Skin is the largest human organ. It is made of two main layers; the inner skin (dermis) and the thin outer skin epidermis. It’s also made of proteins, like collagen which gives the skin its structure and elasticity. A scientific review of wrinkles made in 2008 thought that collagen losing its structure was the key to the appearance of aging skin.
In humans collagen is very stable, and unlike other cells of the body that are constantly dying and replicating, collagen cells will hang around for a long time (approximately 30 years) without being replaced. This is partly because humans only make a few enzymes that can breakdown collagen. The fact that collagen is stable and doesn’t breakdown quickly seems like a good thing, but it isn’t.
Old collagen starts develops alterations, and becomes what scientists call, “fragmented collagen”. Fragmented collagen causes wrinkles, which also leads to skin tearing and bruising easier than it otherwise would.
Fibroblasts are cells that make collagen. In young skin, fibroblasts attach to collagen and stretch. When they stretch fibroblasts make more collagen, and stop producing enzymes that would breakdown collagen. But as collagen becomes more and more fragmented the fibroblasts can’t attach to it anymore. This means fibroblasts shrink instead of stretching, and because they can’t stretch, they can’t make new collagen. The fibroblasts also start making more enzymes will break down collagen.
What can we do?
Since collagen fragmenting is the main cause of wrinkles, therapies that build up collagen have been shown to reduce wrinkles most effectively. Retinoic acid and retinol, a form of Vitamin A, was one of the first treatments on the market that was shown to do this. These products put new collagen into aged skin, which but also encourages fibroblasts to attach to collagen and stretch. This naturally encourages a positive cycle of collagen growth.
While moisturisers might help reduce wrinkles, they are still, and always will be a part of life. If you live long enough, you will get them. But hey, at least you’ve lived.
There haven’t been too many studies showing the effectiveness of vitamin B as an anti-aging ingredient, and even less long term studies. But a few small ones show significant improvements in fine lines and wrinkles in two weeks. In a study where a group of middle-aged women applied topical niacinamide B3 daily to one side of their face and compared it to the other side as a control for 12 weeks, there were reduced fine lines and wrinkles, spots, red blotchiness, and skin yellowing.
In one study, a product with 5% vitamin C applied to one forearm of volunteers and placebo to the other forearm for 6 months lead to increased expression of collagen, and a protein that inhibits enzymes that breakdown collagen. **This is because Vitamin C is broken down to vitamin D, which is used for the production of Melanin (the stuff that helps you tan), and is a major component in the formation of collagen.**
-Wendy Zukerman
**(added after episode airing)
In humans collagen is very stable, and unlike other cells of the body that are constantly dying and replicating, collagen cells will hang around for a long time (approximately 30 years) without being replaced. This is partly because humans only make a few enzymes that can breakdown collagen. The fact that collagen is stable and doesn’t breakdown quickly seems like a good thing, but it isn’t.
Old collagen starts develops alterations, and becomes what scientists call, “fragmented collagen”. Fragmented collagen causes wrinkles, which also leads to skin tearing and bruising easier than it otherwise would.
Fibroblasts are cells that make collagen. In young skin, fibroblasts attach to collagen and stretch. When they stretch fibroblasts make more collagen, and stop producing enzymes that would breakdown collagen. But as collagen becomes more and more fragmented the fibroblasts can’t attach to it anymore. This means fibroblasts shrink instead of stretching, and because they can’t stretch, they can’t make new collagen. The fibroblasts also start making more enzymes will break down collagen.
What can we do?
Since collagen fragmenting is the main cause of wrinkles, therapies that build up collagen have been shown to reduce wrinkles most effectively. Retinoic acid and retinol, a form of Vitamin A, was one of the first treatments on the market that was shown to do this. These products put new collagen into aged skin, which but also encourages fibroblasts to attach to collagen and stretch. This naturally encourages a positive cycle of collagen growth.
