Some time ago, we discussed the matter of beauty in the context of life extension; in particular, we tried to dispel the belief that the motivation behind life extension might be simply vanity. The article argued that there is nothing wrong with wanting to preserve youthful looks and attempted to explain the evolutionary reasons for our perception of beauty, but it did not discuss a perhaps even more important fact: aesthetics are not the main problem of elderly looks. The main problem, as it always is with age-related decay, is a decline in health and functionality.
What do elderly people look like?
If I ask you to imagine an old person, you’re likely to imagine somebody with grey hair, slack, wrinkled skin, and weak and flaccid muscles. While these features may vary from person to person, this is an accurate enough description of anyone past the age of 70, and it generally gets worse and worse as aging progresses. Exercise might help improve your physical condition, and perhaps a good facial cream might make you look slightly younger than your chronological age, but, after a certain point, the signs of age-related decay are unmistakable and irreversible.
Whether this is an eye-pleasing look is a dubious matter that doesn’t concern us right now; what we are interested in is understanding why this look is certainly not healthy.
Skin function and skin aging
Skin is not just “skin deep”. It consists of two main layers that are further subdivided into several sublayers, and it performs a number of essential functions. Besides containing all kinds of receptors that allow you to perceive temperature, pressure, touch, vibration, pain, and even pleasure, your skin acts also as a thermal regulator and a barrier to reduce fluid loss. It is also where vitamin D is synthesized from cholesterol through sunlight exposure, and skin acts as your body’s very first line of defense against foreign threats [1].
As we age, a number of interacting processes gradually impair many of these critical functions, significantly increasing the chances of disease, injury, and infirmity. Perhaps the most striking part of this synergistic, collusive damage is that it raises our susceptibility to infectious diseases through an untimely failing of both our internal defenses and our external barricade, the skin.
Two of the hallmarks of aging are cellular senescence and the accumulation of extracellular cross-links [2]; the latter might be considered as a part of the loss of proteostasis hallmark, although there are arguments that it should be a hallmark in its own right. We have discussed cellular senescence many times, but in a nutshell, it is a response to external stress that prevents potentially aberrant cells from spreading. When a cell becomes senescent, it stops dividing, and it is normally disposed of by the immune system; however, some senescent cells manage to escape this fate, thereby accumulating throughout life. A typical feature of senescent cells is the secretion of a toxic concoction of chemicals called the senescence-associated secretory phenotype (SASP). This mixture is not only harmful to other cells, it may drive neighboring cells to become senescent themselves, including stem cells [3].
Cellular senescence is observed in all kinds of dividing tissue, so the skin, which has a rather high turnover, is a prime example of where this phenomenon occurs. In order to carry out its functions, skin tissue needs to maintain normal thickness and elasticity as well as the ability to replace lost cells. However, cellular senescence in the skin contributes to its thinning, wrinkling, and loss of elasticity [4], making it less resistant to mechanical stress and therefore more prone to breaking. Additionally, while short-lived senescent cells have been shown to promote wound healing, persistent ones impair it and contribute to the formation of chronic wounds [4-5]. The issue is further exacerbated by the fact that stem cells may also turn senescent as an effect of SASP and therefore fail to replenish skin tissue and regenerate wounds.
Extracellular crosslinks are unwanted bonds that tie together different parts of the extracellular matrix, which is a sort of cellular scaffolding. Although the research community hasn’t yet reached consensus on whether crosslinks really play a role in aging, they have previously been associated with skin stiffening, wrinkling, and loss of tissue elasticity [6-7] and might thus contribute to the impairment of skin function.
All of this means that aging causes our skin to look slack and wrinkled while also compromising its role as a protective barrier against pathogens, as wounds tend to happen more often and take a longer time to heal. If you consider that, as we age, our immune systems fail us as well, becoming less responsive to vaccination and less able to produce immune cells [8], it becomes clear that taken together, these two things are a recipe for disaster. Not only are the castle guards weak and sluggish, the walls are fragile and crumbling. Therefore, skin aging is far from being just a problem of aesthetics.
