Anxiety disorders increase risk for the early development of several diseases of aging. Elevated inflammation, a common risk factor across diseases of aging, may play a key role in the relationship between anxiety and physical disease. However, the neurobiological mechanisms linking anxiety with elevated inflammation remain unclear. In this review, we present a neurobiological model of the mechanisms by which anxiety promotes inflammation.
In anxiety disorders, such as posttraumatic stress disorders and phobias, classical conditioning pairs natural (unconditioned) fear-eliciting stimuli with contextual or discrete cues resulting in enduring fear responses to multiple stimuli. Extinction is an active learning process that results in a reduction of conditioned fear responses after conditioned stimuli are no longer paired with unconditioned stimuli. Fear extinction often produces incomplete effects and this highlights the relative permanence of bonds between conditioned stimuli and conditioned fear responses.
Fear and anxiety are debilitating conditions that affect a significant number of individuals in their lifetimes. Understanding underlying mechanisms of these disorders affords us the possibility of therapeutic intervention. Such clarity in terms of mechanism and intervention can only come from an amalgamation of research from human to animal studies that attempt to mimic the human condition, both of which are discussed in this review. We begin by presenting an outline of our current understanding of the neurobiological basis of fear and anxiety.
Anxiety disorders are highly prevalent and debilitating psychiatric disorders. Owing to the complex aetiology of anxiety disorders, translational studies involving multiple approaches, including human and animal genetics, molecular, endocrinological and imaging studies, are needed to get a converging picture of function or dysfunction of anxiety-related circuits.
Gene expression and regulation is an important sculptor of the behavior of organisms. Epigenetic mechanisms regulate gene expression not by altering the genetic alphabet but rather by the addition of chemical modifications to proteins associated with the alphabet or of methyl marks to the alphabet itself. Being dynamic, epigenetic mechanisms of gene regulation serve as an important bridge between environmental stimuli and genotype. In this review, we outline epigenetic mechanisms by which gene expression is regulated in animals and humans.
American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics
Genetic factors appear to be highly relevant to predicting differential risk for the development of post-traumatic stress disorder (PTSD). In a discovery sample, we conducted a genome-wide association study (GWAS) for PTSD using a small military cohort (Systems Biology PTSD Biomarkers Consortium; SBPBC, N?=?147) that was designed as a case-controlled sample of highly exposed, recently returning veterans with and without combat-related PTSD.
BACKGROUND: While many cancer patients derive strength from spiritual or religious faith, concern often remains regarding how different patient subgroups and other community members might react to faith-based services when sponsored by a secular health care organization. METHODS: "A Sacred Gathering for Those Touched by Cancer" was presented in 2 Catholic and 2 Protestant churches. The service included key themes (surrendering fear, peace, hope, community support, and God's love) reinforced by Scripture, music, ritual, and prayer. Patients, clergy, and staff participated.
From the perspective of the terror management health model (TMHM), expectancies as to whether a health behavior is likely to effectively protect one's health (i.e., response efficacy) and whether an individual is optimistic about the outcomes of his or her health risk assessment (i.e., health optimism) should have a more potent influence on health decisions when thoughts of death are conscious and the health risk domain is potentially fatal.
OBJECTIVE: Fear of pain and pain catastrophizing are prominent risk factors for pediatric chronic pain-related maladjustment. Although resilience has largely been ignored in the pediatric pain literature, prior research suggests that optimism might benefit youth and can be learned. We applied an adult chronic pain risk-resilience model to examine the interplay of risk factors and optimism on functioning outcomes in youth with chronic pain. METHOD: Participants included 58 children and adolescents (8-17 years) attending a chronic pain clinic and their parents.
Despite many studies on the age-related positivity effect and its role in visual attention, discrepancies remain regarding whether full attention is required for age-related differences to emerge. The present study took a new approach to this question by varying the contextual demands of emotion processing. This was done by adding perceptual distractions, such as visual and auditory noise, that could disrupt attentional control. Younger and older participants viewed pairs of happy-neutral and fearful-neutral faces while their eye movements were recorded.
