Alright, time for the science delivery. check out this review paper: Hursting, S. D., Lavigne, J. A., Berrigan, D., Perkins, S. N., & Barrett, J. C. (2003). Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans*. Annual review of medicine, 54(1), 131-152.

It's a review, so it cites and compiles a lot of individual studies. They cite a ton of studies if anyone wants to look at the actual studies. It's from 2003, so it's fairly new. It's also a bullshit excuse to ignore a study because it's old, but it's one less thing to try to weasel out with. You probably won't have access, but if you (or anyone) wants a copy I do have a PDF of it. The abstract:

Calorie restriction (CR) is the most effective and reproducible intervention for increasing lifespan in a variety of animal species, including mammals. CR is also the most potent, broadly acting cancer-prevention regimen in experimental carcinogenesis models. Translation of the knowledge gained from CR research to human chronic disease prevention and the promotion of healthy aging is critical, especially because obesity, which is an important risk factor for several chronic diseases, including many cancers, is alarmingly increasing in the Western world. This review synthesizes the key biological mechanisms underlying many of the beneficial effects of CR, with a particular focus on the insulin-like growth factor–1 pathway. We also describe some of the opportunities now available for investigations, including gene expression profiling studies, the development of pharmacological mimetics of CR, and the integration of CR regimens with targeted, mechanism-based interventions. These approaches will facilitate the translation of CR research into strategies for effective human chronic disease prevention.

Honestly this paper is great and I think anyone that argues with hambeasts regularly should keep it laying around. But some highlights

both investigators demonstrated that calorie restriction (CR), an experimental mode in which test animals receive a lower-calorie diet than ad libitum (AL)-fed controls, inhibited the growth of transplanted tumors in mice (3).

a reduced food intake increased lifespan in rodents (4). This work was extended by Tannenbaum and colleagues, who consistently showed that the incidence of tumors in mice decreased when food intake was reduced (5, 6). To date, CR has been the most widely studied and most effective experimental strategy for increasing the survival of mammals (7) and is also the most potent, broadly acting dietary intervention for preventing carcinogenesis in experimental models (8).

Unfortunately, CR is often incorrectly equated with starvation, and this misconception has, at least to some degree, limited the translation of important findings from CR research into human disease prevention strategies. In actuality, adequate nutriture is designed into CR regimens to avoid the confounding effects of malnutrition, and modest calorie decreases of 20%–30% relative to an AL diet can be equated to a normal, healthy level of intake. In fact, CR animals are almost always healthier, sleeker, and more active than their AL counterparts, which tend to develop obesity in mid-life. CR regimens administered throughout life are generally more protective than adult-onset CR (7, 9). However, both modalities prevent adult-onset obesity, significantly extend lifespan, and suppress tumorigenesis, prompting many investigators to suggest that obesity prevention may be a key underlying factor in the anti-aging and anti-cancer effects of CR (8, 10, 11)

CR is the only established intervention that extends lifetime survival (including mean and maximal lifespan) in mammals (7, 19). Figure 1 summarizes the average lifespan extension observed in response to CR in selected mouse and rat strains, as well as in dogs and cows. The anti-aging effects of CR have been observed in diverse organisms, including protozoa, yeast (Saccharomyces cerevisiae), nematode (Caenorhabditis elegans), several insect species including fruitfly (Drosophila melanogaster), mouse, rat, hamster, guinea pig, dog, cow, and preliminarily in several non-human primate species (7, 19–22). Thus, the mechanism(s) underlying the survival extension in response to CR, imposed using a variety of dietary compositions, feeding strategies, and levels of restriction, appears to be evolutionarily conserved. This suggests that a better understanding of these mechanisms will reveal important clues about the biology of aging

And here is the graph the last quote is talking about, showing the percent increase in life with CR. This review is before it was tested much in primates, but here is a more recent (2009) study on disease prevention with CR in monkeys.

Caloric restriction (CR), without malnutrition, delays aging and extends life span in diverse species; however, its effect on resistance to illness and mortality in primates has not been clearly established. We report findings of a 20-year longitudinal adult-onset CR study in rhesus monkeys aimed at filling this critical gap in aging research. In a population of rhesus macaques maintained at the Wisconsin National Primate Research Center, moderate CR lowered the incidence of aging-related deaths. At the time point reported, 50% of control fed animals survived as compared with 80% of the CR animals. Furthermore, CR delayed the onset of age-associated pathologies. Specifically, CR reduced the incidence of diabetes, cancer, cardiovascular disease, and brain atrophy. These data demonstrate that CR slows aging in a primate species.

Colman, R. J., Anderson, R. M., Johnson, S. C., Kastman, E. K., Kosmatka, K. J., Beasley, T. M., ... & Weindruch, R. (2009). Caloric restriction delays disease onset and mortality in rhesus monkeys. Science, 325(5937), 201-204.

Again, if anyone wants the full study, just ask.