which does harm the skin. So is HEVIS from a screen is not causes screen dermatitis, what does? Overall, there is an overlap with skin complaints in buildings with ‘climate control’ problems (2), which may explain why screen dermatitis is relatively more common in atopic patients. The same authors found psychosocial conditions and high work-related stress to be indicators for developing VDT-related facial skin problems. Berg et al. (3) found that these patients frequently have sensitive skin: they are so-called ‘stingers’, reacting with stinging or itching when lactic acid (5%) (LAST-test or Lactic Acid Sting Test). In a large literature study, screen dermatitis was found to show many similarities with skin damaged by UV light or ionizing radiation (4). Ionizing radiation consisting of particles, rays with sufficient energy to cause ionization in the medium through which it passes. Examples are heat or light from the sun, microwaves from an oven, X rays from an X-ray tube and gamma rays from radioactive elements. In this large literature study, not only clinical but also immuno-histological manifestations were evaluated. Most striking was the increased number of mast cells in screen dermatitis, containing histamine. The latter is known to be released when mast cells are exposed to UV light and may be responsible for symptoms of itch, pain, oedema and erythema in screen dermatitis. Furthermore, Langerhans' cells in the epidermis were significantly decreased or virtually absent in screen dermatitis as well as in skin damaged by UV light or ionizing radiation. On the other hand, levels of some neuropeptides were determined, and although several differences were found with normal skin, no single marker was 100% able to distinguish between healthy skin and screen dermatitis (1). It is unclear whether VDTs leak electric or magnetic fields that affect our cells (4). In keeping with these findings are the conclusions of a case-referent study, stating that screen dermatitis most likely is the result of non-specific or irritant factors in subjects with sensitive skin (2). In conclusion: It is highly recommended to use SPF and protect the skin from natural HEVIS (with for example product containing Licochalcone A). However protection against artificial blue light won't likely prevent or improve screen dermatitis symptoms. Always consult your dermatologist for a proper diagnose and treatment. Take care. References:
2/23/2023 Comments Cosmetic Intolerance Syndrome
Dermatologists and pharmacy-assistants or pharmacists are regularly confronted with consumers or patients who have tired about a 100 skin care products and "react" to almost all of them. This could be seen as sensitive or hyper-sensitive skin: self-reported facial presence of different sensory perceptions including tingling, stinging, burning, tingling, pain and pruritis (itch). Sensitive skin was first described by Maibach in 1987 under the name of Cosmetic Intolerance Syndrome. Irritant contact dermatitis (ICD) is caused by the non–immune-modulated irritation of the skin by a substance, leading to skin changes. Allergic contact dermatitis (ACD) is a delayed reaction in which a foreign substance comes into contact with the skin; skin changes occur after re-exposure to the substance. Sounds dramatic, and it is. Buying products to find out that you can not use them is a waste of money, disappointing and if you don't know the cause it is utterly frustrating or problematic. Symptoms can appear local systemic, occur immediately or sometimes with a delay of several hours or days and range from mild to very severe in case of a serious allergic reaction (even life threatening anaphylaxis) and may impact quality of life and/or sleep.
An easy way to avoid wasting your money on a new product is to ask for a sample. It is the most important reason why they exist. Usually with a few applications you can tell if you like the product and your skin likes it too. To find out specifically why your skin is (hyper-)reactive it is smart to go to your dermatologist and ask him/her/they for a test and advice after doing some home-work. You can prior to the appointment make a report as detailed as possible. Checklist for the appointment for a dermatologist / allergologist should contain: symptoms with timing, affected areas (face, scalp, body), co-medication, (family) history of skin diseases (for example atopic dermatitis, psoriasis, rosacea), occupational hazards (for example hair dressers exposed to chemicals), dietary changes, stress, menstrual cycle, use of washing detergents / fabric softeners, sun exposure (photosensitivity) or environmental triggers or changes (like mega-city pollution or skiing by low temperatures or wind), wear of (tight) clothes and anything you deem relevant like recently undergone (aesthetic) treatments. Of course cross-check the INCI's or ingredient lists of the products you use if there are common ingredient(s) listed. Most common triggers in cosmetics are easy to find: latex, dyes, metals and fragrance. Some ingredients are beneficial for skin, but your skin may need slowly adjust to them, like tretinoid or retinol. Some ingredients may be beneficial for some, however not good for your skin when used on a daily base like alpha-hydroxy-acids in high concentrations. I know that many mention preservatives as a potential trigger. Some certainly can be. However my experience (about 9 years of clinical tolerability and safety tests with modern dermatological skin care) is that almost all users tolerate products containing evidence based modern preservatives really well (rarely any side effects) and benefit from them as they reduce the risk of contaminations by unwanted growth of microflora in a product. Hence, they are there for your safety. Large companies have thousands of people working in R&D every day and know what they are doing and are there to provide you with the best they can offer, based on the latest regulations, insights and science. Moreover, they would not market products risking high complaint rates or more dermatological skin care without clinical proof of good / very good tolerability (even in sensitive skin). I therefor like to challenge the negative reputation preservatives in general have. We all remember that parabens were "killed" by reputation and because companies want to produce products consumers enjoy and love, they started formulating all their products without them. Truth is