Updated: July 4, 2020
What is photoaging?
We’ve all heard the term photoaging, but what does that really mean?
Our skin changes how it functions as we grow older, and that process can be accelerated by sun exposure (photoaging).
Photoaging manifests itself in our physical appearance as fine lines, wrinkles, and uneven skin tone.
Today, we’re going to take a look at how our skin changes due to both chronological aging and photoaging.
Sun exposure hastens the effects of chronological aging, so protecting your skin from the sun by using anti-oxidant rich skincare products, shade, and clothing is important.
We’re starting out with a quick anatomy lesson. Then, we’ll talk about how cellular turnover rates change due to photo-exposure (and regular aging) and we'll also talk about something called cellular senescence.
Be sure to stay tuned for the next post in this series where we dive deeper into the sun's impact on our skin’s structure and function.
A brief skin anatomy lesson
Before we start talking about how our skin changes due to sun exposure, we need a basic understanding of both skin anatomy (how our skin is structured) and skin physiology (how our skin functions).
This information is technical, but my job is to describe it in plain English, and I hope you’ll stick with me.
Let’s start out with a basic cartoon showing the layers of the skin. The epidermis is the outermost layer of our skin and the dermis lies below it.
Layers of the Epidermis
The epidermis itself is composed of several skin layers as shown in the illustration below. One thing to note – the stratum lucidum is only present on the soles of our feet and the palms of our hands.
That outermost layer of the epidermis, the stratum corneum, is just layers of dead skin, but LIVING cells down in the epidermis' stratum basale layer constantly migrate up from the innermost layer of the epidermis to the outermost replenishing the stratum corneum as dead skin cells naturally slough away.
Cell Turnover Rate Slows
There’s some debate about how long it takes for a cell in the stratum basale to migrate to the stratum corneum.
Part of the reason for this debate is that our epidermis varies in thickness in different parts of our bodies from about 0.04 mm thick on our eyelids (about half as thick as a strand of hair) to about 1.6 mm thick (about twice as thick as that strand of hair) on our palms and soles.
For this reason, migration of epithelial cells in some parts of the body takes longer when compared with other parts, and migration times vary considerably based on which part of the body is used to evaluate the "turnover rate".
What is known is that this cellular migration rate or cellular turnover rate slows by approximately 30% to 50% from our 30s to our 80s (Reference 4), and this happens while the total thickness of all our epidermal layers DECREASES (mostly due to flattening of rete ridges, which we’ll talk about in the next post).
Chronic sun exposure also slows down the cellular turnover cycle.
As we age, our cells are more prone to enter a state of senescence where they no longer divide. For skin cells, our chronological age AND the amount of time we've spent in the sun promote senescence.
Senescent cells no longer divide, and senescent cells also release different signaling molecules than when they were normal healthy cells.
Signaling molecules are how the cells of our body communicate with one another, kind of like talking or texting with nearby cells.
Here’s where I'll throw out a technical term. Why? Because you cannot search for senescence without coming across this acronym. If you don’t care to get so technical, skip to the next non-italicized paragraph.
SASP – senescence-associated secretory phenotype. Just what the heck does that mean?
Phenotype is a set of characteristics displayed by (or in this case a set of behaviors that) distinguish senescent cells from normal cell types.
Senescent cells have the following differences when compared with normal skin cells:
- Senescent cells express (or secrete) high levels of inflammatory signaling molecules
- Senescent cells resist programmed cell death (apoptosis)
- Senescent cells no longer divide
Whereas SASP means ALL three of those characteristics, we normally see the term SASP when talking solely about the signaling molecules that senescent cells produce and the term SASP environment when talking about the micro-environment around those senescent cells.
Normal Cell Life Cycle vs. Senescent Cells
You may have heard of the Hayflick limit, and even if you haven’t, you may remember from high school biology that we have extra sequences of DNA nucleotides (DNA base pairs). These extra base pairs, known as telomeres, don't code for any of our genes but are really important for DNA replication, which is why they're tacked onto the DNA strands that code for our genes.
Telomeres allow DNA replication to occur by giving room for the enzymes responsible for replicating our DNA to attach onto the DNA molecule.
