Originally posted on LifeApps…
Millions of years ago, in the middle of Africa’s jungles, our primate ancestors moved through the treetops in search of their food. The most energy-dense foods they could find were sugar-rich fruits. In an environment where predators could be around every corner, finding a fast-burning food source was essential for their fight or flight response.
However, in our modern day, there’s an over-abundance of sugary treats all around us. Resisting this temptation is now the real challenge. Our ability to perceive sugar’s sweetness initially evolved to guide our ancestors’ foraging activities, but in modern times it has become a vice for some battling the sweet allure of sugar. In this post, we will explore the genetics and evolution of sweet taste perception and how our sweet tooth is impacting us today.
Evolution of Sweetness
It may be difficult to imagine that sweetness is not strictly a property of sugar itself. The pleasant taste that sugar evokes for us is just our brain’s perception of glucose, sucrose or fructose molecules. This taste system, manipulated by evolution over millions of years, has been crucial to our ongoing survival.
The diet of our early hominid ancestors mainly consisted of forest fruit and leaves. But as the changing climate forced them out of the treetops and onto the African savannah, their dietary repertoire had to greatly expand. With all their novel food sources, taste became an important tool to identify food items that were rich in high-energy simple sugars, which were relatively scarce nutrients at that time (Mennella et al., 2017). The pleasurable sensation we experience when tasting something sweet developed as reward system to encourage us to seek out nutrient-rich food.
An extreme example of this occurs during pregnancy, when women’s taste perceptions become heightened (Faas et al., 2010). During pregnancy, acquiring sufficient nutrients becomes imperative, leading to unusual cravings and altered feeding behaviour. On the other hand, avoidance of toxins is vital for the protection of the unborn child. This leads to increased sensitivity for bitter-tasting, potentially toxic foods during pregnancy (Breslin, 2013). Dangerous compounds are now commonly experienced as bitter, even across a wide range of structurally diverse toxins.
But how exactly does taste perception arise and how has it been manipulated by evolution? To get an idea of this, we must venture down from our anatomy, to the genetic and molecular level.
You have around 10,000 taste buds, which are small structures known as papillae that are found on our tongue, cheek, throat, palate and tonsils. Within these papillae are taste pores, a small cluster of cells with little hair-like projections that interact with the food molecules that we eat. Each of the cells within the taste pore cluster use surface receptors (on the surface of cells) to detect different flavors such as sweet, salty, sour, bitter and umami.
When you eat, a sour, salty, sweet, bitter or umami cell receptor binds to its molecular target (compounds in your food). This triggers a molecular pathway that releases neurotransmitters (brain signaling compounds) and ATP (the energy currency of the cell) to communicate the signal to nearby neurons (nerve cells). Ultimately this pathway transmits the flavor stimulus to your brain. Taste receptors on the surface of different cells within the taste bud have evolved to bind with their specific molecular targets to elicit a certain flavor.
“In general, simple carbohydrates are experienced as sweet, the amino acids glutamate, aspartate and selected ribonucleic acids are experienced as savoury (or umami), sodium salts, and salts of a few other cations, are experienced as salty, acids are experienced as sour, and many toxic compounds are experienced as bitter.” – Breslin, 2013
Researchers at the University of Queensland recently used a taste test among genetic twins to explore variation in how intensely people perceive sweet taste. Based on their results, the researchers estimated that our genes help explain approximately 30% of the variance in how we perceive sweet taste (Hwang et al., 2015). The other 70% is partly due to environmental influences and our experiences with taste throughout life, as we know that taste is the most malleable of the senses. Age and other factors such as circulating insulin and leptin levels, which can vary from day to day and even by time of day, can also impact sweet perceptions. For example, children typically prefer higher concentrations of sucrose in a drink than adults.
Researchers have also recently identified novel genes associated with taste perception (Hwang et al., 2019).
Genetics of Sweetness
Our genetics can impact our sweet taste perceptions in two ways – directly and indirectly. The direct genetic link to taste perception involves the taste receptors themselves. Taste receptors are simply proteins, the product of genes once they have been translated. Two taste receptor genes, T1r2 and T1r3, are directly involved in sweet taste perception.
Genetic mutations, the means by which evolutionary change occurs, are carried through from the gene to the protein itself (a cell receptor in this case). A genetic mutation can change a taste receptor’s orientation. This change in orientation due to a mutation impacts how well food molecules can interact with the receptor, eliciting a stronger or weaker taste perception.
