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A Taste for Fat

Taste

There is evidence for a direct role of the taste system in the consumption and preference of high-fat foods. Image: iStockphoto

By Russell Keast

Desensitisation to the taste of fat may be an important factor in the obesity epidemic.

The sense of taste presumably evolved to inform us about the nutritious or toxic value of potential foods. The primary organ responsible for the sense of taste, the tongue, contains taste receptors that identify non-volatile chemicals in the foods and non-foods we place in our mouth.

When food chemicals activate taste receptors, signals are sent from the taste receptors to processing regions in the brain. The signals are decoded by the brain and we perceive the taste of the food as one of five distinct qualities: sweet, sour, salty, bitter and umami (a savoury-like flavour that is very similar to chicken stock).

Taste can be regarded as a nutrient detection system. For example:

• sweet tastes are elicited by sugars, reflecting the presence of carbohydrates;

• sour tastes are elicited by free hydrogen ions, reflecting excessive acidity;

• umami is elicited by glutamic and other amino acids, reflecting protein content;

• salt is elicited by sodium and other ions, reflecting mineral content; and

• bitter reflects potential toxins in foods.

Excessive bitterness or sourness is aversive to us, and informs us that the food in our mouth may cause harm so the best action is to spit it out rather than swallow it. In contrast the qualities sweet, umami and salty are all appetitive, and tell us that the food contains essential nutrients such as carbohydrate, proteins and minerals, respectively.

As the taste system has evolved to detect the nutrients or toxins in foods prior to ingestion, it makes sense that fats, an essential energy-dense macronutrient required in limited amounts for energy and nutritional needs, would be detected through taste just like other macronutrients, namely carbohydrates and proteins, are detected through the tastes of sweet and umami.

My research program is investigating the ability to taste fat. The intake and regulation of dietary fats is especially important in the development of obesity, given their high energy density and palatability alongside their ability to promote excess energy intake. The intake and regulation of fats in the obese state appears especially problematic given that obese people prefer higher fat foods so that these represent significant portions of the obese diet.

Fat was classified as a taste as early as 330 BC by Aristotle and later in a 1531 AD text on physiology by Jean Fernell. More recently fat has been associated with texture, flavour release and thermal properties in foods, but not the sense of taste.

For fat to be generally accepted as a taste it must meet four criteria. There must be:

• a distinct class of stimuli;

• transduction mechanisms including receptors to change the chemical code of the stimuli to electrical signals;

• nerves fibres to carry the electrical signal to processing regions of the brain; and

• perceptual independence from other taste qualities.

The first evidence that fat may be a taste came from research on rodents in the late 1990s that clearly demonstrated a taste response that was specific to fat. This finding was the beginning of a sequence of discoveries in humans.

An effective class of stimuli in humans, fatty acids, was demonstrated when detection thresholds for a range of fatty acids was established under strictly controlled conditions in which other sensory inputs such as smell, touch and sight were all minimised as variables. This, along with mounting evidence in animals, strongly suggested that fatty acids, the components that make up fats, were the stimuli needed to elicit a fat taste.

Specific receptors that responded exclusively to fatty acids were also located on taste buds, partially satisfying the second criteria regarding transduction mechanisms.

The third criterion is supported by animal research demonstrating independent neural pathway for fat that interacts with brain processing regions associated with taste.

Perhaps the weakest evidence for a fat taste comes from perceptual studies relating to the fourth criterion, and this is where my research focuses.

I suspect that the term “taste”may be a misnomer, as taste implies a clear perception such as sweetness or salty. Fat, at levels we investigate, does not have a perceptual taste quality; rather, it is identified in solution at detection threshold, meaning that you know it is there (can perceive a difference from the same solution without the fatty acid) but cannot describe what it is.

At this point in time there is mounting evidence across species that fat is a taste that perhaps lacks a defined perceptual quality, such as sweetness.

