In this article, I begin assembling several of the concepts from previous articles. I’ve linked to them whenever possible—but if you find yourself confused by concepts or terminology, you might find it worthwhile to re-read the series starting from Part I.
Summary: Our Story Thus Far
In previous installments, we’ve established the following:
- Hunger is not a singular motivation: it is the interaction of several different clinically measurable, provably distinct mental and physical processes.
- In a properly functioning human animal, likes and wants coincide; satiation is an accurate predictor of satiety; and the combination of hunger signals (likes and wants) and satisfaction signals (satiation and satiety) results in energy and nutrient balance at a healthy weight and body composition.
- Restrained eating requires the exercise of willpower to override likes, wants, and the lack of satiation or satiety; the exercise of willpower uses energy and causes stress; and stress makes you eat more. Therefore, a successful diet must minimize the role of willpower.
- A lack of satiety will leave us hungry no matter what else we do to compensate. We fail to achieve satiety by not ingesting (or not absorbing) the energy and/or nutrients our body requires, and by an inability to retrieve the energy and/or nutrients our bodies have stored due to mitochondrial dysfunction.
- Satiation is an estimate of future satiety based on sensory input. As with satiety, we fail to achieve it by not satisfying our nutritional needs. We can also bypass satiation by decreasing sensory exposure to our foods. Some common enablers are eating quickly, eating while distracted or on the run, and eating calorie-dense packaged and prepared foods.
- The role of reward in hunger constitutes hedonic impact (“liking”, palatability) and incentive salience (“wanting”, the drive to consume more food). The process of learning modifies both. Furthermore, reward is not limited to food, is neither static nor an intrinsic property of the food itself, and is modified by many experiences besides its taste during the act of consumption.
(Those of you who have read Part VI have already seen this disclaimer, and can skip it.)
I’ve put off writing these next few articles because they’re likely to cause some controversy, which I don’t enjoy. My objective with the articles I write here at gnolls.org is to organize, distill, and summarize the bewildering variety of nutritional information into succinct, helpful articles, to share them with my readers, and to improve them as new information comes to my attention.
(An aside: I thank you, my readers, for continuing to provide references, intriguing leads, and constructive criticism. Please continue to do so.)
Please note that I have no horse in any of the current races: I am neither selling diet books nor defending a career-building hypothesis, and “Why Are We Hungry?” started long before the AHS and any still-simmering disputes.
Finally, and most importantly, I am not proposing any new theories of hunger or obesity. The current literature is both comprehensive and, I believe, more than adequate to explain and understand observed phenomena.
That being said: let’s get started!
Reward Is Fundamental And Necessary: We Have “Likes” And “Wants” For Very Important Reasons
Even the irreligious tend to take the theological viewpoint on hunger: the desires of the body are sinful, and exist to tempt us into gluttony and sloth. (See: doctrine of original sin.)
This type of thinking leads us astray. Our tastes are the product of millions of years of natural selection, during which animals that didn’t have our tastes died out and were replaced by those that did. They don’t exist to make us fat: they exist to keep us alive. As I’ve said in Part II, “Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would have been strongly selected against.”
For example, we both “like” and “want” salt because all animals, including humans, require salt to live. Life never left the ocean: we carry it within us, in every cell.
Proceedings of the National Academy of Sciences, July 11, 2011
Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite
Wolfgang B. Liedtke, Michael J. McKinley, Lesley L. Walker, Hao Zhang, Andreas R. Pfenning, John Drago, Sarah J. Hochendoner, Donald L. Hilton, Andrew J. Lawrence, Derek A. Denton
“Salt appetite and hedonic liking of salt taste have evolved over >100 million years (e.g., being present in Metatheria).
An instinctive behavior pattern of which salt appetite is an exemplar reﬂects a genetically hard-wired neural organization naturally selected because of its high survival value.”
(Also see “The Salt-Mining Elephants of Kitum Cave”, from Part IV.)
And the fact that our taste for salt generally exceeds our needs can be explained by the fact that excess salt (within limits) is not harmful, whereas insufficient salt leads to death.
Among other interesting facts, Liedtke et.al. point out, somewhat breathlessly, that the desire for salt is mediated by the same brain circuits that mediate drug addiction. This is true—but those same brain circuits mediate all our motivations, from shelter to sex to social status. As I’ve said before, reward is not a concept limited to food. Reward is the reason we’re motivated to do anything at all.
To illustrate, here’s an actual graph of neural firing rates in the ventral pallidum, a hotspot of “liking” (hedonic reward). As we’d expect, rats liked intensely salty water when salt-deficient—even more than sugar water—and disliked it when previously fed a diet with sufficient salt.
Amy J. Tindell, Kyle S. Smith, Susana Peciña, Kent C. Berridge and J. Wayne Aldridge
Ventral Pallidum Firing Codes Hedonic Reward: When a Bad Taste Turns Good
AJP – JN Physiol November 2006 vol. 96 no. 5 2399-2409
We compared VP neural firing activity in rats during aversive “disliking” reactions elicited by a noxiously intense NaCl taste (triple-seawater 1.5 M concentration) in normal homeostatic state versus in a physiological salt appetite state that made the same NaCl taste palatable and elicit positive “liking” reactions. We also compared firing elicited by palatable sucrose taste, which always elicited “liking” reactions in both states. A dramatic doubling in the amplitude of VP neural firing peaks to NaCl was caused by salt appetite that matched the affective switch from aversive (“disliking”) to positive hedonic (“liking”) reactions. By contrast, VP neural activity to “liked” sucrose taste was always high and never altered.
