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Nick King's avatar

Hi Richard. For me, the key point is where the (DNA) damage happens and what the consequences are at that skin layer. My understanding is that melanoma originates in melanocytes in the basal layer and therefore the ~60 fold protection that darker skin affords to DNA damage in the basal layer is relevant to melanoma occurrence.

While something like SCC, which initiates above the basal (melanocyte) layer, benefits less from the protection that darker skin provides (below in the basal layer) and therefore the rates will be more similar to those in lighter skinned folk. Presumably this will apply to other forms of skin damage, reddening etc depending on where they occur.

To shift into your world, melanin is like having the ozone layer in the basal layer of your skin (which is fine for protecting that layer and those below it, but doesn't really help the layers above), while sunscreen enables you to put your ozone on the outside and protect all skin layers.

Most things in evolution are a compromise. It's interesting that the very melanocyte cells that protect our skin are the same ones that develop into something life-threatening. Presumably a melanin-rich melanocyte is well protected while a 'pale' melanocyte is much more sensitive to damage?

And then of course there's the risk x consequence trade off. Melanoma protection is probably under much greater selective pressure than SCC protection or getting wrinkles, but apparently vitamin D production trumps everything as latitude increases.

Nick King

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STAN Randle's avatar

Hi,I suggest you log onto ‘The difference between Collagen 1 ; 2; and 3”

Collagen makes up about 30% of the body and collagen 1 makes up about 90% of all 5 types.

The skin is made up of three layers—Epidermis ; Dermis and Hypo dermis with the dermis consisting of collagen.

Younger skin dermis is collagen 1 which is synthesised to form very stron cross linked flexible fibrils

As one ages dead collagen 1 cells are replaced with inflexible collagen 3 . From about age 20 the Collagen 1 to 3 ratio changes at a rate of about 1% per year and the result is quite a dramatic change in the collagen structure in the dermis layer leading to wrinkles and less flexibility and sagging skin.

The drivers of this change are due to the turning off of genes Coli 1A1 and Col1A2 for Collagen 1 synthesis with Col 3A1 synthesising Collagen 3 replacement. The relentless structural weakness change of the sheet like soft tissues makes them (as well as other collagen tissues like tendons and blood vessel tissue more prone to injury such as tendonitis and aneurysm in blood vessels from high blood pressure)

The penetration of UV Radiation through the epidermis could easily damage the Demi’s layer of collage and with the capillary blood vessels located between the dermis layer of the skin and the hypo dermis layer which consists of hyaluronan and water then one would expect the skin to turn red possibly due to micro tears

Maybe this helps

Stan R

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