A feature of the taste system is the large individual differences in sensitivity to chemicals in foods, and my research group uses these differences to help gain an understanding of the development of diet-related disease. Differential dietary practices among obese and lean individuals are well-established, especially regarding fat consumption and preference. For example, obese individuals have a preference for high-fat foods, and prefer a greater concentration of fat within specific food matrices compared with lean individuals.

However, changes in preferences for high-fat foods have been observed following 12–24-week dietary interventions involving fat restriction. A decrease in the pleasantness, taste and preference for high-fat foods suggests that the experience of fats in foods can be modulated by the diet.

In rodents, differences in sensitivity to the taste of fat appear to influence fat preference, consumption and predisposition to obesity, hinting at a novel role of the taste system in the control of both food intake and weight regulation. It has been established that different rodent strains are selectively more or less sensitive to fatty acids, and that differences in fat taste are inherently linked to dietary intake and preference.

Obesity-prone rodents that are less taste-sensitive to fatty acids have a preference for high-fat chow and become obese when exposed to a high-fat diet, whereas obesity-resistant rodents are more taste-sensitive to fatty acids, prefer carbohydrate-based chow, and resist weight gain by reducing their energy intake when exposed to a high-fat diet. Put simply, the more you taste fat, the less fat you eat.

We used this information from rodent studies to help guide our fat taste research in humans. The questions we wanted to answer was how and why fat taste would have such an important influence on the development of obesity. We provided some insight into these questions when we demonstrated a direct association between responses to fats within both the taste system and the digestive tract.

Differences in both the taste and digestive response to fat appear to play an important role in the regulation of fat intake, which appears to influence the regulation of bodyweight. In other words, if someone is less sensitive to the taste of fat, their digestive tract is also less sensitive to fat, and this seems to be linked to feelings of fullness during and after eating. If your body is not responding to the fat, then the fullness signals generated during the digestion of a meal are reduced.

Data from animal investigations provide strong evidence supporting our research. Robust differences in both taste and digestive sensitivity to fats are apparent among different rodent strains that are either less or more prone to the development of obesity as a result of excess fat consumption.

These data suggest that impaired fatty acid sensitivity at taste and digestive sites may encourage the development of obesity, and that this is promoted by a combination of both impaired taste detection that encourages a greater intake, coupled with impaired digestive detection that fails to induce fullness, thus encouraging the consumption of a larger amount of food.

We have also reported a direct relationship between taste sensitivity and body mass index (BMI) in humans. People who are less sensitive to the taste of fat (i.e. those who require a higher concentration for fatty acids to be detected) also have a higher BMI, and these observations are consistent within healthy and obese populations.

Given that the consumption of a high-fat diet can modulate the physiological response to fat ingestion, dietary patterns that encourage obesity are most likely accompanied by a number of changes that encourage the development of obesity, one of which appears to be reduced taste and digestive response to fat.

The existence of a sixth taste elicited by the digestive products of fat is yet to be confirmed but a growing body of evidence, including our research into humans, provides support for this proposition.

The ability to taste fats may have evolved similarly to the taste of sweet and umami, which indicate the presence of carbohydrates and proteins, encouraging the ingestion of energy-dense, nutritious foods.

In support of the functional significance of fat, we have shown that differences in taste sensitivity to fat appear to predict certain dietary behaviours. That is, decreased sensitivity to fat taste is associated with an increased consumption of fat, and this has been reported in both animal and human studies.

Moreover, we have also shown that sensitivity to fat can be modulated by the diet. Consumption of a high-fat diet appears to maximise the body’s capacity for fat absorption, with no associated changes in appetite, suggesting that such changes may accompany or encourage excess fat intake and obesity.

These data propose a direct role of the taste system in the consumption and preference of high-fat foods, which may be linked to the development of obesity given that differences in BMI have also been linked to oral fatty acid sensitivity. The mechanism we propose is via satiety or fullness signals, because associations in both the taste and digestive mechanisms have been reported for both.

The next 5 years will reveal conclusively whether fat can be classified as the sixth taste but, no matter what, there appears to be a functional significance to oral sensitivity to fats.

Russell Keast is Associate Professor in the Sensory Science Group at Deakin University.