(4) With that trade-off as a fundamental constraint, selection adjusts telomere lengths—longer telomeres increasing the capacity for repair, shorter … - Bret Weinstein

[My] work... looked at the fact that shortening was being looked at by two different groups... by people interested in counteracting the aging process, and... in exactly the opposite fashion, by people who were interested in tumorigenesis in cancer. ...Tumors ...always had active, that's the enzyme that lengthens our telomeres. So those folks were interested in bringing about a halt in the lengthening of telomeres... to counteract cancer, and the folks that were studying the process were interested in lengthening telomeres... to generate greater repair capacity. ...[M]y point was evolutionarily speaking this looks like a pleiotropic effect, that the genes which create the tendency of the cells to be limited in their capacity to replace themselves, are providing a benefit in youth... that we are largely free of tumors and cancer at the inevitable late life cost that we grow feeble and inefficient, and eventually die. ...[T]hat matches a very old hypothesis in evolutionary theory by somebody I was fortunate enough to know, George Williams...

I stood up for three reasons. One... I felt an obligation to do it... it was the right thing to do. Two... manipulative bullies... Three, I thought that I was positioned to endure and repel the accusation that I absolutely knew was going to come back. Why did I think I was well positioned? ...I had tenure. I was well liked by students of every description, who knew me very well... and knew that I was not a bigot. I thought that would protect me. My own personal history was also completely inconsistent with the claim that I am a racist. ...I was wrong.

[C]aptive-rodent breeding protocols, designed to increase reproductive output, simultaneously exert strong selection against reproductive senescence and virtually eliminate selection that would otherwise favor tumor suppression. This appears to have greatly elongated the telomeres of laboratory mice. With their telomeric failsafe effectively disabled, these animals are unreliable models of normal senescence and tumor formation. Safety tests employing these animals likely overestimate cancer risks and underestimate tissue damage and consequent accelerated senescence.