For this third post, I thought I would pass on interesting and relevant scientific news from recent meetings I attended with my wife, Dr. Sharyn Laughlin. The Annual Meeting of the Photomedicine Society and the Annual Meeting of The American Academy of Dermatology were held in March 2014.
More evidence was presented by Dr. Thomas Ruenger for the role of UVA in inducing enzymes that promote the breakdown of collagen and elastin as an important mechanism for photoaging. The findings presented also show that the effect of longwave UVA is the most pronounced and much greater than the effect of UVB. Over the past decade, there has been a volume of evidence from scientific studies that confirm the important effect that UVA has on photoaging and the induction of cellular damage, leading to all forms of skin cancer. This should come as no surprise to anyone – including those who still do not acknowledge the inherent dangers of UVB-biased sunscreens that give unbalanced protection, and allow the effects of UVA to be mostly unabated and cumulative.
|Our Skin: A Work of Art Worth Saving|
Not everything in science needs a study. Many definitive studies cannot be done in humans for ethical and practical reasons. Sometimes critical thinking, cognitive analysis, deductive reasoning – fancy terms for common sense – is all that is required. UVA penetrates to the deeper dermis where the important elements regulating genetics, immunity, and cell function reside, while UVB barely penetrates through the epidermis. UVA is ubiquitous, essentially the same at any latitude and time of day, and is 15-16 times more potent than the dose of UVB that only accounts for 5% of the UV band. It should be logical that the adverse effects of UV radiation may have more to do with UVA than UVB. Erythema or redness of the skin, the first sign of sunburn, and the eventual sunburn, is commonly believed by many people (even some physicians), to be UVB (290-320 nm) mediated skin damage, with a minor contribution from UVA-2 (320-340 nm). It is the basis of the sun protection factor (SPF) that is a label standard that indicates the degree to which a sunscreen reduces the sunburn reaction. The new labelling rules to be adopted in N. America changes the meaning of SPF to denote sunburn protection factor, a more accurate definition. It should convey to the consumer that SPF is a measure of the sunscreen’s ability to reduce or protect from sunburn but is not an adequate measure of protection to other adverse effects of the sun. The erythema-sunburn reaction and its genesis is actually more complex and is also related to UVA-1 effects.
Anyone who has had a sunburn by not applying a sunscreen on a very cloudy day has experienced a UVA sunburn. It is a deeper burn and much more painful that the usual sunburn that starts with UVB initiation. A sunscreen that completely blocks only UVB will not always prevent sunburn and over time a gradual or delayed sunburn develops to the UVA part of the sun. UVB is more efficient in causing sunburn and produces the immediate redness. UVA accounts for 95% of UV exposure and this higher absolute amount contributes to erythema. The early or mainly UVB initiated sunburn reaction, is a protective response telling you to get out the sun when the damage is early and more superficial. Continued sun exposure, even with a sunscreen of high SPF, but minimal UVA-1 protection, eventually leads to a more severe sunburn and the deeper damage that causes irreversible consequences- photoaging and the DNA changes that may lead to cancer many years down the road. SPF values > 15 can only be attained if the UV filters used are reducing transmission of UVA-2 and UVA-1, but is primarily a measure of UVB attenuation.
Industry consultants continue to push the trend arguing for high SPF sunscreens with values > 50 even approaching 100. There is a minor photometric basis for using a higher SPF. Looking at the transmission, rather than what is blocked does show that SPF 30 gives twice the protection than SPF 15, a SPF 60 twice that of SPF 30 and four times SPF 15. An SPF 15 blocks 93.3% of incident UV compared to 96.6% with SPF 30, a difference of 3.3% for doubling the concentration of filters. However, considering what gets through by counting photons of light shows that only half the amount gets through with the higher SPF. The higher SPF also compensates for the lower application amounts used by consumers in practice than the amount applied for laboratory SPF testing. There is some truth in a consumer thinking that a higher SPF allows you better protection and a SPF 30 allows you to stay out twice as long as a SPF 15. The danger is that the higher SPF will have some UVA protection but not nearly enough, if it does not contain one of the limited number of filters that give adequate UVA-1 protection. I am cynical enough to think that industry pushes high SPF sunscreens knowing that the public assumes they are better in every respect. Given a choice between a SPF 30 and a SPF 50, always select the more balanced sunscreen with better UVA-1 protection. This is easy to do in the UK or Europe. Look for Boots 4 or 5 stars in the UK or a UVA-PF to SPF ratio of > 1/3 in Europe. The more this ratio approaches 1, the better the sunscreen is for affording you balanced and proper protection. North American consumers have no such ability to use the label metrics for selection. The new rule of using a Critical Wavelength (CW) of 370 nm or greater as proof of truly broad spectrum activity, particularly the most important UVA-1 extinction, will not necessarily be valid.
