You make it sound like telomere length is something that can be affected by transitory events, over a short period of time. Isn't telomere length the result of gradual changes over time? How is it possible for a drunk night and a short intervention (days) able to change anything to any significant degree or were you just rationalizing what you want to believe?
Below is a detailed explanation I planned to post in any case, but it covers your question. In summary, white blood cells turnover every 6 days or so, and are replaced from the progenitor pool. Therefore various positive or negative lifestyle interventions can make your leukocyte telomeres get longer or shorter, but really all you're doing is varying their rate of attrition and/or replacement.
Here is the more detailed answer.
Telomeres shorten progressively with divisions and this changes gene expression. This is an intentional program to limit the lifetime of a cell line, necessitating their replacement from a stem cell source. It’s like clockwork – white blood cells, fat cells, muscle cells, skin cells – they all follow this pattern, with a small stem cell pool expanding out into a larger, more differentiated progenitor pool, and this feeding an even larger pool of somatic cells doing the job of keeping the body alive. For each compartment, the progenitor pool is an appropriate size for the rate of replacement needed by the tissue it serves [10.1038/ncomms2602]. White blood cells need rapid replacement; skin, fat and muscle have a smaller pool but with longer telomeres giving an equal regenerative capacity overall. Michael West has shown that no stem cells have significant telomerase activity after the embryonic-fetal transition [10.2217/rme-2019-0062]; they must have some telomerase activity in my view, but insufficient to prevent shortening.
The telomere length of your white blood cells (for example) can go up and down depending on their relative attrition and replacement rate. This is behind claims of meditation and exercise or clean eating ‘making you younger’. It does not make you younger. It does slow ageing if sustained for long periods by altering the balance of replacement, but the stem cells are still ageing via telomere shortening and this will eventually lead to a reduction in replacement rate of the somatic cells.
A similar but reciprocal argument holds for DNA methylation, which builds up in long lived somatic cells, but is largely reset in cells replaced regularly from stem cell pools. Hence you could reduce your ‘methylation age’ by accelerating ageing with faster replacement or increase your ‘methylation age’ by slowing replacement but keeping more stem cells for the future. Neither is optimal or what we want.
In practice I advocate cyclical telomerase expression combined with an upward pressure on somatic cells to de-differentiate some portion of them back to progenitors. This allows for epigenetic control whilst you extend telomeres (and it makes it easier to extend telomeres as well). In the longer periods between cycles cells can differentiate normally. It is my belief that dividing cells and those with the shortest telomeres benefit the most from telomerase, so stem cells are likely to benefit least, but this also means that over multiple cycles they should gradually be rejuvenated whilst the larger effects on somatic and some progenitors come out in the wash, or at best reduce the demand on stem cells (which might act as a negative feedback loop in the case of continuous telomerase activity).
