We (the royal we) are guilty of thinking that in winter we just need to apply a little more moisturiser. Harsh weather is after all quite drying.
But consider this.
95% of ultraviolet radiation (UVR) is UVA. This is the non-burning variety and as it has a longer wavelength than UVB, it penetrates deeper into the skin. It also travels through clouds (and glass) so we are fooled into thinking we don’t need protection when it’s overcast.
And as UVA doesn’t result in sun-burn, there are no immediate signs of damage.
UVA affects the immune protective function of the skin, especially ‘Langerhans cells’. It is also linked to formation of ‘free radicals’ which are linked to DNA mutations and cancer promotion.
We do actually have some natural defences for protection including the ‘cutaneous’ barrier, vitamins and radical scavenging enzymes. And the enzymes, including catalase and superoxide dismutase, do fare better in winter as they’re heat sensitive. But sadly we have less enzymes in the skin as we get older.
UVB is less an issue in winter, especially our winters with almost constant cloud cover. Do bear in mind that the winter sun will contribute to our long term UVB exposure which is linked with Squamous Cell Carcinoma and Actinic Keratoses.
Sadly it doesn’t get easier as we do actually need some sun exposure due to our requirement for Vitamin D to prevent a variety of illnesses.
I present a common scenario relevant to many of us. Some reference is made to trial evidence with references available on request.
A Caucasian (Fitzpatrick Type 2) woman in her 40-50s presenting with moderate pigmentation and sun-damaged skin who seeks improvement of her skin's appearance alongside her regular Botox and fillers treatment.
This lady, already receiving aesthetic treatments, is recognising the aesthetic (if not health) benefits to addressing sun-damage(photodamage).
Most soft-tissue damage results from free radicals produced by Ultra-violet (UV) radiation exposure. Another contributory factor is Infrared A (770-1400nm), also responsible for generation of reactive oxygen species(ROS), induction of matrix metalloproteinase-1 (MMP-1) and hence photodamage.
This condition manifests as accelerated skin ageing with clinical signs including pigment change, lines and wrinkles, thread-veins, yellow complexion and leathery skin. Microscopically it is characterised by variable thickening in the stratum corneum, epidermal thinning, reduced glycosaminoglycan levels(resulting in dehydration of the dermis), reduction and fragmentation of elastin and collagen, and reduced basal cell division.
While the skin has integral antioxidants to suppress free radicals, this function declines with age, often overwhelmed by levels of free radicals produced during UV assault.
In the skin, lipid biomolecules are most vulnerable to free radical attack and cell membranes, being rich in polyunsaturated fatty acids (PUFAs), are readily exposed to this process called “lipid peroxidation”. A biochemical process particularly responsible for photoageing involved glycation (attachment of glucose and ascorbic acid) of proteins including collagen and elastin with formation of Advanced Glycation End Products (AGEs). These AGEs are highly reactive in cross-linking proteins, an irreversible process responsible for deep wrinkling. Surely treatments reducing UV or Infrared exposure, and their effects, will benefit treatment and prevention of photoageing?
Having wide-ranging biological effects, been vigorously investigated for the treatment of photodamage, utility at therapeutic doses unfortunately is limited by associated skin irritation.
Attempts to reduce irritation by esterifying vitamin A with fatty acids or other organic acids, such as palmitic acid to produce retinyl esters (e.g., retinyl palmitate) result in less effective products.
Alpha hydroxy acids(AHAs)
AHAs are used for many dermatologic indications. Their mechanism of action primarily involves reduced corneocyte cohesion (exfoliation) with effects including brightening through melanin loss, Glycosaminoglycan and collagen stimulation, therefore overall positive benefit on photodamaged skin.
Chemically, AHAs are both acids and alcohols, but reactions where AHAs are reacted as “alcohols” are uncommon.
A group of women with grade 3 photo-damage or higher (Glogau Scale) were treated using a novel bioengineered retinoid ester, a conjugate of AHA(as the alcohol) with a lipophilic retinoid. Canfield VISIA digital imaging and investigator evaluation found significant improvements in photo damage.
Treatment of pigmentation is no longer commonly treated using hydroquinone due to the possibility of carcinogenesis in in-vitro studies. Arbutin, although safe, has quite a mild effect. Kojic acid, though mild and fairly safe, has fallen out of favour in Japan having demonstrated to have mutagenic potential. A new tyrosinase inhibitor deoxyArbutin(dA) was shown to have slight but significant lightening properties and improvement in solar lentiges resulted.
L-ascorbic acid (AsA, vitamin C) affects collagen synthesis, has antioxidant actions and inhibits melanin production by reducing o-quinones, with melanin not being formed by tyrosinase until all AsA is oxidized. Unfortunately, AsA is quickly oxidized and is unstable in water. A solution was found through the synthesis of the more stable magnesium-L-ascorbyl-2-phosphate (VCPMG). VC-PMG is hydrolysed in skin to AsA.
VC-PMG was effective in lightening ephelides and normal skin.
Some photoprotection may result without penetration into the epidermis or the dermis, however to prevention photodamage of collagen and elastin and to effect collagen synthesis, vitamin C must penetrate the dermis.
As we age, there is increased induction of reactive oxygen species(ROS) due to altered mitochondrial physiology. CoQ10 is integral to the mitochondrial respiratory chain, its level declines with age and is also depleted by UV exposure. Supplementation for 7 days was shown to result in a significant improvement in mitochondrial function.
This isoflavone from soybeans has oestrogenic, antioxidant and anticancer properties. A study using topical treatment on patients with fitzpatrick skin type II to IV 60 minutes before UVB exposure showed a protective effect from the treatment.
Standard sunscreen plus antioxidant cocktail
A cocktail of grape seed extract, vitamin E, CoQ10 and vitamin C mixed with sunscreen(SPF30) were compared against sunscreen alone in a double-blind randomised study. Biopsy analyses showed the antioxidant cocktail offers significant protection against MMP-1 up regulation and therefore provides additional Infrared photoprotection.
It is generally accepted that gold-standard treatment and prevention of photo-damage includes daily sunscreen and night-time retinoids. Addition of cosmeceuticals including those detailed above may speed visible results. I believe the addition of antioxidants to sunscreen to be the most interesting finding particularly as it addresses the previously unknown Infrared A mediated photodamage.
And as ever, it's better and easier to prevent rather than to treat.