Glycerin might help ?
Hi folks,
I just came across an interesting article about glycerin and it’s
reported beneficial role in skin diseases. I’ve been using it for
about three weeks to keep my face from drying out during this ol’ New
England winter. I happened to stumble across it in an old formulary
handbook at the library. I think it was called Henley’s Formulas.
Anyway,it had a formula for skin mositurizers and many used glycerin.
I did a little research and found that it is commonly used in
cosmetics as a humectant. It’s non-comedogenic and hypoallegenic. So,
off I went to look for it. I found it in a full service pharmacy in a
4 oz. bottle for $2.79 It’s a crystal clear, thick liquid, sort of
like light corn syrup. It’s mixed with water on a 1:1 basis. It’s
feels bit sticky on the skin, but it’s not greasy or irritating to
me. It has really worked well for keeping my skin moisturized in
spite of the cold, dry winter air. It would be great if it also
helped sebderm a bit. Here’s the article:
Glycerin May Help Skin Disease, Study Finds
December 2003
www.mcg.edu/news/2003NewsRel/glycerin.html
Glycerin, commonly found in skin care products because it attracts
water and helps skin look better, may have therapeutic value as well,
according to researchers at the Medical College of Georgia.
Glycerin, or glycerol, is a natural alcohol and water attractor
that’s been used in skin care products for centuries, says Dr.
Wendy
Bollinger Bollag, cell physiologist.
In research published in the December issue of The Journal of
Investigative Dermatology, she and co-author Dr. Xiangjian Zheng, who
worked as a graduate student in her lab and is now a postdoctoral
fellow at Vanderbilt University, show that glycerol also makes skin
look and function better by helping skin cells mature properly.
"This is a pretty novel hypothesis that is really quite in its
infancy," Dr. Bollag says of the finding that glycerol works as a
signal to help direct skin cells through their four normal stages of
maturity. In the endless cycle of skin-cell production, the youngest
cells move up from the deepest layer and switch from replicating as
their main function to eventually becoming mature surface cells that
spit out lipids to help form the skin’s protective barrier before
they die.
The researchers’ findings about the signaling function of
glycerol
means the readily available fluid, found in its pure state on grocery
store shelves and as a component of many other products, may help
people with diseases such as psoriasis and non-melanoma skin cancers,
that result from abnormal proliferation and maturation of skin cells,
and may augment wound-healing.
The researchers found glycerol’s role in skin cell maturation
while
studying phospholipase D, an enzyme that converts fats or lipids in
the external, protective cell membrane to cell signals.
Phospholipids are fats found throughout the body that make up much of
the plasma membrane lipid bilayer that encases each cell and helps
keep it from mixing with other cells. All cells have this layer and
skin cells secrete extra lipids which help provide an additional
barrier. "Think about it," Dr. Bollag says. "If there was
not some
sort of barrier, when you took a bath, all the water would go into
you and you would blow up like a balloon."
Knowing that phospholipase D can use alcohols, such as ethyl alcohol,
Drs. Bollag and Zheng wondered what it would do with glycerol, a
physiological alcohol used to synthesize fat and subsequently
released during exercise as fat fuels physical exertion.
What they found is that when phospholipase D pairs with glycerol, it
produces a distinctive signal that directs skin cell maturation, Dr.
Zheng says.
They found that, despite its name, a channel called aquaporin 3,
which is expressed in skin cells and allows only certain molecules
through, is not particularly good at transporting water but is good
at transporting glycerin. Inside skin cells, aquaporin 3 and
phospholipase D interact. "We don’t know if it’s direct
or if there
is an intervening protein, but they associate," Dr. Zheng says.
They
theorize that aquaporin 3 funnels glycerol to phospholipase D,
resulting in phosphatidylglycerol, a lipid that appears to signal
enzymes involved in skin cell differentiation, Dr. Zheng says.
"We think the glycerol is serving as a substrate to allow the
skin to
mature properly and, when you don’t have enough glycerol in the
skin,
cells don’t mature properly and that is why you get hyper-
proliferative, thick skin," Dr. Bollag says.
A mouse model for dry, flaky, unnaturally thick and slow-healing skin
recently developed by researchers at the University of California,
San Francisco, may help prove the Augusta researchers correct.
The genetically manipulated mice lack sufficient glycerol in their
skin because they are missing the gene responsible for aquaporin
3. "That is why their levels of glycerol are reduced, because
they
don’t have that glycerol channel," Dr. Bollag says. The mouse
research was published in the Journal of Investigative Dermatology
about the same time Drs. Bollag and Zheng were submitting their
work. "We were thinking, we know why this happens," Dr.
Bollag says.
Water-loving glycerol couldn’t get inside the phospholipase D
cell
without a channel. Consequently, the phosphatidylglycerol that
results from their union doesn’t happen and neither does the
resulting signal that directs normal skin cell maturation.
Another naturally occurring mouse with dry, thick skin has aquaporin
3 but lacks skin fats that are normally broken down to release
glycerol, Dr. Bollag says.
When glycerol was given topically or orally to these animal models,
many of the skin problems resolved. Other water-attracting agents
didn’t work so well, which gives the MCG researchers more fuel
for
their finding that glycerol also plays a key role in normal skin cell
maturation and proliferation.
They hope their findings will not only contribute to a better
understanding of normal skin development but lead to more effective
treatment when development is abnormal.
A process called co-localization helps show that phospholipase D
(red) and aquaporin 3 (green) are together (yellow) in skin cells.
"For instance, in psoriasis, you have keratinocytes (skin cells)
that
grow too much and if we could somehow harness this signal, we might
somehow be able to tell those keratinocytes, `No. It’s time
to
mature. Stop growing. Mature and form good skin. Form this good
barrier,’" Dr. Bollag says. "Another instance in which you
don’t get
normal maturation of the keratinocytes is in skin cancer, the non-
melanoma skin cancers. So here is another way that if we could
potentially harness this signaling pathway, we could maybe bypass the
signal that basically makes them cancer and tell them, `No.
Mature
and form skin and that’s it. Don’t become a cancer,’"
says Dr. Bollag.
The MCG researcher has submitted a grant application to the National
Institutes of Health to further study the signaling mechanism she and
Dr. Zheng have found. The NIH supported her current studies as well.
"(Now we are) trying to find out what the signal activates,"
she
says. "In other words, how does the signal that is produced by
phospholipase D and the glycerol actually tell the cell to mature?
How does that signal then activate certain enzymes and proteins in
the cell to make the cell mature? Other things we are interested in
looking at are ways to manipulate the system, for instance to
increase signal formation, to see if we can then increase
keratinocyte formation and that would potentially be a way to harness
the system to treat skin diseases."