While moisturisers might help reduce wrinkles, they are still, and always will be a part of life. If you live long enough, you will get them. But hey, at least you’ve lived.
There haven’t been too many studies showing the effectiveness of vitamin B as an anti-aging ingredient, and even less long term studies. But a few small ones show significant improvements in fine lines and wrinkles in two weeks. In a study where a group of middle-aged women applied topical niacinamide B3 daily to one side of their face and compared it to the other side as a control for 12 weeks, there were reduced fine lines and wrinkles, spots, red blotchiness, and skin yellowing.
In one study, a product with 5% vitamin C applied to one forearm of volunteers and placebo to the other forearm for 6 months lead to increased expression of collagen, and a protein that inhibits enzymes that breakdown collagen. **This is because Vitamin C is broken down to vitamin D, which is used for the production of Melanin (the stuff that helps you tan), and is a major component in the formation of collagen.**
-Wendy Zukerman
**(added after episode airing)
Tonight's episode of the petri-dish for youth week is on the fountain of youth, and one of tonight's segments is on the genes which causes aging, here is a taster of what is going to be on tonight.
1A Cynthia Kenyon was looking at the genes, which cause aging in a little worm called Caenorhabditis elegans, which has had all of its genes, mapped out, it’s a really basic multi-cellular life-form, they can tell its full cellular lineage. So they thought that they would find the gene that causes aging. And the weirdest thing is that they found some….
The gene is called Daf-2 and when daf-2gets changed, and then worms live twice as long. From 14 to 28 days. When daf2 is damaged, than the worm lives twice as long, so this gene is increasing the rate of aging in the worms.
How does this gene cause aging?
Daf2 receptor squashes the activity of Daf16, causing aging. So you inhibit daf 2, and Daf16 is liberated, and does 100 little good things by up regulating the cellular stress-response, such as resistance to oxidative stress, thermo-tolerance, resistance to hypoxia, antimicrobial and metabolic genes, which makes the worms aging slow down.
So the daf-2 insulin like IGF-1 receptor is a protein, that floats around in the blood, and causes maturation, in C elegans. Bringing them to sexual maturity, and then after this continues to cause what we call ageing. So daf-1 binds to daf-2 It does this through the binding to a tyrosine receptor on the surface of the cell, this triggers an intracellular protein pathway, which continues into the nucleus of the cell, where daf-16 gets inhibited. Which otherwise would be running around transcribing other genes.
They have found analogues for these genes in humans, but scientists are still unsure if they will have the same effect as on the worms.
Why do we have this gene that makes us age?
So the purpose of a gene is so that it passes on its genes to the next generation, so a gene which may help an increased production of offspring, or is closely associated with this would be more likely to survive. But within a species, no only are you competing for a mate, but your also competing for food. So in a population, where the older generations don’t die off, and continue to float around, there might not necessarily be mates for the following generations, as the old males and females could be whole shotting all of the genes. And so this decreases the slow evolution that would take place for a changing environment.
So the populations where there weren’t any dying off, there was no genetic diversity, and when mass extinctions came through, the animals who would be able to evolve through subsequent generations, without any of the much older generations winding back their variation, and without having to feed the older generation would have had an edge than the immortal populations didn’t, giving them a much more evolutionary stable strategy then the undying. [Kind of like the Mayans expending all of their recourses due to an enormous population].
For more information on evolutionary stable strategies try the book “The Selfish Gene”, by Richard Dawson pub 1976
References
1Nature 424, 277-283 (17 July 2003) | doi:10.1038/nature01789; Received 17 December 2002; Accepted 7 May 2003; Published online 29 June 2003
Tonight's show is on @10pm on Joy 94.9FM or stream live on Joy
If you miss tonight's show it will be available via podcast accessible on the front page.
Feel free to email us on thepetridish@joy.org.au or tweet us by adding #pdish in your message
-Kane Day, Producer of "The Petridish"
Posts
No comments:
Post a Comment