Skin quickly tells a person’s age. Of all vital organs, skin, sitting on the outside of the human body, if not cared for appropriately, can prematurely age a person beyond their years.
A 50 year old who has used suitable skincare practises may easily look 10 years younger than a 40 year old who has not. A 40 year old who has paid no attention to the care of their skin, may easily, suddenly and quickly look far older than they really are.
What is the cause of ageing skin? Can it be adjusted for? Can skincare protect a youthful complexion? Can appropriate skincare practises prevent skin ageing?
The 2 distinct causes of ageing
While there are many theories why the human body ages progressively, it is accepted that the proposed factors centring each theory act in one of two ways;
Extrinsic ageing refers to factors acting upon the body from outside forces i.e. sunlight, alcohol, nutrition, pollution and lifestyle. All are choices a person makes and exposure is effected by the incidence and frequency of each. The most attributable cause of extrinsic ageing is UV light1.
Intrinsic ageing refers to a preprogrammed rate of ageing. In the same way a person’s hair colour is determined by inherited genetics, a person’s ageing rate or resistance to stress and therefore ageing is in part also determined by their DNA.
Proposed theories of ageing focus on intrinsic and extrinsic ageing factors from different biological perspectives, weighting each slightly differently. Ultimately if the human race is able to identify the reason for cell death, its foreseeable treatments of prevention and regeneration would be inventible.
This could mean fewer fine lines and wrinkles, improved collagen levels, youthful cellular turnover, higher activity levels and improving physical agility.
How does the human body age?
To date there have been over 300 theories of ageing, while many have fallen by the wayside, a few tried and tested hypothesis have stood the test of time.
- Free radical theory of ageing/mitochondrial theory of ageing
- Cross linking theory of ageing
- Endocrine theory of ageing
- Programmed longevity theory of ageing
What is the free radical theory of ageing?
The free radical theory of ageing is the most popularly accepted explanation for human ageing. Since its proposal in 19542 the theory has evolved and is now also commonly known as the mitochondrial theory of ageing.
Free radicals are high energy atoms and molecules, scientifically they are described as having an unpaired electron and unpaired electrons want more than anything to be one part of a pair. It is energetically preferable. In order to do this, free radicals must steal an electron from another atom, molecule or cell. When this occurs biologically, which is frequently does, antioxidant vitamins such as vitamin E and antioxidant enzymes such as coenzyme Q10 are able to donate an electron to the free radical, thereby halting its activity.
Antioxidants such as vitamins C and E when coexisting are often able to regenerate each other, however in times of drastic free radical attack, malnutrition or extreme stress, a person’s antioxidative defences can quickly become depleted.
When a cell is no longer able to defend against free radicals such as reactive oxygen species e.g. superoxide3, cell damage occurs and the long term accumulation of free radical damage leads to ageing, organ failure and death.
In support of the free radical theory of ageing are studies showing supplementing antioxidant defences can result in an increased life span4. The same theory also holds true for skin ageing specifically, with the topical application of antioxidants such as vitamin C helping to protect and reverse the ageing effects of UV light5.
The free radical or mitochondrial theory of ageing is both intrinsic and extrinsic. Mitocondria are the cells responsible for producing human energy, scientifically described as ATP (adenosine triphosphate). During the reactions needed to create ATP from inhaled oxygen, much energy is released and under these conditions it is not unusual for reactive oxygen species to be formed. Therefore cellular free radial damage and ageing as proposed under the free radical theory of ageing may be both intrinsically and extrinsically determined.
What is the cross-linking theory of ageing?
The cross-linking theory of ageing was first proposed in 19426 and focuses on a concept described as metabolic waste. The human body processes several chemical reactions daily. Ones which turn foods into blood glucose, ones which send nerve impulses to move muscles and ones which allow for the growth and formation of new and healthy skin cells. With so many chemical reactions occurring, inevitably some do not complete fully, others are terminated artificially and sometimes many more progress a little differently than normal. These processes create artefacts described as biological waste. Ingredients that are not helpful to the human body and if left in place may cause inflammation, damage and ageing.
An example of metabolic waste can be seen in the reaction between protein i.e. human skin and tissues with glucose i.e. blood sugar. This reaction is described as glycation and its progression allows the formation of advance glycation end products (AGEs).
