Australasian Science: Australia's authority on science since 1938

Sugar Cravings

Credit: Yurok Aleksandrovich

Credit: Yurok Aleksandrovich

By Daniel Hwang

We all differ in our sensitivity to natural and artificial sweeteners, but how much of this is genetic and how much due to the influences of our sugar-fuelled culture?

While some people love the taste of Tim Tam biscuits, others find them too sweet. Our research suggests that our genes influence these individual differences in the perception of sweetness.

Taste has a significant impact on our life. It contributes to our enjoyment by stimulating a desire to eat, and therefore plays an essential role in our selection of food and nutrients. It also acts as a natural defence against food poisoning by alerting us to spoilt foods and potential toxic compounds.

We can perceive five basic taste qualities – sweetness, saltiness, sourness, bitterness and umami (savoury) – with sweetness generally considered pleasant by most people across all ages. Sweetness signals the presence of carbohydrates, the main energy source for the human body, and hence is essential for feeding, metabolism and early development.

However, not everyone has a normally functioning sense of taste. One in every ten Australian children is unable to taste food properly, and has difficulty distinguishing one taste quality from another. In the USA more than 200,000 people each year seek medical advice for taste or smell problems, which include changes in taste quality, intensity or hallucinations. The exact causes behind this are not fully understood, but may result from normal ageing, head injuries or a side-effect of chemotherapy and radiotherapy.

These taste problems can have a severe impact on health and life quality. For instance, the primary cause of morbidity in 20% of cancer patients is malnutrition rather than malignancy. Cancer treatments can alter sensory perception, with food becoming tasteless or in some cases possessing a metallic taste. This leads to a further decrease in dietary intake and the development of food aversion.

Taste perception also varies widely between healthy individuals – think about how many teaspoons of sugar you and others add to tea or coffee– with such differences affecting health and well-being. For example, people with weaker taste sensitivity are more susceptible to certain diseases, such as obesity, diabetes and hypertension, because they need to consume more salt, sugar or fat to have the same taste sensation.

What are the causes of the differences in sweet taste? When we eat, food chemicals are detected by taste receptors in taste buds on the tongue,. A signal is sent through taste nerves to the brain, where the taste is identified and a sensation of pleasantness or aversion is elicited.

In 1990, researchers found that heightened sweet taste sensations could be due to the increased number of taste buds on the tongue. About 10 years later it was proposed that differences in signal processing in the central nervous system also cause differences in taste perception. More recently, genetic studies have revealed that sweetness perception is related to variations in sweet taste genes. However, the magnitude of the genetic influence has not been resolved.

Is our sensitivity to sweetness simply due to biological inheritance? Or is it acquired through environmental exposure, such as diet, education, socioeconomic status or culture? The aim of our study was to estimate the strength of genetic and environmental effects on our sensitivity to sweetness.

Sugar is the main source of sweetness, and is used to enhance the palatability of food and drink. In the past decade, the use of aspartame, saccharine and many other artificial sweeteners as sugar substitutes has significantly increased because of their low or non-caloric characteristics. Interestingly, mice use different sweet taste systems to detect sugars and sugar substitutes. Whether the same systems exist in humans is unclear.

We studied the sweet tastes of two sugars (glucose and fructose) and two sugar substitutes (aspartame and neohesperidine dihydrochalcone). The two sugars are sources of sweetness in fruits, vegetables, honey and many other natural products. The two sugar substitutes are hundreds of times sweeter than sugars of the same concentration, and are widely used as food additives in sugar-free or non-caloric foods and drinks, such as sugar-free pudding, chewing gum and diet soft drinks and flavoured water.

The project was part of the Brisbane Adolescent Twin Study. Twins are very important for studying genetic effects because of their biological similarities and differences. Since identical twins share 100% of their genes while non-identical twins and siblings on average share only half of their genes, if identical twins have more similar sweet taste than non-identical twins it is evidence of the strength of genetic influence. Utilising this concept, we were able to estimate the extent to which sweet taste is exclusively attributable to differences in our genes.

In order to accurately estimate genetic effects, a large sample size is necessary. After more than 10 years of data collection, the study amassed a sample of 1901 participants, comprising 243 identical and 452 non-identical twin pairs and 511 non-twin individuals. This provided us with sufficient power to examine genetic influences on sweetness perception.

Twins and their siblings aged between 12 and 26 years old were asked to taste solutions of the four sweeteners and then rank them on a scale ranging from no sweet sensation to the strongest imaginable sweetness. Our results revealed that around 30% of sweetness is due to genetics, regardless of the sweetness source tested (sugar or sugar substitute). Since our sweet taste is partially encoded in genes that are passed from our parents and ancestors, it would not be surprising to see family members possess similar preferences towards sweet foods.

In addition, the study results showed that the sweet responses to these four sweeteners were highly correlated. For example, if you perceive glucose to be intensively sweet, then you are also likely to find fructose, aspartame and neohesperidine di­hydrochalcone highly sweet.

The results also suggested that there is a single set of genes responsible for the perception of all four sweeteners. This suggests that, unlike mice, humans use the same system to detect sweetness in both sugars and sugar substitutes.

Intriguingly, your favourite childhood lollies or sweets may become less tasty or even unpleasant as you age. Most people may notice their preference for sweet foods changes with time. Our study showed that human perception of sweetness decreased by 2–5% per year. This suggests that the sweet taste system changes from childhood to adulthood, and may explain why children are more sensitive to sweetness than adults. This lessening of taste perception is also found for bitterness, and applies to the majority of the population.

We also found that individuals with a history of middle ear infection had a stronger sweet response. These results were unexpected, as middle ear infections are generally thought to lower taste sensation by damaging the taste nerve that runs from the tongue to the brain. It has been proposed that middle ear infections can lead to an increase in the number of taste buds in compensation for the loss of taste sensation. Individuals recovering from middle ear infection would therefore have more taste buds than they had prior to the infection, and this in turn may result in a stronger taste response.

If sweet taste is indeed influenced by genetics, does this mean that people with weaker sweet perception are likely to keep adding more sugar to their diet? If so, this could lead to a serious public health problem in which obese individuals become even more obese.

Fortunately, this is not necessarily the case. Our study also suggested that part of the sweetness is related to environmental factors. As such, it is still possible for people to change their dietary habits through education or dietary management.

Our next steps are to identify key genomic regions responsible for individual differences in sweetness, with the hope of understanding the underlying molecular mechanisms of human sweet taste perception. The research may provide new strategies to reduce dietary sugar intake and provide clues to solving taste disorders, which can have a significant impact on eating patterns and nutritional status and consequently are a risk factor for heart disease, diabetes and stroke.

Daniel Hwang is a PhD student in the Genetic Epidemiology Group at the QIMR Berghofer Medical Research Institute.