The goal of the present study was to assess whether MDD, a disorder characterized by anhedonia, [1
] is associated with altered responses to sweet tastes measured via three SST metrics: sensitivity to sucrose, hedonic response, and designation as sweet-liking or sweet-disliking. The STT is a validated assay of sweet reactivity that predicts alcohol abuse disorder, seasonal affective disorder, and binge eating disorder [see 18
for a review]. Contrary to predictions, groups did not differ on the three measures of STT responsivity. Further, despite robust response to psychotherapy, there was no evidence of differential STT change in the MDD group after psychotherapy, relative to repeated STT assessment in the control group. These results suggest that MDD may not impact responses to sweet tastes.
The present findings confirm and extend the finds of Berlin and colleagues [24
] who reported equivalent hedonic responses to a range of sucrose solutions in MDD and stand in contrast to the portions of findings of Amsterdam and colleagues [26
] who found evidence of blunted intensity ratings and higher pleasure ratings to higher concentrations of sweet solutions in MDD. The present data also indicate that adults with MDD have similar hedonic sensitivity slopes and similar sweet liking/disliking status profiles. Though the precise reasons for differences between the present findings and the results of Amsterdam and colleagues [26
] is unclear, the present study is the first to report simultaneously of hedonic response to sucrose, sensitivity to sucrose, and sweet liking/disliking status profiles in individuals with MDD in a treatment context.
The STT has emerged as an indicator of risk for alcohol use disorders: “Sweet-likers” (i.e., those who prefer the highest STT sucrose concentration) are more likely to have alcoholism and/or a paternal history of alcoholism than “Sweet-dislikers” [19
]. Amsterdam and colleagues [26
] reported similar intensity and pleasantness ratings to lower sweet concentrations in MDD relative to a control group, but found that individuals with MDD gave relatively lower intensity and higher pleasantness ratings to higher sucrose concentrations. Kazes end colleagues [25
] reported a preference for sweets in MDD that did not change with antidepressant treatment (despite increased appetite). Finally, Berlin and colleagues [24
] reported equivalent hedonic responses to sucrose in adults with and without MDD. However, no study to date has examined hedonic sensitivity slopes nor the categorical characterization as a “sweet-liker” or “sweet-disliker” [18
A number of studies have indicated that MDD is characterized by disruptions of brain activation patterns in orbitofrontal, insular, and other limbic regions in response to images and monetary incentives [12
]. The present findings raise the possibility that MDD may impair cognitive evaluations of putatively pleasurable stimuli, yet leave intact more basic capacity for pleasure reactions. This pattern of findings raises the possibility that cognitive interventions may not need to focus on the sensory feeling of a pleasurable stimulus, but rather on the downstream cognitive mediation of response to such stimuli.
Response to sweet tastes are mediated by the nucleus accumbens [15
], the same region that is hypoactive to rewards in MDD [8
]. Additionally, orbital frontal networks both respond to gustatory information and regulate mood [38
]. However, brain imaging studies of reward processing in MDD have assessed responses to monetary incentives or responses to pleasant pictures [13
], and future neuroimaging studies that assess accumbens response to sweet tastes are needed. Nevertheless, the present findings suggest that anhedonia in MDD may not in fact extend to subjective responses to sweet tastes. This conceptualization is consistent with theories of anhedonia in MDD that suggest that this symptom domain may not reflect a global insensitivity to pleasure but rather reflect a tendency to undervalue rewards [39
We note that caution is warranted in interpreting our findings that groups did not differ statistically on all STT measures, which in this context is essentially confirmation of the null hypotheses that groups would not differ. Formal validation of the null hypothesis would require a bioequivalence analysis, a method to determine whether groups are sufficiently near each other to be considered equivalent [40
]. However, the sample sizes used here are far too small for such an approach, and thus we instead reported Cohen’s d
effect sizes [37
] in the pairwise contrast of the difference between the two groups for the continuous measures and odds ratios for tests of designation as Sweet-dislikers. All effect sizes were small or less-than-small, with the exception of sensitivity to sucrose, which yielded small-to-medium effects, suggesting that the findings of non-significant differences should be validated in larger samples.
Despite the limitation of small sample sizes, the patterns of data reported here reveal that response profiles of both groups were highly similar. These preliminary findings suggest that STT response profiles do not predict MDD status. This is in contrast to the utility of the STT to predict alcoholism and genetic vulnerability to alcoholism [19
]. These findings constrain the diagnostic utility of the STT in unipolar MDD, and suggest that anhedonia in MDD may not extend to sensory responses.