to naloxone but a dampened response to psychosocial stress compared to 118A carriers32. The authors suggested that with a higher MOR affinity, 118G allele carriers have a greater inhibitory opioidergic tone on corticotropin releasing hormone neurons in the arcuate nucleus. As a result, exposure to naloxone led to the enhanced cortisol response32. Thus, the blunted response to psychological stress may result from a higher affinity of the mutant receptor, for this native opioid ligand brings about a differential response from the hypothalamic-pituitary-adrenal axis. It is, therefore, tempting to speculate that under normal conditions, the 118G allele imparts a ‘protective’ effect on carriers with a higher pain threshold. However, once that threshold is reached, 118G carriers will require higher amounts of opiates to achieve adequate pain control33 that may, unfortunately, not be obtained. As a result, the likelihood of addiction is increased and detrimental to this patient population.
