Skin Aging: The Influence of Time vs. Sun Damage

It is inevitable: from the moment we are born we start to age. Aging can be chronological, the natural aging process that we as humans experience, or photo induced, aging caused by sun exposure. In this blog post we will compare the difference between the two! Photo by Rod Long on Unsplash

 

Many of us would have seen the image to the left of the 69-year-old truck driver who presented to a Dermatology clinic for skin aging concerns. This image is one of the best comparisons of chronological and photoaging, as it clearly shows the difference in skin impact between the two.  The gentleman in this image had been a truck driver for 28 years. His treating physician explained that UVA rays have the capacity to penetrate the truck window glass causing the progressed appearance of aging on the left-hand side of his face, in comparison to the chronological aging present on the right-hand side of the face 1. As you can see, the side of his face that has been exposed to long-term sun damage presents with advanced skin wrinkling, thickening, sagging and poor elasticity: these are all typical signs of sun damage! (Image: Gordon. Brieva, 2012).

 

Chronological aging happens to us all. It is a natural, slow, degenerative process within the body that is irreversible and occurs over our lifespan. Photoaging advances this process, which involves changes within the skin exclusively due to sun damage, which are superimposed over chronological aging. Consequently, for many people the ageing we experience in the skin is a mixture of both chronological and photoaging 6, 7, 8.

 

Typically, chronologically aged skin is characterised by ‘loss’, where the skin loses colour, thickness, volume and hydration. We tend to experience laxity, wrinkling and thinning skin that is dry and dehydrated. A condition called ‘xerosis’ often presents, which is extensive skin dryness that causes itching, flaking, scaling, extreme dehydration and poor wound healing. Blood vessels tend to be fragile, and bruising can occur easily. We also have reduced volume of glycosaminoglycans in the skin. These molecules (which we can just call GAGs) have the role of plumping the skin to give it volume and cushioning.  One form of GAG that you may have heard of is hyaluronic acid, which has the capacity to bind to and hold over 1000 times its own weight in water.  This makes it a crucial structure for skin hydration and volume. So with loss of this molecule, the skin becomes dehydrated with a loss of volume 3, 8, 11. Photo by Cristian Newman on Unsplash

  

In comparison, photoaging is a condition of ‘excess’ caused by UV rays penetrating the skin causing various forms of change.  Photodamage is progressive due to cumulative sun exposure; therefore, the more exposure to UV rays you have the more extensive the damage is.  People with fairer skin types tend to be more susceptible to photodamage than those with darker skin types 2, 8.

 

So what do UV rays do to the skin? They increase the production of oxidative substances. which have the capacity to cause mass-destruction in skin tissues over time by damaging the membranes of cells and attacking DNA. The surface of our skin becomes thickened and coarse with an uneven texture.  UV also damages our collagen and elastic fibres, which upon repeated exposure, damages the skin structure, as the new collagen and elastic fibres that are produced are excessive and of poor quality. This leads to sagging, drooping and loss of desirable skin volume.  You may have heard of ‘solar elastosis’ before – this is a situation where the elastic fibres in the skin are produced excessively, are thickened, fragmented and sitting in a ‘messy ball’ within the skin.  The combined effects of damage to collagen and elastic fibres creates wrinkling and fine lines, rough skin texture, and thickened or leathery skin – how depressing! 2, 3, 8 Photo by Anna Shvets from Pexels

 

The GAGs are also impacted as they become fragmented and poorly structured which does not permit them to function properly.  This alters skin volume and causes dehydration, which in turn enhances the appearance of fine lines, wrinkles and skin laxity 8, 11.

 

 

Naylor, Watson, & Sherratt (2011), p. 252

 

This image by Naylor et al. (2011) gives us a very good visual of what we have just discussed. You will see that the images through the centre represent the structure of young skin. If we compare these images with the top line, which represents chronologically aged skin, you can see that there is a loss of collagen, elastic fibres and glycosaminoglycans. When we compare the middle row to the bottom row, which represents photoaged skin, you can see that the collagen fibres are more spaced apart and rigid, the elastic fibres are unstructured and in excess, and the glycosaminoglycans are fragmented and poorly structured 8.

 

Excess sun exposure also increases the production of melanin (skin pigment). Melanin has the role of protecting the nucleus of the cell. It is produced in response to skin trauma, such as sun exposure, and it moves into the skin cells to sit like an ‘umbrella’ over the top of the nucleus to block the UV rays from damaging the DNA held within. If the DNA becomes permanently damaged, it causes skin mutations which have the capacity to form skin cancer. A lesser effect is the formation of skin pigmentation due to the excess production of melanin. This can present as freckles, mottled pigmentation and in some cases, melasma (2, 3, 9, 10). It must be noted that the formation of skin cancers are another result of photoaging. This is a very serious situation, and it is beyond the scope of this blog to discuss this in detail. For further information on skin cancer formation follow this link to the Cancer Council of Australia. , and then read this link where the Cancer Council of Australia explain how to check for signs of skin cancer. Photo by cottonbro from Pexels

 

One other impact that extensive sun damage had on the skin is damage to the superficial blood vessels. It damages the region which supplies the upper layer of the skin with blood, reducing the amount of oxygen and nutrients entering this region while also impacting cell waste removal. This reduces the capacity of the skin to function optimally and can contribute to the sallow appearance of sun damaged skin. UV rays also increase the production of new blood vessels; however, they have a fragile structure which leak fluids into the skin causing inflammation and redness. This can be known as ‘dilated capillaries’ or ‘telangiectasia’ 2, 3.