Throughout human history, a mutation in a taste receptor gene that improved taste acuity would have been beneficial for the survival of a given individual, allowing that mutation to be passed on to their children. This is how beneficial mutations become more prevalent in a population.
The second, indirect way that genes are linked to taste is more complex and involves the interpretation of signals coming from taste receptors by the brain. While genes indirectly linked with taste perception in this way have been largely unexplored, a recent study investigated how these genes might work in the brain to influence your sugar perception and intake.
In this study, researchers found that sweet taste might be controlled partly by genes involved in the movement of neurotransmitters (signaling molecules) between neurons in the central nervous system and brain, and genes relating to stomach inflammation and food intake (Hwang et al., 2019).
For the more than one billion people living in regions of the world plagued by low food security and severe malnutrition, the evolutionary adaptations of taste perception that help humans identify vital nutrients and calorie-dense foods are still useful. However, for those of us with reliable and ready access to nutrient-dense foods, the pleasure-seeking behavior of sugar overconsumption can be very difficult to resist. Sweet taste activates the reward centers of our brain through a mechanism similar to that of alcohol and other drugs. It has been proposed that the highly-refined and concentrated sugar in processed food is co-opting the neural pathways that were initially designed for advantageous sweet taste perception (Ventura and Worobey, 2013).
But while genes influence the voracity of your sweet tooth, early-life experiences with sugar also shape how much sugar we consume later in life. Sweet taste is also context-dependent. Repeated exposure allows us to get an idea of how sweet certain foods are meant to be. The prevalence of ‘super stimuli’ or ‘supernormal’ sweet foods with added sugar or sweeteners increases the threshold for what is “sweet enough” to our brains. Studies have found that children routinely fed sugar-sweetened water during the first six months of their life had a stronger preference for sweetened food from ages 2-10 years old (Beauchamp and Moran, 1984).
Substituting children’s sugar intake with calorie-free sweeteners has been proposed to counteract metabolic diseases such as obesity and type 2 diabetes. However, artificial sweeteners may actually increase our threshold for sweetness, whether as children or adults, making naturally sweet foods such as fruit not “sweet enough” in the future (Mennella et al., 2017).
Reducing overall intake of sweetness – both caloric sweeteners (sucrose) and non-nutritive sweeteners (aspartame) – may be a better strategy to lower rates of obesity than replacing the former with the latter (Mennella et al., 2017).
Breaking the Bonds of Sugar
While our preference for sugar-packed food was once a beneficial survival skill, we must overcome this evolutionary drive in order to increase our healthspan. The first step is to recalibrate our brain’s perception of sweetness, or to train our taste buds and brain to become more sensitive to sweet substances. We can do this by avoiding super-stimuli food and drinks. Bringing your brain’s sweetness threshold back down to normal levels will open your dietary repertoire to nutritious foods that were previously tasteless. Have you ever had to put sugar on your fruit to make it taste good enough? At one time, we did! But over time by eating things that are less sweet (dark chocolate, plain yogurt, unsweetened smoothies), super-sweet items that were previously a mainstay will become sickly sweet and unappetizing to you.
The second step is to reduce your food consumption in general (or intermittently, through intermittent fasting!). Leptin, the body’s satiety hormone, primarily controls your appetite and how much of your food’s energy is stored as fat. Leptin works in your body through a negative feedback loop – as leptin levels go up with food intake and fat accumulation, your appetite should go down. But the negative feedback loop between leptin levels and appetite becomes broken in obesity.
To achieve successful weight loss, people with leptin resistance have to recalibrate their bodies and cells to better respond to leptin. Slashing leptin levels in the body through interventions like intermittent fasting, reducing sugar intake, loosing extra fat through diet and exercise, and getting high quality sleep, can help.
Beside its role in food intake, leptin has also been shown to be a suppressor of sweet taste perception (Mizuta et al. 2008)! This only works if your body and taste nerves are sensitive to leptin; under healthy conditions, leptin will signal your taste receptors to have less of a preference for super sweet things! Reestablishing the body’s response to normal levels of leptin may turn out to be a two-birds-one-stone approach to weight loss and reducing sugar consumption.
These steps can form the basis for addressing sugar over-consumption and restoring a healthy diet. In the modern world, with sweet temptation all around us, resisting the urge for sugar could be a potent weapon in the fight against the rising tide of metabolic diseases.