Current Psychiatry Reviews - Volume 11, Issue 1, 2015

Objective: To perform an exploratory review of the association between autonomic function and depressive symptoms/major depressive disorder (MDD) with a particular emphasis on their combined impact on cardiovascular health across the lifespan. Method: A review of computerized databases was performed using PubMed, Medline, PsycINFO, Scopus, Google Scholar, and BioMed Central from 1950 – 2013. Articles that primarily focused on the association between depression/ MDD and autonomic function, notably cardiovascular health, were included for review. The search was augmented by tracking citations from reference lists of original reports included in the review. Seven hundred and thirty seven articles were screened, 89 articles met criteria for inclusion and 54 articles were incorporated to the current review. Results: Three large scale epidemiological studies were identified; their results suggest that autonomic dysfunction is consistently present among individuals experiencing depressive symptoms and/or clinically diagnosed with MDD. Moreover, autonomic dysfunction is implicated with elevated risk for cardiovascular disease (CVD) and its associated mortality. Studies have reported that autonomic dysfunction is present in the context of depression (depressive symptoms as well as clinically diagnosed MDD) across the life span with males and females reported to be differentially affected. The role of antidepressants in ameliorating autonomic dysfunction associated with MDD and depressive symptomatology has mixed results. Conclusion: Autonomic dysfunction is a marker of depression. Autonomic dysfunction can be measured, not only in the laboratory, but also in the clinical ecosystem. Among individuals experiencing depressive symptoms and/or clinically diagnosed MDD, autonomic dysfunction may represent a biomarker for a subpopulation at increased risk of developing CVD.

Objective: Anorexia nervosa is a severe pathology often associated with malnutrition. It is known that starvation could result in various anxious and depressive symptoms, often mentioned in eating disorders. Indeed, a lowering of plasma tryptophan through restrictive behaviours could cause a decrease in brain serotonin synthesis and give rise to these symptoms. The aim of this article was to review studies assessing plasma tryptophan and blood serotonin in anorexia nervosa, peripheral markers of the serotoninergic system. Method: A systematic computerized search was performed in Medline for all studies published between 1980 and 2012. A total of 9 studies for tryptophan and 5 studies for serotonin were reviewed for their methods, protocols and results. Results: The characteristics of sample populations and studies protocols are very heterogeneous. Nonetheless, most studies find that during the acute phase of anorexia nervosa plasma tryptophan is lowered but not blood serotonin. Discussion: Further research with longitudinal design and larger samples is needed to confirm these data. Peripheral serotoninergic markers could be a promising and non invasive way to explore how malnutrition really affects the serotoninergic system.

Sudden gains are relatively large, quick, stable drops in symptom scores during treatment of depression that may (or may not) signal important therapeutic events. We review what is known and unknown currently about the prevalence, causes, and outcomes of sudden gains. We argue that valid identification of sudden gains (vs. random fluctuations in symptoms and gradual gains) is prerequisite to their understanding. In Monte Carlo simulations, three popular criterion sets showed inadequate power to detect sudden gains and many false positives due to (a) testing multiple intervals for sudden gains, (b) finite retest reliability of symptom measures, and (c) failure to account for gradual gains. Sudden gains in published clinical datasets appear similar in form and frequency to false positives in the simulations. We discuss the need to develop psychometrically sound methods to detect sudden gains and to differentiate sudden from random and gradual gains.

This article introduces a systems biology model of the psycho-immune-neuroendocrine (PINE) network. It provides a comprehensive synthesis of the network of biological mechanisms which link major depressive disorder (MDD) with several diseases including hypertension, atherosclerosis, coronary heart disease (CHD), cerebrovascular accident (CVA) and type 2 diabetes. The first part of this article provides an overview of concepts such as the PINE physiome and pathome, as well as the application of a systems biology framework to explain the significant reciprocal associations of MDD with the above named medical illnesses. The second part describes the normal physiological pathways of immune mechanisms, the hypothalamic-pituitary-adrenal (HPA) axis, autonomic pathways and central nervous system function, which form the PINE physiome. The third section describes how homeostasis of the PINE physiome is disrupted by chronic stress, on a background of genetic and developmental diathesis factors, resulting in a network of pathophysiological pathways called the PINE pathome. MDD, CHD, type 2 diabetes, CVA, hypertension and atherosclerosis can act to maintain the PINE network in a stable pathological state. This article presents comprehensive topographical maps of both the PINE physiome and the PINE pathome. Implications of the model and the importance of adopting a systems approach to understanding the relationship between these diseases is discussed in the last section, including the possibility of novel treatments for MDD and areas of future research.

Understanding sleep complaints among menopausal women is an emerging area of clinical and research interest. Several recent reviews have focused on mechanisms of menopausal insomnia and symptoms. In this review, we present a discussion on the most relevant and recent publications on the treatment of sleep disorders for menopausal women, with a focus on menopause-related insomnia, insomnia symptoms, and obstructive sleep apnea. We discuss both nonpharmacological and pharmacological treatments, including cognitive-behavioral therapy for insomnia (CBT-I), complementary and alternative medicine, hormone replacement therapy, sedative hypnotics, antidepressants, and continuous positive airway pressure. In addition, we briefly discuss methods and considerations of assessment of sleep disorders in menopausal women.