Sweet taste and blood pressure-related analgesia

Abstract

To test the prediction that sweet taste modifies responses to cold induced pain, 72 young adults held sweet, bitter and water solutions in their mouths, in counterbalanced order, before and during a cold pain stimulus. To test whether or not blood pressure interacts with sweet taste analgesia, measurements of resting blood pressure were also obtained. A significant main effect of taste on pain tolerance was observed, as well as a significant interaction between resting mean arterial pressure (MAP) and taste on tolerance. Sweet taste was associated with a prolongation of tolerance compared to the bitter and water conditions. When participants were split along the median for MAP, sweet taste was associated with an 18.1% increase in pain tolerance compared with water for those with lower MAP. No significant impact of taste on pain sensitivity was observed among participants with higher MAP. Groupwise comparisons revealed a significant difference in pain tolerance between participants with higher and lower MAP in the water condition but not in the sweet condition, replicating previous findings of a reduced sensitivity to pain among those with higher blood pressure. The analgesic effects of sweet tasting solutions seen previously in human infants and children may also be present in adults. Individuals with higher blood pressure may not be as sensitive to the presumably opioid-mediated analgesic effects of sweet taste, perhaps due to opioid dysregulation.

Stress-Induced Eating Dampens Physiological and Behavioral Stress Responses

“…Laboratory experiments have also demonstrated that sweet-tasting substances may provide analgesic effects during acute stressors, e.g. increasing pain threshold latency and pain tolerance during cold-pressor tasks [42,43]. Taken together, these findings suggest a general capability of comfort foods to elicit desirable affective or sensory responses in humans, which may function to reinforce stress-induced eating behavior.…”

Sucrose-induced analgesia is related to sweet preferences in children but not adults

“…Nevertheless, more research is warranted before one can conclude that sucrose is an ineffective analgesic during adulthood. For example, the efficacy of sweet taste in reducing pain appears to be moderated by resting blood pressure in normotensive young adults (Lewkowski, et al, 2003). That the increased pain tolerance induced by sweet tastes during the CPT was attenuated in individuals with high-normal blood pressure suggests that they may not be as sensitive to opioid-mediated sweet-taste analgesia, perhaps because of opioid dysregulation (Lewkowski et al, 2003;see Bruehl and Chung, 2004 for review).…”

“…For example, the efficacy of sweet taste in reducing pain appears to be moderated by resting blood pressure in normotensive young adults (Lewkowski, et al, 2003). That the increased pain tolerance induced by sweet tastes during the CPT was attenuated in individuals with high-normal blood pressure suggests that they may not be as sensitive to opioid-mediated sweet-taste analgesia, perhaps because of opioid dysregulation (Lewkowski et al, 2003;see Bruehl and Chung, 2004 for review). Whether the large proportion of overweight/obese individuals in the adult sample contributed to the lack of the analgesic effect is an important area for future research.…”

“…CPT is a classical experimental model for the induction of pain in children and adults (Miller et al,1994 ;Lewkowski et al, 2003). Modifying the previously published methods of Miller and colleagues (1994), subjects were told that they were going to play a game in which they will put their hand in a cold water bath.…”

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

“…Food 'liking' is conveyed to the frontotemporal cortical structures (Berridge, 2003;Kelley, 2004b) through m-opioid neurotransmission within the scattered network of subcortical and brainstem nuclei (Tanda and Di Chiara, 1998;Saper et al, 2002;Berridge, 2003;Berridge and Robinson, 2003;Pecina et al, 2003;Berthoud, 2004b;Kelley, 2004b;, including the NAc, VTA, ventral pallidum, nucleus of the solitary tract, parabrachial nucleus, and the amygdala. Opioids enhance food pleasantness (Doyle et al, 1993;Pecina and Berridge, 1995;, whereas consumption of high-energy sweet and fat food increases endogenous opiates release (ie, feedforward interaction; Tanda and Di Chiara, 1998;Colantuoni et al, 2002;Grigson, 2002) so that analgesia (Mercer and Holder, 1997a;Segato et al, 1997;Lewkowski et al, 2003), opioid dependence (Schoenbaum et al, 1989(Schoenbaum et al, , 1990Colantuoni et al, 2001Colantuoni et al, , 2002, and compensatory decrease of opiate gene expression in the reward structures (Kelley et al, , 2005 may ensue.…”