that most parabens were and are very safe based on ample evidence. In this case a family of beneficial preservatives suffered significantly because of 1 or 2 bad family-members. We don't formulate with parabens or known potential allergens. A very active and skilled safety department is taking care of that. Don't completely rely on the word hypo-allergenic. It only means that the risk of a reaction to one of the ingredients is reduced and does not provide a 100% guarantee. Don't think that "everything natural" is always good for you. For example latex (a well known potential allergen) comes from nature. Click the button below for a full list of potential allergens in skin care provided by the FDA. There are preservative, fragrance and dye free options available in skin care. Although "free off" claims are frowned upon by the industry or sometimes not even legal. Usually these "minimal" products come in specific safe packaging (mostly pumps) to avoid contamination, often also protecting them from air and light to avoid oxidation of certain ingredients in the formula. There are evidence based dermo-cosmetic products which actively sooth and calm the skin with ingredients like Symsitive®, reduce related redness or inflammation with licochalcone A or cool or reduce itch with methoxy-propanediol or polidocanol or a combination. Sometimes the solution is as simple as the problem. Sensitive (hyper) reactive skin can be caused by barrier impairment, which allows irritants to penetrate the skin, sensors in the skin to be exposed and water to evaporate from the skin.....hence often confused or overlapping with dry skin as the symptoms are identical. If your skin barrier is the problem, the solution is to avoid over-exfoliation or harsh cleansing, maintain the skin's healthy pH (around 5) and use products containing ingredients supporting barrier repair like urea and/or dexpanthenol. These are considered the gold standard as written in this position paper by Prof. M. Augustin et al 2019. In my opinion all skin is "sensitive", and it should be. It is our skin's function to protect us by sensing heat, cold, touch, pressure and pain for example. However when the skin does not tolerate "normal conditions", hence is overreacting to (common) ingredients in skin care, it is telling you "something is off" and it might be Cosmetic Intolerance Syndrome. Listen to your skin. Don't forget to ask for a sample and advice from the pharmacist when buying a new product or go to your dermatologist/allergologist to get a better understanding of the problem, so they can provide a tailored solution for you. Take care 
The fibroblast is one of the most important cells involved in ageing skin. You can find it in the lower layer of the epidermis and the dermis. It has many functions, one of which is the production of key components like hyaluron (filling + hydration), collagen (strength + structure) and elastin (flexibility + stretch). It particularly has to work hard to replenish hyaluronic acid or hyaluron as this filling component only has a half-life in the skin of several hours up to a day. Good quality collagen can last 15 years and elastin up to 70 years. It is also believed to be involved in the clean-up of dysfunctional components, like for example broken elastin, which is visible photodamage-damage and called solar elastosis. Fibroblast senescence (agedness) does also increase the risk of age spots. In proper ageing skin management, the fibroblast is a key target-cell.
Many aesthetic in-office treatments like ultrasound, radio-frequency, chemical peelings, laser etc. are based on causing controlled damage to the skin provoking wound-healing. This is the base of their rejuvenating or aesthetic impact. The number of new fibroblasts (myofibroblasts) is increased during the wound-healing process. Some injectables, like for example hyaluron-fillers cause the fibroblasts at the injection site to stretch and bio-stimulate collagen production. There are specific bio-stimulating injectable treatments. The most popular ones are Sculptra®, Radiesse®, Ellanse®, and a new one which combines hyaluron-filling and bio-stimulation is HArmonyCa®. As we age the fibroblast is undergoing some changes because of intrinsic and extrinsic factors. It loses it’s production power, it flattens, loses mechanical tension and therewith the ability to interact with other cells in the skin. It is becoming “tired and deaf”. My hypothesis was that injecting large droplets of hyaluron into the dermis might cause the fibroblast to become “lazy” via a negative feedback mechanism: when something is present in abundance, the fibroblast might not be stimulated enough to work hard to replenish it. This is not yet scientifically proven. It is important to keep the fibroblast in good shape and biologically active. We can stimulate it’s biological activity with skincare containing bio-stimulators, or ingredients which activate the production of important skin components by the fibroblast. On the other side we need to protect the cell from damage. Bio-stimulating active ingredients in skincare which have shown to particularly stimulate the fibroblast* are for example:
Protection from photo-damage we can achieve with a combination of sunscreen and anti-oxidants, more specifically Licochalcone A. Licochalcone A has a proven broad ability to protect the skin from damaging free-radicals or oxidative stress from UVA, UVB and HEVIS (High Energy Visible Light) affecting keratinocytes and fibroblasts. I am not yet aware of skincare ingredients which increase the number of (new) fibroblasts, like the semi or minimal invasive in-office treatments. It’s an interesting field to explore if this is possible without injury, inflammation or irritation. However, you probably get "more bang for your buck" by starting a a skincare routine with focus on bio-stimulation and protection of the fibroblast pre- and post minimal and semi invasive aesthetic treatments. This could be something we will proof with a clinical study. Take care *in vitro 2/18/2023 Comments Skincare peri and post menopause
Our life expectance is increasing and the average age when menopause occurs didn't change much in the last decade. This is why more women will have to care for post menopause skin for a longer time. During and after menopause our skin will go through some changes and might even become problematic. In this blog post I will have a closer look into these changes.
