Metabolism is complex - very, very complex. In areas that have been well studied for more than a decade, researchers are still pushing back and forth on whether well known genes and pathways are actually important in longevity. In this sort of environment a single study in a few dozen mice isn't worth much, as the results from these various studies are either are all over the map, or prone to being overturned by a more careful, well-funded, and larger research project. That is what seems to have happened here for IGF-1 and longevity:
One of the major discoveries in aging during the past decade has been the observation that mutations in insulin/IGF-1 signaling led to increased longevity in various invertebrate models.
The most direct evidence that mutations affecting the insulin/IGF-1 signaling pathway lead to increased longevity in mammals has come from studies with Igf1r+/− mice ... i.e., mice lacking one copy of the gene coding for IGF-1 receptor ... In 2003, Holzenberger et al. reported that female Igf1r+/− mice exhibited a 33% increase in lifespan. ... However, the lifespan data in the Holzenberger study are problematic because of the small sample size and the very short lifespan of both the wild type (WT) and Igf1r+/− mice studied.
therefore, we have reassessed the effect of reduced expression of the IGF-1R on lifespan using the rigorous criteria recommended by Ladiges et al., e.g., lifespan and end-of-life pathology were assessed using large sample sizes and husbandry conditions that permitted the control lifespan to approach its full potential, which are necessary if the longevity differences in the experimental group are to be relevant to healthy aging.
In agreement with Holzenberger et al., we found that the female Igf1r+/− mice were more resistant to the oxidative stress than were WT female mice while no difference was observed between the male Igf1r+/− and WT mice. However, there was only a modest increase in the mean lifespan (4.7%) of female Igf1r+/− mice compared to their WT littermates and no significant change in end-of-life pathology. Thus, our data show [that] reduced IGF-1R signaling in mammals does not play the same major role in aging that is observed in invertebrates.
And so it goes - sometimes the early results achieved in small, prospective studies with small budgets don't hold up to closer inspection. Some fundamental processes relating to the link between operation of metabolism and longevity are very similar between lower animals (like worms) and higher animals (like mammals). You might think of the effects of calorie restriction, for example. But clearly other processes are significantly different between species, and this is one more layer of complexity that will increase the cost and slow the progress of efforts to slow aging by manipulating metabolism - such as by altering IGF-1.