New strategies needed for investigating taste–obesity relationships
- Correspondence to Professor David G Laing, School of Women's and Children's Health, Faculty of Medicine, University of NSW, Level 3, Sydney Children's Hospital, High Street, Randwick, NSW 2031, Australia;
- Accepted 9 September 2012
- Published Online First 11 October 2012
Overberg and colleagues report that obese children and adolescents exhibited a lower ability to identify bitter, salty and umami taste qualities and perceived several sweet taste solutions to be weaker than their normal weight counterparts.1 These results disagree with those found in a recent study of taste perception in massively obese and non-obese adolescents,2 where the obese children detected lower levels of sucrose and sodium chloride than the non-obese group and gave higher ratings of perceived intensity of sucrose and salt. Poorer than normal taste perception by obese individuals has been reported by others as has the opposite claim that they have better perception of tastes. Although the findings from obesity and taste studies favour a lowering of taste perception in obese individuals, the association between taste and obesity is at best weak. For example, in the Overberg et al 1 study only 12% of the variability in the data was accounted for by the four variables examined, namely, weight status, age, sex and ethnicity.
The inconsistent results obtained using measures of taste sensitivity, identification and perceived intensity in various studies are mirrored in measurements of liking of the high energy-related tastes of sweet and fat. Thus, studies of liking for sucrose by obese subjects have reported that liking (1) increases with a monotonic increase in concentration, (2) increases to a maximum then decreases as concentration increases and (3) decreases with increased sweet concentration. The inconsistency in the data suggests a significant design feature is missing. Here I suggest that the design of studies of the relation between taste and obesity require a more sophisticated approach that focuses on the characteristics of the subjects chosen. A new strategy is needed.
It is well known that variations in obesity are largely inherited to the extent that the heritability of body mass index (BMI) calculated from population studies is about 70%.3 It is also well known that humans differ markedly in their ability to perceive a taste and there is a growing body of evidence that indicates genetic factors are important in determining taste perception in individuals and in causing obesity. Accordingly, it is suggested here that the missing feature in taste–obesity studies is the lack of attention to genetic differences when selecting individuals.
As regards a genetic basis for the variation in taste responses of individuals, the recent discoveries of receptors for sweet, bitter and savoury (umami) tastes provide opportunities to select individuals with particular genetic features that can result in wide differences in the ability to perceive particular tastes. To date, only the genetic basis for bitter taste perception by humans and sweet perception by different species have been studied in detail. In both types of investigation, the genetic factors were the alternative forms (alleles) of taste receptor genes. Thus, naturally occurring alleles of the bitter receptor gene (TAS2R38) are reported to be responsible for well-described individual differences in the ability to taste the bitter substance phenylthiouracil and its chemical relative propylthiouracil (PROP). Some people can taste very low concentrations of these substances while others cannot perceive even high concentrations. Family-based genetic studies have revealed the molecular basis of these latter effects and have shown that three variants of the gene account for 55%–85% of the variance in phenylthiouracil sensitivity. Of particular relevance to taste–obesity studies was a phenotype–genotype study of PROP sensitivity.4 Mothers and their children were genotyped and grouped according to one of the three variants and their bitter sensitivity determined. The data indicated that 64% of children of one variant type and 43% of their mothers were sensitive to the lowest concentration of PROP. Importantly, the phenotype–genotype relationship was modified by age with heterozygous children being more sensitive to the bitterness at the low concentrations of PROP when compared with adults with the same genotype. The authors suggest the difference may be due to adults becoming less sensitive with age because of experience, ageing and/or disease. Interestingly, the bitter gene variants also predicted sweet preferences in the children but found no relationship for adults where race/ethnicity was the stronger determinant. Importantly, the latter study represents a turning point for future studies of taste and obesity, which should recruit subject groups on the basis of genetic variation in relation to BMI and taste.
Unfortunately, genetic variation in taste sensitivity in humans has largely been confined to studies of bitter taste, a taste for which there are few foods that contribute to obesity. Encouragingly, studies of genetic variation in inbred strains of mice have shown that different alleles of the sweet receptor gene TAS1r3 correlate with sweet intake. Given the high level of interest in nutrition and health and the role of sweet-tasting foods to obesity, knowledge of the role of genetic variation in sweet taste in humans, therefore, may not be far off.
Defining groups of individuals on the basis of obesity-related characteristics, however, is already occurring. Several major genes contribute to the variation in obesity-related phenotypes in humans. For example, a strong genetic relation exists between serum leptin levels and obesity, and phenotypes have been found for per cent body fat and respiratory quotient, a metabolic measure. Leptin, the product of the obese (ob) gene, regulates adipose tissue mass through hypothalamic effects on satiety and energy expenditure. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Importantly, leptin is reported to provide a graded response in terms of body composition across a broad range of plasma concentrations. Interestingly, leptin receptors are expressed on sweet-sensitive taste cells in the human tongue and the diurnal variation in serum levels of leptin control sweetness sensitivity and food intake. Given the increasing number of genetic studies involving leptin and obesity, it would appear that leptin and its genetic variants provide strong candidates for incorporating into taste–obesity studies.
Another candidate is propiomelanocortin (POMC), a food intake reducing substance whose expression is regulated by leptin in the hypothalamus. Mutations in a POMC gene are reported to cause hyperphagia (high food intake) and the mutation MC4R is reported to cause a dominantly inherited obesity syndrome in different ethnic groups. Thus, in 500 severely obese individuals in the UK, 5% had pathogenic mutations of the MC4R gene, making this one of the commonest monogenic causes of obesity in humans.5 Furthermore, in a Danish study of young men, 2.5% of those with a BMI >30 had a pathogenic mutation in MC4R.6 These examples of genetic variation and relationship with obesity represent only a few of the potential factors that could be incorporated as variables in taste–obesity studies.
In summary, whether there is a relationship between taste and obesity is unresolved. The Overberg et al study provides results which agree with some findings but are different to those found in others. In essence, the study further highlights the inconsistent results reported from different studies over many decades. In this editorial, I have suggested that the underlying problem with these studies is that the choice of subjects has not been based on factors that are linked to variation in taste perception of the most common tastes, for example, sweet, salt, sour and umami, and obesity. Until this can be achieved, inconsistent data will continue to be reported.
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.