| Summary: | Thesis (Ph.D.)--Memorial University of Newfoundland, 1995. Psychology Bibliography: leaves 131-161 Previous studies with animals and human infants have found that the ingestion of palatable sweet solutions produces a morphine-like analgesia (e.g., Blass, 1986; Blass & Hoffmeyer, 1991). This "sweet-induced analgesia" can be reversed by minimal doses of naltrexone, an opioid antagonist, suggesting that sweets operate through an endogenous opioid system (e.g., Blass, Fitzgerald, & Kehoe, 1987). This thesis investigated whether sweet-induced analgesia occurs in human adults. In the present experiments, subjects (330 university undergraduates) were exposed to cold water (Expt.l), pressure (Expts. 2a-2c), or contact heat (Expts. 3a-3b) and then assessed for pain sensitivity. Subjects then consumed either nothing (control group), or foods that they rated previously as unpalatable (e.g., black olives), neutral (e.g., rice cakes), or palatable (e.g., chocolate-chip cookies). Following a brief delay (approx. 5 min) , subjects were exposed a second time to the cold water, pressure, or contact heat and again assessed for pain sensitivity. Pain sensitivity was assessed with four pain measures: pain threshold, pain tolerance, and visual analogue scale (VAS) ratings of painintensity and unpleasantness. Tactile thresholds were also measured before and after treatment. Results showed that sweet palatable foods appeared to produce significant increases in females' pain tolerance to contact heat and to pressure. However, pain thresholds, VAS measures, and tactile thresholds were not consistently affected by sweet intake. Gender differences in pain perception were also present; females reported lower pain thresholds and pain tolerances and rated the pain as more intense and more unpleasant than did males. -- These data constitute the first demonstration that sweet-induced analgesia occurs in human adults. Sweet induced-analgesia is thought to operate through an endogenous opioid system whereby sweet consumption causes the release of opioids into the CNS, resulting in pain- inhibition. However, the present results also indicate that this sweet-induced analgesia is influenced by a number of factors, including the method of pain induction, the type of pain measure, and the gender of the subjects. Moreover, the palatability of the ingesta seems to be a critical factor in producing analgesia. Collectively, the present results suggest that a more accurate label for sweet-induced analgesia may be "palatability-induced analgesia".
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