Could the a link between food and obesity be right on the tip of our tongue? Prof Russell Keast from the School of Exercise and Nutrition Sciences attempts to answer this question.
When food is eaten, nutrients (fats, carbohydrates, and salt) or their digestive products (fatty acids, sugars, and sodium) are ‘sensed’ by specialised receptor cells within the mouth and in the gastrointestinal (GI) tract. These interactions lead to taste perceptions and alterations in the GI tract, such as the slowing of food leaving the stomach and hormone secretion, which lead to the development of satiety or feeling full.
Impaired oral and GI sensing to the breakdown products of dietary fat (i.e. fatty acids) may be associated with increased energy consumption. To test this, in a recent blinded crossover study, participants were asked to consume a high fat, high protein, high carbohydrate and a balanced macronutrient breakfast on four separate days. Following each breakfast, participants were required to consume a buffet-style lunch until they felt comfortably full.
Following the high fat breakfast, participants with an impaired ability to taste fat in foods, consumed significantly more energy (2.1 ± 0.8 MJ) and grams of food (237.70 ± 46.37g) at lunch compared to other participants. There were no significant differences in the amount of energy or grams of food consumed at lunch or in perceived satiety, between participants after consumption of the other breakfasts.
This study demonstrated that impaired fatty acid sensing was associated with excess energy consumption following a high fat meal. As excessive consumption of fat is a common feature in obesity, impaired ability to taste fat may be a causal factor in the development of obesity.
While there are undoubtedly many factors involved in the development of obesity, the identification of a potential causal factor is an important finding in the search for strategies to reduce the incidence of obesity.
Prof Russell Keast
School of Exercise and Nutrition Sciences, Deakin University