The CW is a measure of the wavelength at which 90% of the area under the absorption or extinction curve occurs. This relates to broad spectrum activity as to achieve this CW of 370 nm, usually requires a significant UVA absorbance. However, the threshold of 370 nm can be attained by some sunscreens with little overall UVA-PF, particularly in the more problematic UVA-I spectrum approaching 400 nm. Sunscreens with low UVA-PF and those with moderate UVA-PF can both have the same CW of 370 nm. The shape of the extinction curve is a factor and a UVB biased sunscreen SPF 30, with inadequate or a low UVA-PF < 10 can attain the same CW of 370 nm as a sunscreen with UVA-PF of ≥ 10. One would fail the EU criteria but both would pass in the USA and Canada, under new regulations being enforced this year. My preference for adequate UVA protection is that SPF 30 values should have a UVA-PF exceeding 20 with the ratio approaching 1. More about these considerations in a later post.
The other important topics discussed at these meetings included the use of anti-inflammatory(AI) agents
or antioxidants (AO) in sunscreens, and the role for oral
photoprotection as a component of a sun protection strategy. The use of AI
ingredients will be discussed in detail in a future post. Dr. Salvador Gonzales
reviewed the present status of oral
nutrients that afford some measure of UV protection, and its use in oral
photoprotection is increasing in Europe at an annual rate of about 5%. He also
reminded us that a lifetime UV radiation exposure is attained 1/3 through
vacation, compared to 2/3 from every day or non-vacational time. This supports
our view that a balanced
sunscreen is for daily use all year round. In addition 70-80% of sunburns occur
can occur in your backyard. Dr. Mary Matsui presented evidence that certain nutrient
and botanical ingredients applied on the skin are a source of non-sunscreen photoprotection.
The list of useful agents for oral or topical photoprotection is extensive.
Some of these and other agents also may reduce skin damage from visible light
(400-770 nm) and near infrared (IRA at 770 -1400 nm), now shown to be relevant
in addition to UV in the genesis of adverse effects from sunlight. This an area
I am presently researching at CyberDERM. While developing a balanced sunscreen
that mimics the UV protection afforded by black clothing or shade, we are
identifying the single best antioxidant to add to the formula. Some of the
effects of UV and IRA on inducing immune suppression may also be reduced by oral
therapy. Longer wavelengths UVA-1 near 400 nm and visible through IRA at 400-
1400 nm, tend to produce deeper damage to the dermis. Oral antioxidants may be
more rational and efficient than topical application. The concept of skin
therapy from within via the dermal blood vessels is not new. I recall an
ad-campaign from many years ago- “have you taken your skin care today”? For
therapy to cell damage in the dermis, ingestion and delivery by the dermal
blood supply seems more logical than topical administration, which requires
absorption through the epidermis, and the agent is not always sure to reach the
deep dermis. We are also working on an antioxidant mix for oral supplementation
that best achieves all the objectives. For now it appears that taking 2 Gms. of
Vitamin C and 1200 IU of Vitamin C increases the minimal erythema dose – the visible sign of sun damage – by 20% after
1 week and 40% at 3 months (Gonzales et al). Flavonoids and the subgroups- anthocyandins,
catechins, flavonols, and isoflavones – all play important roles in modulating
and inhibiting the various adverse effects. A diet rich in blue and red
berries, red or purple grapes, 1-2 glasses of red wine/day, dark chocolate,
green and white teas, apples, broccoli, onions and scallions, kale, soybeans,
hot peppers, apricots and celery, provides Flavonoids. This diet with Vitamin C
and E as described above may be a useful adjunctive measure to using a balanced
sunscreen and sun avoidance for those at
greater risk of cancer and photodamage. These nutrients, along with ingesting
curcumin, resveratrol, and pomegranate, are already recommended for a myriad of
health benefits. Skin cancer is considered an occupational disease in some
provinces of Germany, and in Canada we need a National Occupational Strategy
for those involved in outdoor work. For these workers and anyone at higher risk
for skin cancer, a dietary approach as outlined is a complementary and
responsible self- help initiative.
|Can a diet rich in anti-oxidants protect you from the sun?|