Obesity is complex but certain factors are simple. Obese people prefer calorie-dense foods because they taste better. That’s how we become obese. That raises an interesting question. Why do the least healthy foods taste so good? Rich, sugary, fatty foods aren’t good for anyone. Yet, everybody loves them. Why is that? Aren’t our taste buds supposed to be a protective mechanism? And, of course, why do overeaters seem to like calorie-dense foods more than normal eaters? As it turns out there’s more to taste than meets the tongue. Also, what meets the tongue in normal eaters and overeaters is very different. More importantly, these differences are a key part of the obesogenic puzzle.
Origins of Taste
Taste appeared over 500 million years ago as a way of avoiding toxins and finding nutrients. All vertebrates have taste. Taste was so important to humans it changed our history; the European’s pursuit of spices launched the age of exploration.
Personal taste preferences begin before birth. In utero, amniotic fluid, which contains glucose, fructose, amino and fatty acids, is our first food. Humans also have an innate taste for sugar because newborns prefer the sweet taste of breast milk. However, maternal eating habits during pregnancy and nursing can influence children’s taste preferences. A study showed pregnant and nursing women who consumed anise, carrots, mint, vanilla, and blue cheese conveyed a taste preference for these items to their offspring. It’s basic survival. When a child begins eating solid food, eating what the mother ate is a safe bet. The taste preferences that start in the womb endure for a lifetime.
The Physiology of Taste
When I think taste, I think tongue. So let’s begin there. There are four types of papillae (filiform, fungiform, foliate, and circumvallate) that give the tongue its rough surface. The filiform papillae only determine texture, but the fungiform, foliate, and circumvallate contain five different types of taste receptors (taste buds). Each taste receptor is densely packed with taste cells, which are capped with sensors. When these sensors receive taste signals, various neural pathways swing into action, saliva production increases, and stomach secretions activate. Five taste receptors correspond with the five known tastes: sweet, sour, salty, umami, and bitter. When I read that I thought, what, there are more than five tastes left on my fingers from my last meal. However, though they are often misused interchangeably, taste, taste perception, and flavor are not the same.
Taste is a chemical process: Sweetness sensors react to sugar molecules. This relates to food with high caloric energy value. Sourness measures pH because humans have an aversion to acidic foods because they could be spoiled. Saltinessmeasures positive ions in alkali metals, in particular sodium, because of our need for mineral salt. Umami, the savory meaty taste, is detected by a receptor for glutamate. This detects protein. Bitterness is poorly defined. It may be an umbrella term for various chemical reactions that are toxic, because many dangerous compounds are bitter, although not all bitter foods are toxic.
Hot and astringent oral sensations are important, though not classified as taste or texture. When you eat a chili pepper, the capsicum molecule dissolves in your saliva. The trigeminal nerve triggers a burning sensation. This nerve also detects heat, cold, and pain. Although spicy is not classifiably a taste, it is a trigeminal sensation, like pepper, garlic, ginger, and menthol.
Taste and the Other Senses
I used to think taste was the only sense involved in enjoying food—not true. Actually, gustatory enjoyment is not taste, but taste perception. Taste perception involves taste, sight, hearing, touch, and smell. Besides taste, smell is the sense most engaged in the enjoyment of food. The olfactory epithelium detects aromas by interacting with odor molecules entering via the nose or the back of the mouth. It has millions of neurons, with specific receptors that combine odor molecules and subsequently produce an electrical impulse. This in turn transmits a signal to the olfactory bulb, then to the cortex and simultaneously to the limbic system, where human emotions and memories are stored. Also, smell is the only sensory input that is not first processed through the thalamus, the brain’s clearinghouse for sensory information. This direct connection to the limbic system is why smells can spark deep memories and very emotional responses.
Smell is also more complex than taste. We have five receptors for taste. Taste occurs when molecules bind to these five receptors on the tongue. From there, signals travel to specific brain regions. We have 350 different types of receptors that can perceive over 10,000 different odors. When odor molecules bind to nasal receptors smell occurs and goes to certain brain regions. Chewing releases volatile molecules that go from the back of the mouth to receptors in the lining of the nasal passages. Odors traveling through the back of the throat while tasting are perceived differently in the brain. When taste and smell arrive simultaneously in the insula, the insula creates flavor because taste and smell have distinct overlapping pathways in the insula. This allows us to identify the combination of sensations that lead to flavor, which bears little resemblance to actual taste. That’s why food “tastes funny” when you have a cold. The taste is not missing, but the flavor is. You can determine, sweet, sour, salty, bitter, or umami, but not the flavor. For flavor, you need smell. It is the endless possible combinations of taste and odor that create our wide variety of recognizable flavors.
