Literature suggests that occupational stress is associated with a higher risk of metabolic syndrome; yet less is known whether other sources of stress have similar effects. This review aims to examine whether the relationship between psychological stress and metabolic syndrome differs by sources of stress. Three databases (PubMed, Web of Science, and CINAHL) were searched for eligible articles; metaanalyses were conducted using the random effects model. After controlling for covariates, adults in the high-stress groups had 45% higher chance of having metabolic syndrome than adults in the low-stress groups (odds ratio [OR] = 1.450; 95% confidence interval [CI], 1.211-1.735; P < .001). The subsequent meta-analysis based on cross-sectional studies suggested that occupational stress showed the strongest effect (OR = 1.692; 95% CI, 1.182-2.424; P = .004), while perceived general stress showed the weakest effect (OR = 1.217; 95% CI, 1.017-1.457; P = .032).Unfortunately, there is a lack of longitudinal studies for subsequent meta-analysis based on sources of stress. There is a need for continued research to examine the long-term relationship between different sources of stress and the risk of metabolic syndrome. Traditional recommendations for preventing metabolic syndrome (eg, low-fat diet and exercise) may not achieve the best outcome if clinicians overlook patients' psychosocial stress. KEYWORDS metabolic syndrome, occupational stress, perceived stress, psychological stress 1 | INTRODUCTION About 30% of adults have metabolic syndrome worldwide. 1,2 The economic burden of metabolic syndrome is substantial. For instance, the annual medical costs for Americans with metabolic syndrome are 60% higher than those without metabolic syndrome. [3][4][5] The development of metabolic syndrome is a multifaceted continuum of metabolic dysregulation, including hyperglycemia, hypertension, visceral adiposity, and atherogenic dyslipidemia. 6 Psychological stress has been linked to metabolic syndrome for decades, but its underlying mechanism is not yet fully understood.Allostasis refers to a normal physiological process where the brain activates the sympathetic-adrenal-medullary (SAM) and hypothalamic-pituitary-adrenal (HPA) axes and stimulates adrenal glands to release stress hormones (eg, corticosteroids) and catecholamine (eg, epinephrine and norepinephrine) to combat against stressful environmental demands. 7 According to the allostatic load framework (ALF), the repeated cycles of activation and deactivation of allostasis over time, or a failure to disengage the stress response during and after each stressful life demand, could alter adults' diurnal cortisol rhythm and decrease the capacity of glucocorticoids to suppress endotoxin-stimulated cytokine production, resulting in a