CFC
Bluelight Crew
- Joined
- Mar 9, 2013
- Messages
- 18,171
An interesting study published last week suggests that AAS (in this instance Danazol, and possibly via an oestrogen-response element) reverses the shortening of the chromosomal telomere that typically precedes cell aging, dysfunction, apoptosis and/or malignancy (tumours).
I should reiterate that this is pretty profound stuff. Shortened telomeres from some hereditary diseases lead to premature illness and death via a number of mechanisms, and are in general linked to ageing in most lifeforms.
In essence the telomere is the 'cap' on the end of the chromosome that holds it together and helps protect the DNA, preventing the development of cancer.
It's length can be thought of as analogous to the cell's 'clock', since it shortens during normal DNA replication. As it becomes shorter and shorter, replicative senescence (ageing) develops, and the cell begins to stop replicating, becoming faulty and eventually dying.
People with shorter telomeres are thus thought to die younger and often endure poorer lifetime health/QOL scores. In theory telomere lengthening could immortalise human cells and extend lifespans quite dramatically, though in practice it's unlikely to be anything like that straightforward.
Nevertheless the prospect of AAS improving cellular lifespans could prove to be an interesting tool, and suggests testosterone replacement therapy in older men may actually be more beneficial than simply improving cosmetic or psychological outcomes - it may actually slow ageing altogether.
Anyway, it's well worth a read if you're interested in the subject. I'd have a look at the editorial first, and you can read the full paper for free here.
I should reiterate that this is pretty profound stuff. Shortened telomeres from some hereditary diseases lead to premature illness and death via a number of mechanisms, and are in general linked to ageing in most lifeforms.
In essence the telomere is the 'cap' on the end of the chromosome that holds it together and helps protect the DNA, preventing the development of cancer.
It's length can be thought of as analogous to the cell's 'clock', since it shortens during normal DNA replication. As it becomes shorter and shorter, replicative senescence (ageing) develops, and the cell begins to stop replicating, becoming faulty and eventually dying.
People with shorter telomeres are thus thought to die younger and often endure poorer lifetime health/QOL scores. In theory telomere lengthening could immortalise human cells and extend lifespans quite dramatically, though in practice it's unlikely to be anything like that straightforward.
Nevertheless the prospect of AAS improving cellular lifespans could prove to be an interesting tool, and suggests testosterone replacement therapy in older men may actually be more beneficial than simply improving cosmetic or psychological outcomes - it may actually slow ageing altogether.
Anyway, it's well worth a read if you're interested in the subject. I'd have a look at the editorial first, and you can read the full paper for free here.
