I saw this comment by Michael Rae,
"as with most conditions related to aging, there is no single form of aging damage responsible for the various changes that happen in skin as we age, and it's actually far from clear to me that glucosepane is the most important. The elastin protein that gives skin its elasticity becomes crosslinked and snaps, reducing its youthful ability to snap back into place when pulled, but there's a lot more to the visible and functional aging of the skin than loss of elasticity. The anchored system that supports the collagen-producing fibroblast cells degrades, leading fibroblasts to collapse and stop making new protein; the skin accumulates senescent cells, leading to SASP that spews out a range of inflammatory signaling molecules and proteolytic enzymes that degrade the supportive structures in the skin; the skin accumulates years of oxidative damage, leading to mutations; in many people, the dark pigment melanin that normally darkens our skin to give us an even tan clumps together into concentrated deposits known as "age spots" (often mistakenly attributed to lipofuscin in the anti-aging community, propagating an error first introduced by Pearson and Shaw) (and note that age sposts are both functionally one of the least important kinds of damage in aging skin and yet amongst the most visibly obvious such damage; ongoing rising oxidative stress distorts intracellular signaling, leading to aberrant keratinocyte function; etc. Like Seth, I don't have the chops to quantify all of that - and I doubt his dermatologist has them, either."
Thoughts?