Vision is also essential to taste perception. We evaluate the aesthetics of food and then determine if it looks okay to eat. EEG studies have shown, compared to low-calorie foods, calorie-dense foods cause stronger cortical activity in the bilateral insula and frontal operculum. Pleasant changes in taste were correlated with medial orbitofrontal cortex activation. Even shape can affect taste perception. In one study, after subjects completed an unrelated task involving geometric figures, the taste perception of pointed pieces of cheese was sharper than rounded pieces of cheese.
Sound also affects taste perception, e.g., the sound of a crisp apple or potato chip. Studies have shown playing crisp audio cues, while apples are being eaten, enhances their taste perception.
Touch is another marker for differentiating taste perception, e.g., a fresh juicy ripe peach compared to a mealy dry peach, or a very hard unripe peach. Nerve endings on the taste buds provide consistency and texture information about food. This is especially true of fats, e.g., the creamy feel of ice cream or the texture of a well marbled grilled steak, compared to a very lean cut. Dedicated neurons in the orbitofrontal cortex respond specifically to the texture of fat in the mouth. Feel influences taste perception in soda as well. The taste perception of flat beverages is much different than that of fully carbonated beverages.
Overeating and Decreased Taste Sensitivity
Studies have shown that the five tastes, except sour, have distinctive regional representations on the gustatory cortex. Those studies also say while bitter and sweet receptors are intermingled on the tongue they are separated by 2.5 millimeters in the brain. This could span hundreds of neurons. The brain is probably wired this way so that bitter resides in a region that drives aversion, and sweetness in an area of attraction. The important thing about this topographical segregation is that the encoding of taste signals can drive aversive and attractive behaviors. This could begin to explain why obese people are more responsive to certain foods.
Taste receptors are unique. An overpowering sweetness to one tongue may be barely detectable to another. So, differences in satiety would also differ among individuals. This is especially important to overeaters. Conceivably a person’s taste receptors could mitigate taste perception and influence food preferences, eating habits, and subsequently weight management. Obesogenesis is complex, but studies increasingly suggest that taste receptors are a major factor. Continuous studies dating back as far as the 1950’s link a decreased ability to detect sweetness with obesity. So, is it possible that it is a decreased sensitivity to sweetness that actually causes overweight people to eat more sweets than regular eaters? Diminished ability to perceive taste, and subsequently encode flavor and satiation in the brain could be one of the reasons overeaters overeat. In other words obese people are seeking the same satiety levels that all people seek, but we just have a diminished capacity for determining when those levels are achieved because of a signal breach that begins with our taste buds. So, it’s not about liking sweets more, it is about needing more sweets to achieve satiety.
Certainly, that’s theoretically possible, and according to scientists, probable. The overeater in me is ready to jump on that train—but one problem. I’m not a big sweet eater. I am a grease monkey, and not the kind that fixes your car. Like most obese people, I crave fat more than carbohydrates. “When I die, bury me deep, with a bowl of gravy at my feet, and a platter of deep fried fatty meat in my hand, and I’ll smack my way to the promised-land” has been my spiritual mantra for years. And fat isn’t even one of the basic five tastes. Hmm… looks like this train might not be coming. It’s curious all around. The tongue has receptors for two of the three mandatory macronutrients—sweet for carbohydrates, and umami for protein. It would logically conclude that humans would have some form of taste response for fat, the remaining macronutrient. While fat is not one of the basic tastes, it affects food’s taste perception, appearance, texture, and even smell. Obese people are much less sensitive at detecting fatty acids (the breakdown of fats) than people who are not overweight. This low sensitivity leads to significantly more fat consumption and subsequent weight gain. Predisposition to this can have various causes, beginning with genetics, in utero and neonatal exposure as well as signal breaches in taste sensitivity, flavor construction in the insula, and abnormalities in the orbitofrontal cortex.
So the key issues as I see them are the heavy involvement of smell with taste, and decreased sensitivity for detecting the five basic tastes, and fatty acid insensitivity, in achieving satiety. Could this be the reason normal eaters, “get enough” and I just never do when it comes to food? Also,direct communication between smell and the limbic system is a likely factor. Amygdala and hippocampal remodeling, due to adverse early life experience, has been reliably associated with obese populations. This raises the question, if the amygdal-hippocampal complex has undergone restructuring, how does this effect receiving, processing and responding to signals from the olfactory epithelium. That’s all fine and well: the train has arrived and we’re on it. Now for the important question: where is this train going, and more importantly where do we get off?
The bad news for chronic overeaters, such as myself, is that our taste detection, driving our taste perception, and subsequent eating habits is impaired and placing us in harm’s way. The good news is we can compensate for these breaches in taste detection insensitivity and change our taste perception. Stay tuned for the next post and we will explore that. Until then, remain fabulous and phenomenal.
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