Humans have a unique long postmenopausal lifespan, which may have evolved due to mother-child food sharing. This practice allows aging females to enhance their daughters' fertility, reducing selection for senescence. Combined with Charnov's dimensionless assembly rules for mammalian life histories, this hypothesis explains human late maturity, small weaning size, and high fertility. It also has implications for past human habitat choice, social organization, and the importance of extended learning and paternal provisioning in human evolution. Mother-child food sharing is common among primates, but only human mothers provide a significant portion of their weaned children's diets. This allows mothers to use resources they can gather efficiently, which children cannot. Postmenopausal women can earn high rates, helping feed their daughters' and nieces' offspring. This support is especially important for weaned children when their mothers forage less after a newborn's arrival. This division of labor suggests a solution to the riddle of menopause in humans. Other apes live no longer than about 50 years, with fertility failing alongside physiological decline. In humans, fertility ends around half that age, well before other physiological frailty. The question is how natural selection favored this distinctly human "postreproductive" component of life history. The "stopping early" hypothesis suggests that early termination of fertility would evolve when extended maternal care is crucial to offspring survival. Aging mothers who stop being fertile and focus on ensuring the survival of children already born would leave more descendants than those who continue risky pregnancies. However, this hypothesis is challenged by evidence from other primates, such as chimpanzees, where fertility does not end early. Human reproduction does not end early compared to other apes, and the difference lies in low adult mortalities, leading to long average lifespans after menopause. Two evolutionary explanations for aging are mutation-selection balance and inter-temporal tradeoffs in reproductive effort. Mutation-selection balance occurs when the force of selection is no greater than the mutation rate, leading to accumulation of deleterious effects. Inter-temporal tradeoffs lead to senescence because genes have multiple effects. Genes that are beneficial at younger ages may be disfavored at later ages. Senescence results from this antagonistic pleiotropy. Grandmothering could slow aging by either means. It would strengthen selection against late-acting deleterious mutations by increasing the contribution of longer-lived females through the reproductive success of their daughters. It would also change the tradeoffs between opposing effects expressed at different ages. Slower senescence generally comes at the cost of reduced fertility at younger ages. If ape adult mortalities are in equilibrium on this tradeoff, then apes age early by human standards because mutations that would increase adaptive performance at later ages are continually removed by the reductions those mutations impose on fertility earlier in life. Regular mother-child food sharing could perturb that equilibrium by increasing the payoffs for late somatic performance as vigorous seniorHumans have a unique long postmenopausal lifespan, which may have evolved due to mother-child food sharing. This practice allows aging females to enhance their daughters' fertility, reducing selection for senescence. Combined with Charnov's dimensionless assembly rules for mammalian life histories, this hypothesis explains human late maturity, small weaning size, and high fertility. It also has implications for past human habitat choice, social organization, and the importance of extended learning and paternal provisioning in human evolution. Mother-child food sharing is common among primates, but only human mothers provide a significant portion of their weaned children's diets. This allows mothers to use resources they can gather efficiently, which children cannot. Postmenopausal women can earn high rates, helping feed their daughters' and nieces' offspring. This support is especially important for weaned children when their mothers forage less after a newborn's arrival. This division of labor suggests a solution to the riddle of menopause in humans. Other apes live no longer than about 50 years, with fertility failing alongside physiological decline. In humans, fertility ends around half that age, well before other physiological frailty. The question is how natural selection favored this distinctly human "postreproductive" component of life history. The "stopping early" hypothesis suggests that early termination of fertility would evolve when extended maternal care is crucial to offspring survival. Aging mothers who stop being fertile and focus on ensuring the survival of children already born would leave more descendants than those who continue risky pregnancies. However, this hypothesis is challenged by evidence from other primates, such as chimpanzees, where fertility does not end early. Human reproduction does not end early compared to other apes, and the difference lies in low adult mortalities, leading to long average lifespans after menopause. Two evolutionary explanations for aging are mutation-selection balance and inter-temporal tradeoffs in reproductive effort. Mutation-selection balance occurs when the force of selection is no greater than the mutation rate, leading to accumulation of deleterious effects. Inter-temporal tradeoffs lead to senescence because genes have multiple effects. Genes that are beneficial at younger ages may be disfavored at later ages. Senescence results from this antagonistic pleiotropy. Grandmothering could slow aging by either means. It would strengthen selection against late-acting deleterious mutations by increasing the contribution of longer-lived females through the reproductive success of their daughters. It would also change the tradeoffs between opposing effects expressed at different ages. Slower senescence generally comes at the cost of reduced fertility at younger ages. If ape adult mortalities are in equilibrium on this tradeoff, then apes age early by human standards because mutations that would increase adaptive performance at later ages are continually removed by the reductions those mutations impose on fertility earlier in life. Regular mother-child food sharing could perturb that equilibrium by increasing the payoffs for late somatic performance as vigorous senior