A narrative review of the construct of hedonic hunger and its measurement by the Power of Food Scale.

INTRODUCTION: The term 'hedonic hunger' refers to one's preoccupation with and desire to consume foods for the purposes of pleasure and in the absence of physical hunger. The Power of Food Scale (PFS) was developed as a quantitative measure of this construct in 2009. Since then, over 50 published studies have used the PFS to predict appetite-related outcomes including neural, cognitive, behavioural, anthropometric and clinical measures. OBJECTIVE: This narrative review evaluates how closely the PFS captures the construct it was originally presumed to assess and to more clearly define hedonic hunger itself. METHODS: The measure's relationship to four domains is reviewed and summarized: motivation to consume palatable foods; level of actual consumption of such foods; body mass; and subjective loss-of-control over one's eating behaviour. Findings are synthesized to generate a more accurate understanding of what the PFS measures and how it may relate to the broader definition of hedonic hunger. RESULTS: Results suggest that the PFS is closely related to motivation to consume palatable foods and, in extreme cases, occurrence of loss-of-control eating episodes. PFS scores are not consistently predictive of amount of food consumed or body mass. CONCLUSIONS: Implications of these findings are discussed in the context of behavioural health, and avenues for further inquiry are identified.

Genetic heterogeneity for autosomal recessive pyridoxine-dependent seizures.

Pyridoxine-dependent seizure (PDS) is a rare autosomal recessive intractable seizure disorder only controlled by a daily supplementation of pharmacological doses of pyridoxine (Vitamin B6). Although glutamate decarboxylase utilizes pyridoxal phosphate as a cofactor during conversion of the excitatory amino acid, glutamate, to the inhibitory neurotransmitter, gamma-amino butyric acid (GABA), several studies have failed to demonstrate a linkage to either of the glutamate-decarboxylase-encoding genes (GAD1 and GAD2) and PDS excluding involvement of this functional candidate. However, in 2000, a locus for PDS was mapped to a 5 cM interval at chromosome 5q31 in four consanguineous and one multisib pedigree (Z(max)=8.43 at theta=0 for marker D5S2017) [Cormier-Daire et al. in Am J Hum Genet 67(4):991-993 2000]. We undertook molecular genetic studies of six nonconsanguineous North American families, using up to ten microsatellite markers to perform haplotype segregation analysis of the 5q31 locus. Assignment to the chromosome 5q PDS locus was excluded in one of the six North American PDS pedigrees, as chromosome 5q31 haplotypes were incompatible with linkage to this locus. The remaining five PDS pedigrees showed haplotype segregation consistent with linkage to 5q31, generating a maximum combined lod score of 1.87 (theta=0) at marker D5S2011. In this study, we establish genetic heterogeneity for PDS, catalog 21 genes within the originally defined PDS interval, and identify additional recombinations that indicate a higher priority interval, containing just 11 genes.