Cracking the code on aging remains one of the biggest challenges in science today. As recently as a decade ago, the general aging theory focused on the oxidative stress model. Basically, the idea was that aging is due to the sustained accumulation of cellular damage and a lifetime of reactive oxygen species and free radicals coursing through our veins.
Imagine driving in city traffic. The lights are timed so that, if you’re lucky and there aren’t any accidents or crazy drivers cutting in front of you, you can drive several blocks before a red light stops you. But realistically, multiple factors often throw the system off balance and the traffic rarely flows smoothly…
Our children and grandchildren continually remind us of our younger days, when we could perform physical and mental feats with seemingly no effort or fatigue. So, why the age-related loss of energy? And can we do anything to stop or attenuate its progression? Recent research suggests the answer to the second question is “yes.” But first questions first.
Structurally, the difference between the acetyl-L-carnitine (ALC) and L-carnitine (LC) is that ALC is an LC molecule that also contains an attached acetic acid group. This structural difference is small, but it produces a considerable difference in the biochemical properties of the molecule and, consequently, in its effects on metabolism.