The Role of Anxiety in Metabolic Syndrome

Aline Sardinha; Antonio E Nardi


Expert Rev Endocrinol Metab. 2012;7(1):63-71. 

In This Article


MS is likely to develop in patients in whom genetic predisposition, chronic stress, negative emotion and unhealthy lifestyle habits converge. Anxiety and depressive disorders are linked to higher cardiometabolic risk, higher incidence of acute cardiovascular events and poorer prognosis for cardiac patients. In addition, they seem to be comorbid to a range of other chronic internal diseases. The current literature on the metabolic mediation of this relationship provides evidence for an association between psychological characteristics and the development of MS, which could eventually increase cardiovascular disease risk.

The authors consider the results presented here of considerable interest, once the link between psychological variables, such as depression and stress, and cardiovascular problems have long been established and the current literature points to an independent role of anxiety and negative cardiovascular outcome. This review shows that even though there is considerable evidence for the role of anxiety in cardiovascular problems, state-of-the-art literature does not support that metabolic alterations are a plausible physiological underlying pathway for this association. Negative health behaviors and hypothalamic dysregulation and sympathetic hyperactivation are the most commonly mentioned plausible underlying pathways (see Figure 1).

Figure 1.

Psychological factors, metabolic syndrome and cardiac risk. HPA: Hypothalamic–pituitary–adrenal.

Prospective data, although limited, suggest that depression, stress, hostility and anger, but not anxiety, independently predict increased risk of developing MS. The coexistence of anxiety in MS patients seems to be a byproduct of anxiety–depression or anxiety–stress comorbidity. The HPA axis dysregulation observed in MS patients may also be explained by alternative factors, such as visceral obesity's influence on HPA axis activity. Adverse functioning of the ECS can also mediate the stress–fat distribution relationship.

More prospective studies conducted with diverse samples are needed to delineate the direction of this relationship and to assess the roles of the proposed behavioral mechanisms. To test for causality, further animal experimental investigations might provide more reliable evidence. Even though the details of the causal process remain unclear, one can certainly affirm that patients presenting with psychological distress, such as anxiety, depressive symptoms and chronic stress, are in danger of metabolic alterations and of a negative cardiovascular prognosis. This is because the constant activation of the HPA and the sympathetic nervous system promoted by anxiety responses triggers cardiovascular dysregulations such as elevated heart rate and blood pressure.[53]


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