In my latest issue of Plastic and Reconstructive Surgery Journal with the antiaging special, there was an article “NAD+ in Regenerative Medicine.” Being Plastic Surgeons, there was a whole section dedicated to the role of NAD+ in skin aging.
Cell damage in skin:
- DNA damage and genomic instability is seen, likely caused by UV radiation
- Your body’s ability to repair the DNA damage is dependent on NAD+
- As NAD+ wanes with aging, you can’t repair the DNA damage as well, so it accumulates —> leads to cellular senescence.
Senescence = bad. When skin cells enter this, they are present and are metabolically active, but they do NOT PERFORM THEIR USUAL FUNCTION. They can’t make collagen and elastin. They cannot repair damage. They have inflammation, which leads to altered intercellular communication. The inflammation also leads to thinning of the epidermis, so the skin’s function as a barrier is impaired.
NAD+ levels:
It is thought that fasting and exercise help aging in part due to their increase in NAD+ levels. NAD+ levels decrease as you age because more is needed due to increased DNA damage and inflammation, and you don’t recycle it like you did when you were young, so you actually make less of it.
Sirtuins (yes, I know all these words are overwhelming. We will call it SIRT1 for short) are dependent on NAD+, and are linked to preserving collagen in the dermis, wound healing, and regeneration of the skin.
Mitochondrial dysfunction is seen. NAD+ is critical for mitochondrial function.
When damaged proteins accumulate, the skin does not function correctly. It is stiffer, less flexible, becomes more fragile, has less collagen and elastin. You need to clear the damaged proteins. NAD+ and SIRT1 are important to do all this.
So how can you get NAD+?
Read on.