Here is an question to think on while you recover from the excesses of the recent holiday: should we expect there to be, in humans, mice, or other species, many simple genetic alterations that are unambiguously beneficial for the individual, yet which evolution did not select for? Another way of looking at this question: why is it that there exist a range of ways to engineer slightly-genetically-altered mice that are stronger, healthier, and longer-lived than the standard wild variants?
The classical answer to this question suggests that these improvements come with fitness costs in the wild, or - more subtly - have the effect of dramatically reducing ability to survive under some rare combination of environmental circumstances. This is obviously the case when you look at mice lacking growth hormone, which live 60-70% longer than their peers, but are absolutely unfit for life in the wild due to their small size and, more importantly, issues with maintaining body temperature due to that small size. But for unambiguously all-round beneficial mutations like myostatin knockout, one has to think harder about how this could be a disadvantage.
Here is another example of a mutation that everyone would want for their offspring, should it turn out to work much the same way in humans:
Cardiotrophin 1 (CT-1), an interleukin 6 family member, promotes fibrosis and arterial stiffness. We hypothesized that the absence of CT-1 influences arterial fibrosis and stiffness, senescence, and life span. In senescent 29-month-old mice, vascular function was analyzed by echotracking device. Arterial histomorphology, senescence, metabolic, inflammatory, and oxidative stress parameters were measured.
Survival rate of wild-type and CT-1-null mice was studied. ... The wall stress-incremental elastic modulus curve of old CT-1-null mice was shifted rightward as compared with wild-type mice, indicating decreased arterial stiffness. Media thickness and wall fibrosis were lower in CT-1-null mice. CT-1-null mice showed decreased levels of inflammatory, apoptotic, and senescence pathways, whereas telomere-linked proteins, DNA repair proteins, and antioxidant enzyme activities were increased. CT-1-null mice displayed a 5-month increased median longevity compared with wild-type mice.
The absence of CT-1 is associated with decreased arterial fibrosis, stiffness, and senescence and increased longevity in mice likely through downregulating apoptotic, senescence, and inflammatory pathways. CT-1 may be a major regulator of arterial stiffness with a major impact on the aging process.
I look forward to the day on which one can take a flight across the Pacific as a medical tourist, drop into a reputable clinic, and have a few genetic alterations done: myostatin, cardiotrophin 1, and others that arise and are shown to have no downsides for people living in a society with access to modern medicine.