Patients with depression tend to have higher inflammatory activities as evidenced by elevated levels of pro-inflammatory cytokines including interleukin (IL)–6 and tumor necrosis factor alpha (TNF–α) [10], higher activity of sympathetic nervous system (SNS) and sympathetic outflow to the heart [11], disruption in the normal circadian rhythm of cortisol secretion [3], endothelial dysfunction [12] and metabolic risk factors [13]. This evidence concerns the gene TNF and depressive symptom measurement.