Abstract
It is well known that the taste of sweet solutions produces a morphine-like analgesia in both rats and human infants, and under certain conditions, possibly in human adults. To further explore whether ingestion analgesia persists into human adulthood, the present study was the first to utilize contact heat, a method of pain induction used commonly in both behavioural and pharmacological studies with laboratory animals. Left arms of 120 university undergraduates were exposed to a hot-plate, with pain responsivity assessed both before and after consuming 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). Pain responsivity was assessed with four pain measures: pain threshold, pain tolerance, and visual analogue scale (VAS) ratings of pain intensity and unpleasantness. Between-groups comparisons in 2 separate experiments revealed that women (but not men) who consumed a palatable food showed increased pain tolerance, relative to the nothing, unpalatable, or neutral groups. Collectively, these data support our previous findings that “palatability-induced analgesia” exists in human adults, at least in females. Moreover, the findings support contact heat as a suitable method for assessing ingestion analgesia to experimental pain with human adults.
Highlights
It is well established that the consumption of sweet ingesta increases endogenous opioid peptide (EOP) ac-How to cite this paper: Mercer, M.E., Holder, M.D. and Adams, R.J. (2015) The Effects of Palatable Sweet Ingesta on Human Responsivity to Heat Pain
The present findings are the first to demonstrate that contact heat is a suitable, if not superior, method for the assessment of ingestion analgesia in human adults, at least among females
Women who ingest palatable food endure contact heat pain for longer durations than women who consume nothing, or foods rated as unpalatable or neutral. It appears that ingestion analgesia, or perhaps more accurately, palatability-induced analgesia (PIA), does persist beyond infancy
Summary
It is well established that the consumption of sweet ingesta increases endogenous opioid peptide (EOP) ac-How to cite this paper: Mercer, M.E., Holder, M.D. and Adams, R.J. (2015) The Effects of Palatable Sweet Ingesta on Human Responsivity to Heat Pain. Experimental studies show that intraoral sweet solutions (either dextrose/saccharin, or sucrose) increase rats’ paw-lift latencies from a hot-plate [8]-[10], an analgesic effect resembling that produced by morphine This “sweet-induced” analgesia (SIA) is reversed by minimal doses of an opioid antagonist (e.g., naltrexone, naloxone), suggesting that EOPs are primarily responsible for mediating the analgesic effect [8] [9] [11]. Rat pups who consumed one of a variety of other preferred foods (e.g., milk, corn oil, polycose, or chocolate) showed reduced pain responsivity [19]-[22] These findings support the hypothesis that it is the pleasant or desirable taste of the ingesta that produces the analgesic effect, as opposed to its specific sugar or caloric content per se
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