Change During the start of menopause, also called peri-menopause, women will notice some changes to their skin. This is because estrogen levels start to decline (-35% between age 35-50) and as estrogen level decline, androgen level proportionately become more dominant. As a result, the majority of women experience drier skin. Or when the hormone levels are differently balanced they may get a more oily skin or develop acne tarda (adult acne), because the oil gland activity is increased. Another problem is that the skin's pH level will increase, which will impact skin health, barrier and microflora or microbiome. A higher pH value may result in problematic skin. Loss of biological activity Around this period the metabolic biological activity in the skin will decrease faster than in our 20s or 30s. The production of important components like hyaluronic acid (filling + hydration), collagen (strength + structure) and elastin (flexibility + stretch) by fibroblasts (a very important skin cell) isn't sufficient, while the speed of their degradation is inclining because the skin's natural resilience against damaging free radical activity is reduced and the activity of degradation enzymes, like hyaluronidase, collagenase and elastase is elevated. Therewith the presence of those important skin components is declining 30% in the first years. This leads to more advanced signs of ageing skin and an overall loss of skin quality: skin firmness, skin surface eveness, skin tone eveness and glow (Goldie, Clin Cosmet Invest Dermatol, 2021). Solution Skin ageing is a multifaceted continuous biological degenerative process, with an impact on overall skin quality, self perceived attractiveness, confidence and comfort (Quality of Life). The optimal solution should improve all 4 emergent perceptual categories or EPG's of skin quality (an important component of human attractiveness) as mentioned above. This can be achieved by supporting skin's own resilience against the inclined loss by degradation (reduce free radical and enzymatic activity) and increase skin's own biological activity, hence skin's own production of hyaluron, collagen and elastin with bio-active ingredients or bio-stimulators and inhibit human tyrosinase activity (reduce age spots). I will explain the 4 key actions below: 1. Bio-stimulators Some evidence based bio-actives we can find in skincare are:
2. Enzyme inhibitors Some ingredients in skincare which inhibit enzymatic degradation are:
3. Anti-oxidants Damaging free radical activity is increased in mature skin and ROS (Radical Oxidative Species) increase degradation of all components, enzymatic degradation and human tyrosinase activity, a powerful cocktail of anti-oxidants is a "must-have". The combination of fresh activated L-Ascorbic-Acid (primary defence with instant neutralisation of extra-cellular free radicals) and Licochalcone A (secondary defence with long-lasting intracellular stress protection is a valuable addition in any day or nighttime skincare regimen. Licochalcone A is moreover one of the most powerful anti-oxidants (if not the most powerful one) proven to reduce (deep) oxidative stress from High Energy Visible Light or HEVIS. As we know, free radicals from HEVIS damage the important skin-cell called the fibroblast and increase the risk of age spots. A product which development was initiated, supported and clinically tested by me is Eucerin's Hyaluron-Filler Vitamin C Booster. I highly recommend this product, especially after a collagen-stimulating in-office procedure. 4. Human tyrosinase inhibition A relatively new, effective and safe ingredient in skincare which was tested on inhibiting human tyrosinase is Thiamidol. Other ingredients in skincare were tested on mushrooms (Hornyak, Journal of Investigative Dermatology 2018 & Mann et al. 2018) and are not potent in reducing human tyrosinase activity. It took 10 years of pioneering research (dr Ludger Kolbe) and comparing 50.000 actives to patent and market it. In the mean time Thiamidol is loved and recommended globally by many dermatologists and evidence based with 35+ studies including >2000 participants with all Fitzpatrick phototypes. Every AM routine should at least have a skincare product with SPF of 15 or higher. An improvement of skin quality leads to an improvement of quality of life (van Geloven et al. EADV 2022). Hope this was helpful. Take care 
Vitamin C is a "must have" skin care ingredient our skin needs at any age.