Telomeres are not part of the sequence necessary for gene coding, and every time a cell divides (or replicates), the telomere length gets shortened a little (this is due to how replication of the DNA strand occurs and I'll go into this in more detail after this illustration).
Notice the big green blob in the figure above. That's the enzyme responsible for replicating the DNA strand. You'll see that enzyme is pretty large (quite a few base pairs long).
Due to its size, when that enzyme attaches and detaches from the DNA strand, it can't start replicating at the very end of the strand because it just doesn't attach to the very end of the strand, it inserts itself as close as possible at the end of the DNA strand, but there are base pairs that don't replicate during the process.
That's why telomeres are SO important.
Telomeres reside at the end of our DNA strands adding length onto the DNA strand, and each time a cell divides and our DNA gets copied as part of that process, the telomere length gets a little shorter.
After a certain number of divisions, these telomere lengths are too short to allow the cell to continue dividing so that the full DNA sequence gets copied, so replication (and cell division) stops.
The natural order of things is that this cell would destroy itself through programmed cell death (apoptosis). However, it's also possible that these cells enter a state of senescence. And, senescent cells resist programmed cell death.
The choice of a path towards programmed cell death or senescence presents for all cells at the end of their division life cycle in all the tissues of our body.
Senescence isn't a phenomenon unique to skin cells, but of course photo-aging is unique to skin cells.
Senescent skin cells tend to build up both in chronically photo-exposed skin and also naturally as we age (even in non-photoexposed skin).
Cascade effect of senescence
Remember we mentioned earlier that once a cell stops dividing (becomes senescent) that it starts producing different signaling molecules than it did when it was a normal cell?
Some of those signaling molecules produced tell nearby cells to stop dividing also.
So, a single non-dividing senescent cell can start a cascade or domino effect because it constantly tells nearby cells to stop dividing and they listen.
This is how one senescent cell can demoralize its neighboring cells and turn the once happy, joyful, viable neighboring cells into other demoralized cells like itself spreading the message to stop dividing to their neighbors and propagating the whole process.
How to encourage removal of senescent skin cells
Researchers have linked certain genes to higher rates of senescent cell removal (yep, good genes help) and have shown that certain supplements and ingredients boost the elimination of senescent cells.
When we’re talking about senescent skin cells in particular, we’re in luck because some ingredients have been shown to reduce the number of senescent skin cells or reduce the expression of the demoralizing signaling molecules that the senescent cells release.
Here’s a short list of ingredients shown to help reverse the effects of senescence in skin cells (we're just talking about skin on this list even though some of these ingredients have been shown helpful for reversing senescence in other cells within our body).
- Vitamin C (Reference 5)
- Goldenrod extract (Reference 6, Reference 7, and Reference 8)
- An extract from the microorganism Sphingomonas hydrophobicum (Reference 9 and Reference 10)
- The peptide, JuvelevenTM (technical name: Acetyl Hexapeptide-51 Amide)
Disclaimer: Please keep in mind that these studies have not been evaluated by the FDA.
You can either add Vitamin C to your diet or apply it topically (both ways have been studied for reducing the number of senescent cells).
Goldenrod isn't nearly as common in skincare, but JuvelevenTM, an incredible peptide, is often found in skincare products because of its ability to protect skin from the effects of UV.
If you're interested in picking up a great serum with JuvelevenTM, we offer the peptide packed oil free Abigail's Serum, and you can find it here.
And, be sure to stay tuned for our next post on more ways sun exposure impacts our skin.
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Reference 1 Basic Skin Layers
Reference 2 Wikipedia: Epidermis
Reference 3 The Skin
Reference 8 https://www.ncbi.nlm.nih.gov/pubmed/29675264
About the Author
Brandy Searcy is an outdoor girl who loves hiking, gardening, bird-watching, and body boarding. Her innate curiosity means she's constantly researching something, and she's likely sharing what she's learned here on the blog.
Nearly obsessive about her skincare, she started developing products to pack with her on day hikes and soon realized her backpacking friends were searching for a portable skincare routine as well, and that's how Rain Organica started.
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