Exposure to early - life adversity — involving repeated and prolonged separation of a pup from its mother — results in
hyperreactivity of the sympathetic nervous system (SNS) and the hypothalamic — pituitary — adrenal (HPA) axis in adolescence and adulthood and elevations in anxiety, fearful behaviors, and hypervigilance (1 ⇓ ⇓ — 4).
Some studies document
hyperreactivity of the SNS and HPA axis following early - life adversity (15 ⇓ ⇓ ⇓ — 19) and others observe blunted HPA axis reactivity (20 ⇓ — 22) or discordance between SNS and HPA axis responses (23).
Although early - life adversity results in
hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic — pituitary — adrenal (HPA) axis in rodents, evidence from human studies is inconsistent.
Not exact matches
There was a significant association between the level
of exposure and bronchial
hyperreactivity: firefighters with a high level
of exposure were more likely to have
hyperreactivity than were those with a moderate level
of exposure (relative risk, 21.0; 95 percent confidence interval, 1.8 to 164; P = 0.01).
Our finding
of sinusitis, bronchial
hyperreactivity, and bronchial responsiveness in firefighters with World Trade Center cough is important but not surprising.17 - 20 An unexpected finding was that 87 percent
of such firefighters reported symptoms
of gastroesophageal reflux disease; such symptoms are generally reported by less than 25 percent
of patients with chronic cough.1, 21,22 Despite the strong associations between gastroesophageal reflux disease and chronic cough17 - 20 and between gastroesophageal reflux disease and asthma,23 - 25 it remains unclear whether gastroesophageal reflux disease causes either condition.26 The causative mechanism may be repeated aspiration
of minute amounts
of refluxed material; vagally mediated esophageal, tracheobronchial, or laryngobronchial cough reflexes; or neurally mediated bronchial inflammation.23, 24,26 Involvement
of the posterior nasopharynx is common in patients with gastroesophageal reflux disease, 27 whereas bronchial
hyperreactivity may not be present.25, 26 For these reasons, we classified gastroesophageal reflux disease as an upper - airway symptom (Figure 2).
Arhgef1 is required by T cells for the development
of airway
hyperreactivity and inflammation.
One study found a five-fold increase in bronchial
hyperreactivity in people with the lowest intake
of vitamin C.
With this deduction follows that the clinical picture
of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA - axis.
In animals, physiological
hyperreactivity induced by exposure to early - life adversity can be ameliorated by placement in an enriched environment during puberty (33), indicating that the neurobiological consequences
of early - life adversity may be reversed, at least in part, through improvements to the environment.