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Benefits of Meditation and Yoga in Clinically Depressed Patients
Published in Anne George, Snigdha S. Babu, M. P. Ajithkumar, Sabu Thomas, Holistic Healthcare. Volume 2: Possibilities and Challenges, 2019
Madhuri Tolahunase, Rajesh Sagar, Rima Dada
Early-life adverse events and yoga in early life: The HPA axis is at the center of the comprehensive neurobiological model that seeks to explain the long-lasting consequences of stress. Early-life stress produces persistent increases in the activity of corticotropin-releasing hormone-containing neural circuits. Individuals who suffer from adverse life events in childhood show, as adults, a markedly enhanced activity of the HPA axis when exposed to stressors. Indeed, glucocorticoid receptor function is reduced in these individuals (so-called glucocorticoid resistance). These individuals also show increased activation of the inflammatory system, which is under physiological inhibitory control by cortisol. Indeed, glucocorticoid resistance, HPA axis hyperactivity and increased inflammation are all evident in depression. Practitioners of yoga show resilience to stress and don’t show decreased levels of cortisol and inflammatory markers. Yoga interventions in depression have shown to decrease cortisol and inflammatory markers. Therefore, to decrease the impact of childhood adversity on the health and wellbeing of the individual and prevent depression in adulthood, yoga may be adopted from the earliest point of life possible.
Antidepressants in pregnant and breastfeeding women
Published in Kathleen A. Kendall-Tackett, Depression in New Mothers, 2016
Until recently, researchers believed that antidepressants’ efficacy was due to their effects on the monoamine neurotransmitters, such as serotonin and norepinephrine. That conceptualization is accurate, but incomplete (Leonard, 2010; Maes et al., 2009). In a review of the literature, Maes (2001a) noted that most major classes of antidepressants, including TCAs, SSRIs, SNRIs, heterocyclics (e.g. trazodone), and MAOIs downregulate proinflammatory cytokines, including IL-1β and TNF-α, and increase glucocorticoid receptor functioning. Long-term therapy normalizes the inflammatory response system, including downregulating IL-6 and acute-phase proteins (such as C-reactive protein). He concluded that antidepressants may have their effect because of their immunoregulatory effects, an effect noted by several others (Kubera et al., 2004; Leonard, 2010; Pace et al., 2007; Roumestan et al., 2007; Vollmar et al., 2008). In addition, anti-inflammatory COX-2 inhibitors, such as Celebrex, boost the effects of the antidepressant reboxetine (Kiecolt-Glaser et al., 2015; Pace et al., 2007). COX-2 is a signaling molecule that can contribute to glucocorticoid resistance. Blocking it with a COX-2 inhibitor increases glucocorticoid resistance.
Endocrine hypertension
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Frances McManus, John M. Connell, Marie Freel
Glucocorticoid resistance is a rare, genetic disorder characterized by hypercortisolemia without the characteristic phenotype of cortisol excess. The syndrome is inherited in an autosomal recessive or dominant manner, and the most common genetic defects identified exist within the glucocorticoid receptor gene.52 This causes reduced peripheral activity of cortisol, and the ensuing compensatory increase in ACTH drive results in stimulated production of cortisol as well as adrenal androgens and ACTH-dependent mineralocorticoids deoxycorticosterone and corticosterone by the adrenal cortex.
Sleep disruption induces activation of inflammation and heightens risk for infectious disease: Role of impairments in thermoregulation and elevated ambient temperature
Published in Temperature, 2023
Sleep disturbance that becomes chronic induces repeated and recurring activation of the HPA axis. In turn, chronic elevation of cortisol leads to glucocorticoid resistance. In this instance, there is a decreased sensitivity to cortisol and glucocorticoids show a reduced potency or ability to constrain an inflammatory response [229]. For example in patients with chronic insomnia and short sleep duration, there is evidence of both increases in cortisol and increases in inflammation as evidenced by elevated levels of CRP and IL-6; elevated levels of cortisol do not effectively reduce inflammation because immune cells no longer “hear” this message [230]. The mechanisms that lead to glucocorticoid resistance with chronic sleep disturbance are not known. However, chronic stressors have been found to induce increases in endogenous damage-associated molecular patterns (DAMPs), along with activation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome. When the NLRP3 inflammasome is upregulated, leading to caspase- mediated cleavage of the glucocorticoid receptor, glucocorticoid resistance emerges [231]. A second mechanism pertains to the polymorphic variation in the gene encoding the glucocorticoid receptor; such variation correlates with anti-inflammatory signaling of glucocorticoids at the cellular level. This latter observations might explain heterogeneity in risk of inflammatory disorders among short sleepers at the population level; namely that chronic short sleep duration is associated with variance in glucocorticoid sensitivity [232].
Key considerations in the pharmacological management of treatment-resistant depression
Published in Expert Opinion on Pharmacotherapy, 2021
Mani Yavi, Ioline D. Henter, Lawrence T Park, Carlos Zarate
Another area of interest is traumatic childhood experiences. Studies have suggested that the association between the severity of such experiences and poor antidepressant treatment response may be due to the effects of trauma on the HPA axis, as evidenced by increased cortisol levels and glucocorticoid resistance [99]. This suggests that this subgroup with glucocorticoid resistance could be targeted for specified treatment. In this context, the second-generation tetracycline antibiotic minocycline is being investigated as a potential treatment for CNS inflammatory disorders; this agent, which has known immunomodulatory effects and has been shown to normalize glucocorticoid levels through its actions on the HPA [100], is able to cross the BBB and suppress inflammatory pathways directly at the microglia [101]. In addition to normalizing glucocorticoid levels and acting on the HPA axis, minocycline has also been implicated in the kynurenine pathway [102]. A large randomized controlled trial is in progress to validate the antidepressant efficacy of adjunctive minocycline treatment [103].
The impact of maternal asthma during pregnancy on fetal growth and development: a review
Published in Expert Review of Respiratory Medicine, 2020
Ashley S. Meakin, Zarqa Saif, Nabila Seedat, Vicki L. Clifton
Female placentae from pregnancies complicated by uncontrolled maternal asthma upregulated the nuclear expression of GRα A and GRα D3 translational isoforms and increased cytoplasmic GRα C expression in the presence of elevated cortisol concentrations [34]. These GR isoforms mediate glucocorticoid induced antiproliferation, apoptosis and inhibition of inflammatory cytokine function suggesting female placentae remained sensitive to glucocorticoids due to the localization and expression of specific GR protein isoforms. Male placentae of pregnancies complicated by uncontrolled asthma and elevated cortisol had increased cytoplasmic GRβ when compared with non-asthmatic controls (Figure 1) [34]. GRβ is a splice variant of GR gene known to antagonize the effects of GRα A and block glucocorticoid induced mechanisms. It is often associated with inducing a state of glucocorticoid resistance. Expression of GRβ protein in male placentae from asthmatic pregnancies was positively correlated with cord blood cortisol concentrations and suggested that as glucocorticoid concentrations increased intracellularly in the presence of maternal asthma, the male placenta induced a state of glucocorticoid resistance which would allow growth pathways to continue to function normally. The observed sex-specific differences in placental GR isoform expression and localization likely contributed to distinct differences in growth outcomes for male and female fetuses of pregnancies complicated by asthma.