This study investigates the association between metabolic syndrome (MetS) and epigenetic aging using two epigenetic clocks, GrimAge and DunedinPACE, in a population covering the adult lifespan. The study used twin data to control for genetic and familial confounding factors. The findings showed that individuals with MetS had higher epigenetic age acceleration compared to those without MetS, independent of lifestyle factors such as physical activity, smoking, and alcohol consumption. The association was stronger for GrimAge, but remained significant for DunedinPACE even after adjusting for lifestyle factors. Within-twin-pair analyses suggested that genetics fully explains the association for GrimAge and partially for DunedinPACE. The replication analyses confirmed that the association between MetS components and accelerated aging is independent of lifestyle factors considered in this study, suggesting that genetics is a significant confounder. The study highlights that MetS is associated with accelerated epigenetic aging, which may be explained by genetic factors. The results suggest that MetS components, particularly waist circumference and triglycerides, are associated with accelerated aging. The study also found that high blood pressure was associated with accelerated aging, although the association was weaker compared to other MetS components. The study concludes that genetic factors play a significant role in influencing the relationship between MetS components and epigenetic aging. Further research is needed to determine which lifestyle factors may mediate or moderate this association. Understanding the effects of different MetS components on epigenetic aging may lead to interventions that can slow down the aging process and prevent age-related diseases.This study investigates the association between metabolic syndrome (MetS) and epigenetic aging using two epigenetic clocks, GrimAge and DunedinPACE, in a population covering the adult lifespan. The study used twin data to control for genetic and familial confounding factors. The findings showed that individuals with MetS had higher epigenetic age acceleration compared to those without MetS, independent of lifestyle factors such as physical activity, smoking, and alcohol consumption. The association was stronger for GrimAge, but remained significant for DunedinPACE even after adjusting for lifestyle factors. Within-twin-pair analyses suggested that genetics fully explains the association for GrimAge and partially for DunedinPACE. The replication analyses confirmed that the association between MetS components and accelerated aging is independent of lifestyle factors considered in this study, suggesting that genetics is a significant confounder. The study highlights that MetS is associated with accelerated epigenetic aging, which may be explained by genetic factors. The results suggest that MetS components, particularly waist circumference and triglycerides, are associated with accelerated aging. The study also found that high blood pressure was associated with accelerated aging, although the association was weaker compared to other MetS components. The study concludes that genetic factors play a significant role in influencing the relationship between MetS components and epigenetic aging. Further research is needed to determine which lifestyle factors may mediate or moderate this association. Understanding the effects of different MetS components on epigenetic aging may lead to interventions that can slow down the aging process and prevent age-related diseases.