I’m not convinced this is a problem with the reasoner rather than a problem with the scenario.
Let’s say we start with an infinite population of people, who all have as a purpose in life to play Russian Roulette until they die. Let’s further say that one in a trillion of these people has a defective gun that will not shoot, no matter how many times they play.
If you select from the people who have survived 1000 rounds, your population will be made almost entirely out of people with defective guns (1 / 1e12 with defective guns vs 1/6e80 with working guns who have just gotten lucky).
Alternatively, we could say that none of the guns at all are defective. Even if we make that assumption, if we count the number of observer moments of “about to pull the trigger”, we see that the median observer-moment is someone who has played 3 rounds, the 99.9th percentile observer-moment has played 26 rounds, and by the time you’re up to 100 rounds, approximately 99.999999% of observer-moments are from people who have pulled the trigger fewer times than you have survived. If we play a game of Follow the Improbability, we find that the improbability is the fact that we’re looking at a person who has won 1000 rounds of Russian Roulette in a row, so if we figure out why we’re looking at that particular person I think that solves the problem.
My impression is that DNA repair mechanisms get dramatically less effective with age, and that piRNA and siRNA (and other such transposon repression mechanisms) are effective but not 100% effective even in germ cells. Since germ cells in males continue to divide through the entire lifespan, my naive expectation would be that the children of very old men to age faster than the children of younger men (not just “have worse health outcomes in general” but specifically “express the specific marks of senescence earlier”).
Is that a valid prediction of the “transposons make more transposons and eventually the exponential increase in the number of transposons kills the cell” hypothesis?