One of the best researched skin care ingredients and proven to be very beneficial for skin is Vitamin C. Our skin uses Vitamin C as an anti-oxidant and the dermal fibroblasts need Vitamin C for the production of collagen. Two very good reasons to add this ingredients into your daily skincare routine whether you are twenty or eighty. Moreover, our skin depends on us for the needed supply, as our skin is not able to produce Vitamin C itself. We can either include enough Vitamin C in our diet or apply Vitamin C topically there where we need it the most. Usually this is the skin which is exposed to (sunlight) as this increases damaging free radical activity in our skin. An active form of vitamin C can reduce the free radical activity, which we call anti-oxidative effect. There are 4 things to consider when buying a skincare product containing Vitamin C:
Day or night? Some recommend to use Vitamin C during the night, as the active form of Vitamin C will oxidize in daylight. Hence, your skin can benefit from the Vitamin C longer during the night. I would recommend Vitamin C to be used during daytime (thus added to your morning routine), as we need protection from damaging free radicals the most during daytime and the oxidization of Vitamin C is actually a sign that the ingredient is doing it’s job! It’s even better to add Vitamin C both to your day & night time skincare routine. Is L-Ascorbid Acid enough? Vitamin C is counteracting free radicals from UV light. However, UV is not the only damaging light form as there is also High Energy Visible Light or abbreviated HEVIS. This penetrates even deeper into the skin where also the dermal fibroblasts reside. The dermal fibroblasts are our collagen and hyaluronic acid producing cells and a key target in an effective anti-ageing skincare strategy. Lichochalcone A (Licorice-root extract) has proven to be the most potent anti-oxidant to protect the dermal fibroblasts and neutralize free radicals from HEVIS. Moreover, Lichocalcone A increases Glutathione, which is a skin’s own anti-oxidant. Licorice-root extract is an anti-ageing hero. Summary The combination of Vitamin C and Lichocalcone A will protect our skin and dermal fibroblasts from free radical damage by UV and HEVIS and will provide superior biological cell protection in comparison to Vitamin C only. For me this is a good reason to use a product containing both ingredients as a first step after my cleansing routine in the morning. If you have sensitive eyes, I recommend to use an eye care prior, which will form a barrier to help to prevent the low pH Vitamin C product to migrate into the eye area. Afterwards you can use the other products of your skincare routine. I would like to put emphasis on using a SPF of 30 or higher during the day. This will not only help to protect your skin, but also support the anti-oxidative benefits and make them last longer. Hope this was helpful. Take care! 7/22/2018 Comments Skin care with something blue
Lately I was trying out several skin care products with a very similar smell, which I actually started to appreciate during my evening skin care routine.
Usually, an overpowering fragrance in a product puts me off, however I consider this one soothing. The (in my opinion) pleasant odour comes from an ingredient called Tanacetum Annuum or Blue Tansy (Moroccan Blue Chamomile - not to be confused with Tanacetum Vulgare) and is found as the signature ingredient in some more luxury "Blue" products like May Lindrom's beauty balm concentrate called "The Blue Cocoon", Sunday Riley's tranquility cleansing balm called "Blue Moon" (Blue Tansy Leaf oil) and her sleeping night oil called "Luna". All products are relatively "oily" and you only need the littlest amount. Blue Tansy is "calming", as it supposed to have anti-inflammatory and anti-allergenic, anti-histaminic and anti-fungal properties. Tanacetum Annuum is an essential oil with a very dark blue collar due to chamazulene. The aromatic description is sweet, warm fruity, with subtle floral, camphorous and herbaceous undertones. It's most often mixed in with other oils or ingredients to dilute it, as the recommendation is not to use concentrations above 5%. Although it has anti-inflammatory properties, some might have intolerance for it as it contains camphor, which can cause sensitivity. Therefore, I would not recommend to use multiple products containing Blue Tansy in conjunction. Pure Blue Tansy oil is not easy to get hold of, thus an expensive ingredient. If I was asked choose one product, I would pick Sunday Riley Luna sleeping night oil which also contains Retinol. Luna is easy to use and incorporate in a night time regimen, is less expensive when compared to May Lindrom's "The Blue Cocoon", very popular amongst "beauty guru's" and receives many positive reviews. Alternatively, there are other evidence based skin care ingredients with proven anti-inflammatory properties, for example Arctiin (anti-inflammageing, stimulates hyaluronic acid and collagen production) and Licochalcone (also powerful anti-oxidant). They don't have the blue colour or "calming" odour, which some may find offensive. Hope you enjoy healthy skin & take care. |
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