An extensive literature has linked off-time pubertal maturation to adverse health outcomes among adults. Childhood adversities are also linked to both pubertal development and cardiometabolic disease. Despite the racial and ethnic disparities in pubertal timing and cardiometabolic health in midlife, few studies have investigated if off-time pubertal maturation is associated with Latino individuals' metabolic syndrome. Furthermore, there exists limited data assessing early life risk factors affecting the association between timing of pubertal maturation and metabolic syndrome by sex and in young adults. This dissertation used a life course perspective to test developmental hypotheses of stress on reproductive strategies and cardiometabolic health to address these limitations. The three primary aims of this dissertation research were to 1) estimate the association between family dysfunction and timing of pubertal maturation in Latino boys and girls, 2) systematically review the impact of the timing of pubertal maturation on metabolic syndrome in young adults age 18-40 years, and 3) estimate the association between timing of pubertal maturation and metabolic syndrome in young adult Latino men and women. The analytic aims were explored using data from two population-based cohorts that include different age groups: the Hispanic Community Health Study/Study of Latinos (HCSH/SOL) Youth Ancillary Study (cross-sectional design) (8-16 years), and the Boricua Youth Study Health Assessment Ancillary Study (prospective design) (5-10 years and 18-23 years). The first empirical study, using HCHS/SOL Youth data, found that the presence of family dysfunction may be associated with delayed pubertal maturation in Latino children and adolescents. The systematic review highlighted the lack of diversity by sex, measurements, and racial/ethnic representation in this area of research, but also suggested that childhood BMI may account for much of the association between pubertal timing and metabolic syndrome. The second empirical study, based on the BYS HA study, did not find meaningful associations between timing of pubertal maturation and metabolic syndrome and cardiometabolic traits in young adults. These results do not support the prevailing hypotheses nor quantitative evidence linking off-time pubertal maturation to poorer cardiometabolic health. Overall, this dissertation utilized a life course perspective to advance understanding and support of the origins of adulthood cardiovascular risk that may begin in childhood. Future investigations should be designed to be longitudinal and include measures characterizing childhood body size, health behaviors, and environmental exposures. Future studies should also explore the specific mechanisms explaining the observed associations, particularly the complex interaction between hormonal and metabolic factors that appear to affect adult health among individuals with off-time pubertal maturation adversely.