When glycation occurs spontaneously it allows cross linking of neighbouring molecules. During this process previously separate cells able to flex against each other become irreversibly linked and stiffened. This reaction shares similarities with the setting of a two part super glue.
Glycation can occur within blood vessels, skin and organ tissues where they result in inflammation and oxidation, two biological reactions linked to premature ageing, diabetes and cardiovascular fatigue7
What is the endocrine theory of ageing?
The endocrine theory of ageing revolves around the concept of hormone pace control. Endocrine glands or the endocrine system describes a part of the human body whose job it is to secrete hormones in addition to other chemical messengers. These hormones are excreted directly into a person’s blood stream and therefore effect the body as a whole.
Hormones control growth, puberty, menopause and ageing. As hormones such as estrogen decline, so too do collagen levels fall with studies showing that topical reapplication can help to reverse skin ageing in addition to reducing wound healing time8.
In particular it is theorised that the insulin and insulin like growth factor (IGF-1) pathways play a particularly important role in the control of ageing. Studies show that diminished activation in animal models can increase lifespan to over twofold9.
What is the programmed longevity theory of ageing?
The programmed longevity theory of ageing focuses solely on intrinsic ageing factors, being based on the concept that all cells have a pre-programmed lifespan before they become defunct10. In biological terms this process is described as cell senescence.
The programmed longevity theory compliments a concept commonly known as the Hayflick limit, proposing human cells have a limited ability to replicate, namely they may only replicate themselves 50 times11. After 50 replications cells become senescent and can technically be described as dead. Organs are made up of many individual cells and as more and more reach senescence the organ i.e. heart, lungs or brain find it harder to perform their functionality and ultimately stop working.
This theory of ageing also fits well with telomere theory. Telomeres can be through of as bottle caps surrounding individual strands of DNA. As cells and therefore their DNA strands are replicated, telomere caps shorten and adult cells lack the ability to relengthen them, meaning with each successive replication telomere caps become shorter and shorter. Eventually as telomeres become unworkably shortened, cells may no longer replicate and therefore die12.
Can you delay ageing?
If we understand the mechanisms of ageing, we can take precautions and treatments to help avoid premature ageing, delay inherited rates of ageing and potentially in the very distant future significantly extend anticipated life expectancy.
As there are many proposed and evidenced theories of ageing, we can currently only infer what may help to delay the ageing process. The following steps are dictated by the above described theories of ageing and may help to delay both a person’s physical and cosmetic ageing processes;
- Eat a diet rich in antioxidants
As described by the free radical theory of ageing, oxidative damage may be primarily responsible for the ageing process. Indeed extrinsic ageing factors such as UV light, being quickly acting oxidants are noted to significantly speed up the ageing process of skin13. Eating a diet full of antioxidant rich fruits and vegetables helps to replenish antioxidant reserves and therefore extend protection against oxidative attack.
Some of the richest natural sources of antioxidants include; Prunes, strawberries, blackberries, plums, kale, broccoli, brussel sprouts, spinach, beets and red bell peppers.
- Take an antioxidant based supplement
In the same approach to eating a diet rich in antioxidants, supplementing a diet with an antioxidant rich supplement may also help to delay the process of ageing. Studies have shown antioxidant supplementation e.g. vitamin C and E combined can help reduce the risk of oxidative conditions such as Alzheimer’s disease14.
Although topical antioxidant application is known to help combat the oxidative nature of UV light, it should be noted that antioxidant supplementation is not a proven extender of longevity.
- Avoid large intakes of sugar
The cross linkage theory of ageing focuses on chemical side reactions i.e. reactions that are not required for healthy human biology. One such significant reaction is described as glycation and requires the presence of both glucose and protein. Glucose is sugar energy that is transported through a person’s blood stream to provide fuel to all living cells. Maintaining constant blood sugar levels i.e. avoiding blood sugar spikes helps reduce the risk of glycation type reactions.
In conditions of diabetes where impaired insulin release prevents the natural control of blood sugar levels, premature ageing and oxidative stress is prevalent. In conditions of diabetes it is very common for skin to therefore age prematurely15. Ensuring a low sugar diet helps to avoid insulin fatigue, risk of type 2 diabetes and premature ageing.
