Emotional dysregulation, working memory dysfunction, pro-inflammatory cytokines and appetite hormones in adolescents
Shao-Lun Ko1, Ya-Mei Bai2, Ju-Wei Hsu3
1Department of Psychiatry, Taipei Veterans General Hospital, Taipei, Taiwan; Department of Medical Education, Taipei Veterans General Hospital, Taipei, Taiwan.
Background:
Emotional dysregulation (ED) is common in adolescents with major affective disorders (MADs), including major depressive disorder and bipolar disorder. Its relationships with cognitive function, appetite hormones, and proinflammatory cytokines remain unclear.
Methods:
We studied 43 healthy adolescents and 104 adolescents with MADs, classified as without-ED (n = 25), deficient emotional self-regulation (n = 52), and severe ED (n = 27) based on the Child Behavior Checklist Dysregulation Profile scores. Cytokine levels such as C-reactive protein, interleukin-6, and tumor necrosis factor-α; appetite hormone levels such as leptin, adiponectin, ghrelin, and insulin; and cognitive functions were assessed. Group differences were analyzed using generalized linear models.
Results:
Adolescents with MADs and severe ED showed the fewest correct responses and the highest errors on working memory task, and had the highest C-reactive protein levels. Elevated leptin levels were associated with deficient emotional self-regulation in group comparisons, whereas increased tumor necrosis factor-α and insulin were linked to MADs regardless of ED severity. Interestingly, correlation analyses showed positive link between ghrelin levels and ED severity scores.
Discussion:
Severe ED in adolescents with MADs is associated with working memory dysfunction and higher CRP levels, while tumor necrosis factor-α and insulin elevations reflect MAD-related processes independent of ED. Ghrelin may be more of a state-dependent hormone then leptin that characterize ED and potentially linking pathological eating styles and broader psychopathological traits. Larger, longitudinal studies with additional control of eating disorder-related symptoms are needed to clarify the neurobiological mechanisms linking ED, working memory, and inflammatory-metabolic pathways.
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