 

How can we prevent extensive photoaging in our skin? Slip, slop, slap, slide, and seek shade! Through rigorous sun protection strategies, we have the capacity to reduce the impact the sun has on our skin and consequently, how extensively we photoage. There is also a SunSmart app (which is fabulous) for Apple and Android which tells us the sun protection times each day using forecast information from the Bureau of Meteorology and live UV data from the Australian Radiation Protection and Nuclear Safety Agency.  You can check the app each day, or set an alert on your phone, to identify when you need to use sun protection measures to reduce the risk of skin cancer formation. The best news is that it is free as a public health initiative.

Of benefit to the younger generations is the banning of sunbeds in Australia, which also have the capacity to enhance the aging process in Generation X and above, while also reducing the risk of skin cancer formation 2, 3, 12.

 

Aesthetic Clinic products and treatments have the capacity to target multiple aspects of photodamage. It is beyond the scope of this blog post to discuss them all, however, here are a couple of examples.  Antioxidant products have the capacity to counteract the oxidative substances which cause so much damage to the skin. Topical Vitamin A products are also very effective as they have the ability to regulate abnormal processes within the skin that are caused by UV rays. For example, they can regulate collagen and elastin production, balance the production of melanin and improve the integrity of blood vessels. There are also multiple treatments that have the capacity to improve aged skin. As a brief indication, lasers, LED, chemical peels, micro needling, facials, microdermabrasion and antiwrinkle injections, alongside a homecare regime, all have the capacity to enhance photo and chronologically aged skins 3, 4, 5, 12.

 

Chronological and photo aging are two separate processes that occur together in most people. Chronological aging is a condition of loss, whereas photoaging is a condition of excess. The more sun exposure we experience, the more advanced the photo aging we see in our skin. The best strategy for sun protection is following the advice from the Cancer Council of Australia: Slip, slop, slap, slide, and seek shade! If you have any questions leave us a comment below!

 

Photo by Philipp Berg on Unsplash

 

 

1. Gordon, J. R. S., & Brieva, J. C. (2012). Unilateral Dermatoheliosis. New England Journal of Medicine, 366(16), 1466. DOI: 10.1056/NEJMicm1104059
2. Han, A., Chien, A. L., & Kang, S. (2014). Photoaging. Dermatologic Clinics, 32(3), 291-299. http://dx.doi.org/10.1016/j.det.2014.03.015
3. Poon, F., Kang, S., & Chien, A. L. (2014). Mechanisms and treatments of photoaging. Photodermatology, Photoimmunology and Photomedicine, 31(2), 65-74. https://doi.org/10.1111/phpp.12145
4. Petruk, G., Del Giudice, R., Rigano, M. M., & Monti, D. M. (2018). Antioxidants from plants protect against skin photoaging. Oxidative Medicine and Cellular Longevity, http://dx.doi.org/10.1155/2018/1454936
5. McDaniel, D. H., Mazur, C., Wortzman, M. S., & Nelson, D. B. (2017). Efficacy and tolerability of a double conjugated retinoid cream vs 1.0% retinol cream or 0.025% tretinoin cream in subjects with mild to severe photoaging. Journal of Cosmetic Dermatology, 16(4), 542-548. https://doi.org/10.1111/jocd.12381
6. Wu, S., Li, H., Zhang, X., & Li, Z. (2013). Optical features for chronological and photoaging skin by optical coherence tomography. Lasers in Medical Science, 28, 445-450. DOI: 10.1007/s10103-012-1069-4
7. Durai, P. C., Thappa, D. M., Kumari, R., & Malathi, M. (2012). Aging in elderly: Chronological versus photoaging. Indian Journal in Dermatology, 57(5), 343-352. 10.4103/0019-5154.100473
8. Naylor E. C., Watson, R. E. B., & Sherratt, M. J. (2011). Molecular aspects of skin ageing. Maturitas, 69(3), 249-256. doi:10.1016/j.maturitas.2011.04.011
9. Kobayashi, N., Nakagawa, A., Muramatsu, T., Yamashina, Y., Shirai, T., & Mori, T. (1998). Supranuclear melanin caps reduce ultraviolet-induced DNA damage in human epidermis. Journal of Dermatological Science, 16(S1), S98. https://doi.org/10.1016/S0923-1811(98)83586-X
10. Fajuyigbe, D., Lwin S. M., Diffey, B. L., Baker, R., Tobin, D. J., Sarkany, R. P. E., & Young, A. R. (2018). Melanin distribution in human epidermis affords localised protection against DNA photodamage and concurs with skin cancer incidence difference in extreme phototypes. The FASEB Journal, 32(7), 3700-3706. https://doi-org./10.1096/fj.201701472R
11. Papakonstantinou, E., Roth, M., & Karakiulakis, G. (2012). Hyaluronic acid: A key molecule in skin aging. Dermato Endocrinology, 4(3), 253-258. doi: 10.4161/derm.21923
12. Visscher, M. O., Pan, B. S., & Kitzmiller, W. J. (2013). Photodamage. Facial Plastic Surgery Clinics of North America, 21(1), 61-75. http://dx.doi.org/10.1016/j.fsc.2012.10.004