DrG's Medisense Feature Article
15121-Old_Looking_Skin
Old
& Old-looking Skin
by Ann Gerhardt, MD
December 2015
Print Version
Skin is a complex organ with multiple layers and functions.
Other
than holding our insides in and sensing touch and temperature, skin
provides a protective barrier against hazardous substances, infections,
and mechanical, thermal and physical injury. It prevents loss
of
moisture and regulates temperature by sweating. It reduces
harmful effects of UV radiation while using that light to make vitamin
D.
The top layer, the epidermis, contains protective barrier cells,
melanocytes which confer skin color and a base membrane that separates
it from more sensitive structures below. Under the epidermis
is
the dermis, the workhorse of skin. It contains sweat glands,
hair
follicles with muscles to hold them erect, collagen to give firmness,
elastin to provide elasticity, sebaceous glands to make a protective
oil layer, tiny blood vessels, and nerves. Below it all is
the
subcutaneous layer of fat, blood vessels and nerves.
Throughout all the layers is a complex, stacked layering of lipids
(waxy, fatty substances) containing cholesterol, ceramides and
sphingomyelin. These lipid layers, along with
collagen and
elastin hold together all the other structures and are termed
connective tissue. It is this structure that many skin cream
ingredients profess to repair and bolster.
The big three skin destroyers are natural aging, called senescence,
tobacco and ultra-violet radiation (UV). They work via
different
mechanisms, but all lead to sagging dry thin skin with wrinkles,
irregular sallow color, brown “age” spots, and
visible
blood vessels. Aged skin is less likely to resist injury,
infection and cold.
Senescence is an aging process that occurs in all organs in which
functional capacity declines, old cells die at a faster rate (also
called programmed death) and the capacity to regenerate declines with
age. Losing our hormones contributes. Normal age-related
cell,
connective tissue and subcutaneous fat loss cause wrinkling, thinning,
itching and sagging.
Absent extraordinary physical stresses, our genes largely determine the
rate of senescence. The more rapid the process, the older the
skin looks. People with progeria, who have a defect that
impairs
cells’ ability to divide and make new cells, look ancient in
their teens and almost always die by age 20. Other genetic
forms
of senescence result from defective gene repair mechanisms.
Exposure to UV radiation is one of the most important factors
contributing to skin aging and cancers. We may long for the
beauty of deeply tanned skin, but by middle age that skin is deeply
wrinkled, sagging, dry and leathery. It is the Oriental
ladies
with their sun-blocking parasols who are the ones who retain beautiful
skin past middle age.
There are three main types of UV radiation, UVA, UVB, and
UVC. We
previously thought that UVA caused DNA damage that leads to cancer and
UVB burned and tanned the skin. Actually both do both, albeit
via
different mechanisms. UVC does not usually penetrate the
atmosphere, but when it does, it can also play a role in causing DNA
damage.
UV radiation damages most skin cell types, causing wrinkling, loss of
elasticity, irregular pigmentation, tiny visible broken blood vessels
and skin tumors. UV radiation also causes funny-looking
pigmented
spots and crusty lesions that can lead to cancer, and accelerates
changes associated with normal aging.
In addition to damaging DNA, UV radiation also induces oxidative
injury. Normal unstressed cells keep a balance between
potentially damaging reactive oxygen byproducts (ROS) and a variety of
antioxidant enzymes in the cell that neutralize ROS. ROSs are
natural byproducts of metabolism, but are also generated when cells are
exposed to UV radiation, toxins, pro-oxidants or
inflammation.
Under those conditions ROSs may overwhelm the cells’ capacity
to
neutralize them. Oxidative stress accelerates normal skin
aging
also.
This is why people take anti-oxidants and cosmetic companies put
anti-oxidants in skin products. Since there is no guarantee
that
the anti-oxidants we eat, take as pills or smear on our skin actually
neutralize ROS, it’s better to avoid excess ROS in the first
place.
Smoking causes significant skin damage, some of which resolves over
time after quitting. There are thousands of chemicals
including
nicotine in tobacco smoke. These chemicals trigger ROS
production
and an influx of enzymes that destroy collagen and elastin.
They
constrict blood vessels, depriving skin of oxygen and
nutrition. They induce the influx of and damage by
a
particular type of inflammatory cells called mast cells.
Smoking prematurely loosens skin around the eyes causing deep
crow’s feet, makes the skin more susceptible to
‘age
spots’ and turns the cigarette- holding fingers yellowish
brown. In some people it increases hair loss and risk of
psoriasis.
Dehydration and loss of body fat also make skin look aged, without
actually destroying it. Very thin middle aged people generally look
older than their age because their skin doesn’t have the fat
that
would normally puff it out and fill in wrinkles. For the same
reason, dehydration increases wrinkles, just like drying plums makes
the wrinkles of prunes.
Good nutrition is necessary for healthy skin. Skin is one of
the
most actively renewed organs in the body as we continually slough off
then replace the top layers of cells. We need a full
complement
of nutrients to do so, including protein, vitamins, minerals and energy
from carbohydrate and fat.
Cosmetic companies single out particular nutrients for skin health,
usually because the names sound good and seem intuitively connected to
a positive result. Take vitamin C for example.
Vitamin C is
necessary for cross-linking collagen protein, making it
stiff.
This helps connective tissue to keep skin taut. But vitamin C
alone can’t stimulate collagen production. We need
energy,
protein and a full complement of micronutrients to make the protein so
that there’s something to cross-link. For someone
who is
not deficient, a vitamin C supplement or cream won’t boost
extra
collagen production or firmness.
We can’t change our genetically determined senescence rate,
but
we certainly can choose a lifestyle that does not worsen skin aging.
Tobacco and smoke avoidance and using clothing and sun block to protect
against UV radiation go a long way to minimize premature aging skin
damage. Eating healthfully, with enough calories, protein and
nutrients to replenish skin structures and plump out wrinkles, makes
skin look better regardless of its degree of aging.
A few references:
Morita A, et al. Molecular basis of tobacco smoke-induced
premature skin aging.
J Investig Dermatol Symp Proc. 2009; 14(1):53-5
Kaukinen A, et al. Increased numbers of tryptase-positive mast cells in
the healthy and sun-protected skin of tobacco smokers.
Dermatology. 2014; 229(4):353-8
Ortiz A; Grando SA. Smoking and the skin. Int J
Dermatol. 2012; 51(3):250-62
Situm M, et al. Skin changes in the elderly people--how
strong is
the influence of the UV radiation on skin aging? Coll
Antropol. 2010; 34 Suppl 2:9-13
Stern RS. Treatment of Photoaging. N Engl J Med
2004;350:1526-34