- Avoid foods high in advanced glycation end products (AGEs)
It was once thought the human body did not absorb AGEs – ingredients formed in foods during cooking processes, however scientific thought is changing since studies have shown foods high in AGEs lead to inflammation, oxidation and ageing16. In the same manner glycation happens in vivo through the reaction of sugar with bodily tissues, so too may the same reaction happen when foods rich in both protein and sugar are cooked.
These reaction are most prevalent in cooked meats and even more prevalent in meats cooked quickly at high heat. Pre-marinating foods with lemon juice helps to avoid AGE causing reactions while following a passively plant based diet helps avoid food groups prone to AGE formation.
- Use sunscreen daily
Using sunscreen daily, even when indoors and even when in winter, is the easiest outside-in method of delaying ageing. UV light is a well-recognized cause of premature ageing, causing early onset of fine lines and wrinkles with more serious side effects of skin cancer. UV light is an oxidant, high energy light easily able to provoke the creation of free radicals, high energy atoms and molecules which as per the free radical theory of ageing, provoke and promote ageing.
- Topical application of antioxidant based skincare
Antioxidants can be consumed through diet or applied topically to skin. Skincare rich in antioxidants such as vitamin E, as found in the griffin+row Enrich Antioxidant night cream help combat oxidative ageing factors i.e. UV light, replenishing skin’s natural reserves as well as adding to them.
- Farage, M. A., Miller, K. W., Elsner, P. and Maibach, H. I. (2008), Intrinsic and extrinsic factors in skin ageing: a review. International Journal of Cosmetic Science, 30: 87–95. doi:10.1111/j.1468-2494.2007.00415.x
- Gerschman R, Gilbert DL, Nye SW, Dwyer P, Fenn WO. Oxygen poisoning and x-irradiation: a mechanism in common. Science. 1954;119:623–626.
- Jin K. Modern Biological Theories of Aging. Aging and Disease. 2010;1(2):72-74.
- Theories of ageing. Viña J, Borrás C, Miquel J. IUBMB Life. 2007 Apr-May;59(4-5):249-54.
- Darr, D., Combs, S., Dunston, S., Manning, T. and Pinnell, S. (1992), Topical vitamin C protects porcine skin from ultraviolet radiation-induced damage. British Journal of Dermatology, 127: 247–253. doi:10.1111/j.1365-2133.1992.tb00122.x
- The crosslinkage theory of aging. Bjorksten J J Am Geriatr Soc. 1968 Apr; 16(4):408-27.
- Uribarri J, Woodruff S, Goodman S, et al. Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal of the American Dietetic Association. 2010;110(6):911-16.e12. doi:10.1016/j.jada.2010.03.018.
- Philips N, Devaney J. Beneficial regulation of type I collagen and matrixmetalloproteinase-1 expression by estrogen, progesterone, and its combination in skin fibroblasts. Journal of the American Aging Association. 2003;26(3-4):59-62. doi:10.1007/s11357-003-0006-7.
- Insulin, IGF-1 and longevity. van Heemst D. Aging Dis. 2010 Oct;1(2):147-57. Epub 2010 Aug 26.
- Davidovic M, Sevo G, Svorcan P, Milosevic DP, Despotovic N, Erceg P. Old age as a privilege of the “selfish ones” Aging and Disease. 2010;1:139–146.
- Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains. Exp Cell Res. 1961;25:585–621.
- Campisi J. Cancer, aging and cellular senescence. In Vivo. 2000;14:183–188.
- UV-light-induced signal cascades and skin aging. Rittié L, Fisher GJ. Ageing Res Rev. 2002 Sep;1(4):705-20.
- Frank B, Gupta S. A Review of antioxidants and Alzheimer’s disease. Ann Clin Psychiatry. 2005;17(4):269–86.
- Dyer DG, Dunn JA, Thorpe SR, et al. Accumulation of Maillard reaction products in skin collagen in diabetes and aging. Journal of Clinical Investigation. 1993;91(6):2463-2469.
- URIBARRI J, WOODRUFF S, GOODMAN S, et al. Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal of the American Dietetic Association. 2010;110(6):911-16.e12. doi:10.1016/j.jada.2010.03.018.