More trouble
Infections aren’t the only problem. The skin is where your vitamin D is synthesized, and apart from that, there aren’t many other sources of it. Vitamin D is notoriously hard to get from food and is mainly obtained through sun exposure. As we have noted, skin aging also implies skin thinning, which is one of the several risk factors that cause vitamin D deficiency in the elderly. Another factor is diminished sunlight exposure, arguably due to the fact that elderly people have impaired mobility and a higher risk of falling and injuries; this, in turn, is a consequence of the gradual loss of muscle mass and strength that accompanies old age, which results from a number of factors, one of which, in a sort of perverse catch-22, is vitamin D deficiency [9]. Thankfully, you can obtain vitamin D through supplementation, but that’s not a good reason to let your skin get thinner.
Needless to say, structural changes to the skin due to aging also impair its thermoregulatory functions [10] as well as its permeability [11]. Problems don’t stop at the skin, as the flaccid muscles of the elderly are more than just not very nice to look at; they make it more difficult for them to carry out normal activities, let alone vigorous ones such as sports, and they increase the likelihood of falls and injuries. Speaking of grey hair, it appears that there might be a correlation between it and atherosclerosis, to the point that some researchers suggest that graying of hair, especially if it happens early on in life, might be a marker of coronary artery disease; this doesn’t mean that grey hair causes heart disease but rather that the two might share some of their underlying mechanisms and be differently important symptoms of the same deleterious processes [12]. Another interesting correlation is between the presence of crosslinks in the skin and decreased pulmonary function. Again, this doesn’t mean that slack skin harms your lungs; it means that one of the factors suspected to wrinkle and stiffen your skin might make it harder for you to breathe in old age as well [13].
Conclusion
Is looking old an aesthetic problem? For many of us, it is, and while some might think it silly to dwell on your lost youthful looks, the take-home message is that elderly features are symptoms of a dysfunction that may pose a serious threat to your health. Addressing the mechanisms that cause us to look older may make us not only look younger but actually be biologically younger and healthier.
Literature
[1] Proksch, E., Brandner, J. M., & Jensen, J. M. (2008). The skin: an indispensable barrier. Experimental dermatology, 17(12), 1063-1072.
[2] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.
[3] DPM, ABMSP, FASPM, FAPWH(c), & Regulski, M. J. (2017). Cellular Senescence: What, Why, and How. Wounds, 29(6), 168-174.
[4] Dellambra, E., & Dimri, G. P. (2008). Cellular Senescence and Skin Aging. In Skin Aging Handbook (pp. 129-148).
[5] Velarde, M. C., & Demaria, M. (2016). Targeting senescent cells: possible implications for delaying skin aging: a mini-review. Gerontology, 62(5), 513-518.
[6] Snedeker, J. G., & Gautieri, A. (2014). The role of collagen crosslinks in ageing and diabetes-the good, the bad, and the ugly. Muscles, ligaments and tendons journal, 4(3), 303.
[7] Sell, D. R., Biemel, K. M., Reihl, O., Lederer, M. O., Strauch, C. M., & Monnier, V. M. (2005). Glucosepane is a major protein cross-link of the senescent human extracellular matrix relationship with diabetes. Journal of Biological Chemistry, 280(13), 12310-12315.
[8] Hakim, F. T., & Gress, R. E. (2007). Immunosenescence: deficits in adaptive immunity in the elderly. HLA, 70(3), 179-189.
[9] Janssen, H. C., Samson, M. M., & Verhaar, H. J. (2002). Vitamin D deficiency, muscle function, and falls in elderly people. The American journal of clinical nutrition, 75(4), 611-615.
[10] Blatteis, C. M. (2012). Age-dependent changes in temperature regulation–a mini review. Gerontology, 58(4), 289-295.
[11] Parrish, A. R. (2017). The impact of aging on epithelial barriers. Tissue barriers, 5(4), e1343172.
[12] ElFaramawy, A. A. A., Hanna, I. S., Darweesh, R. M., Ismail, A. S., & Kandil, H. I. (2017). The degree of hair graying as an independent risk marker for coronary artery disease, a CT coronary angiography study. The Egyptian Heart Journal.
[13] Kubo, A., Kato, M., Sugioka, Y., Mitsui, R., Fukuhara, N., Nihei, F., & Takeda, Y. (2018). Relationship between advanced glycation end-product accumulation in the skin and pulmonary function. Journal of physical therapy science, 30(3), 413-418.
