Caloric restriction (CR) delays aging and has served as a yardstick to evaluate interventions extending life span. However, mice given unlimited access to food suffer severe obesity. Health gains from CR depend on control mice being sufficiently overweight. Less obese mouse strains benefit far less from CR. Pharmacologic interventions that increase life span, including resveratrol, rapamycin, nicotinamide mononucleotide and metformin, also reduce body weight. In primates, CR does not delay aging unless the control group is eating enough to suffer from obesity-related disease. Human survival peaks at a BMI achievable without CR, and the above interventions are merely diet aids that shouldn’t slow aging in healthy weight individuals. To explain the effects of growth and obesity on longevity, I propose the tumor suppression theory of aging: aging is mostly the consequence of tumor-suppressive mechanisms that evolved to limit the tumorigenic potential of clonally expanding cells. A variation of the somatic mutation theory of aging, oncogenic mutations and clonal expansion, but not functional impairment, are postulated as the most relevant consequence of somatic mutations. Accumulating senescent cells, senescence-associated secretory phenotypes and stem cell exhaustion eventually cause tissue dysfunction and the majority, if not most, phenotypes of aging.