And again, we see that “wanting” and “liking” are not magical properties of food—they’re values we assign to food (and everything else) based on our past experience and nutritional state.
Why Do We Ever Stop Eating Delicious Food?
If incentive salience is the controlling factor of how much we eat, why do we ever stop eating? Why don’t we simply eat until we can’t move, repeat as soon as we’re able, and continue until we all require mobility scooters?
The answer cannot be in the food itself: the last Oreo in the package is no different than the first Oreo. “Palatability” is a value we assign to food, not an intrinsic property of the food itself, as I’ve already discussed here, in Part VI. Otherwise everyone in the world would “like” exactly the same foods.
I’ll repeat this, because it’s important: the Oreo didn’t change. We did.
Obviously there must be some drive within us that modulates incentive salience (“wanting”)—some motivation that causes us to stop eating before we vomit or physically burst. And many of my readers have already come to the correct conclusion: that drive is satiation, which I’ve already described at length here.
Note that satiety can also come into play if we’ve been eating for long enough. Though satiety and satiation are clearly defined, there is no bright line between them as they are experienced: the timing of the satiety response depends dramatically on what’s being eaten and how it’s prepared, and can overlap with the satiation response.
Also note that these drives can become dysfunctional, so there are a few unfortunate people who eat until they vomit and/or require mobility scooters. I’ll discuss this in future installments.
Therefore, in order to estimate how much of a food we are likely to consume, we must examine its power to produce satiation and satiety, as well as its incentive salience.
Modulation Of Reward Doesn’t Require Taste At All
Hedonic impact and incentive salience are modified by the entire set of circumstances around eating, not just taste. Here’s a startling study:
Ivan E. de Araujo, Albino J. Oliveira-Maia, Tatyana D. Sotnikova, Raul R. Gainetdinov, Marc G. Caron, Miguel A.L. Nicolelis, Sidney A. Simon
Food Reward in the Absence of Taste Receptor Signaling
Neuron Volume 57, Issue 6, 27 March 2008, Pages 930-941
Here we show that trpm5−/− mice, which lack the cellular machinery required for sweet taste transduction, can develop a robust preference for sucrose solutions based solely on caloric content. Sucrose intake induced dopamine release in the ventral striatum of these sweet-blind mice, a pattern usually associated with receipt of palatable rewards. Furthermore, single neurons in this same ventral striatal region showed increased sensitivity to caloric intake even in the absence of gustatory inputs.
Not only did the taste-blind rats develop a preference for sugar water over plain water—their preference was just as strong in all measurements as the mice with functional taste receptors!
(Clearly the satiety response can affect our reward responses, irrespective of taste.)
Satiation and Satiety: Putting The Brakes On Liking And Wanting
It is very important to recall here that satiation is an estimate of future satiety, based on sensory input.
“This ﬁnding of concerted gene regulation was attenuated on gratiﬁcation with perplexingly rapid kinetics of only 10 min, anteceding signiﬁcant absorption of salt from the gut.” -Liedtke et.al.
In other words, the satiation response is sufficient to stop salt consumption: we don’t have to wait for satiety (absorption from the gut) to tell us to stop ingesting salt.
As we’d expect, satiation and satiety cause a decrease in “wanting” as well as “liking”. And here’s another blockbuster:
Physiology & Behavior
Volume 98, Issue 3, 7 September 2009, Pages 318-325
Eating what you like induces a stronger decrease of ‘wanting’ to eat
Sofie G.T. Lemmens, Paul F.M. Schoffelen, Loek Wouters, Jurriaan M. Born, Mieke J.I. Martens, Femke Rutters and Margriet S. Westerterp-Plantenga
‘Liking’ and ‘wanting’ scores of all fasted subjects on the two test-days showed 62–73% reproducibility. CM [chocolate mousse] was liked more than CC [cottage cheese] (p < 0.001). Consumption of CM decreased ‘wanting’ for bread, filling, drinks and dessert (p < 0.03). Consumption of CC decreased ‘wanting’ for bread only (p < 0.05). Contrary to CC, CM decreased relative ‘liking’ for the dessert category (p < 0.001). In conclusion, the computer test for measurement of ‘liking’ and ‘wanting’ is sufficiently valid. Eating a highly liked food item induces a more distinct decrease in ‘wanting’ for food items in general and category-specific ‘liking’, than eating a sufficiently liked neutral food item.
Chocolate mousse induced a larger decrease in hunger and desire to eat than cottage cheese, although the offered amount of both food items was isoenergetic.
Lemmens et.al. demonstrates that eating delicious, highly “liked” food (food with high hedonic reward, aka “palatable” food) does not necessarily cause us to eat more. In fact, in their experiment, the subjects were less motivated to earn more food after eating the chocolate mousse than after the cottage cheese!
Given this data, it seems likely that eating the government-recommended low-salt, low-fat diet simply increases the hedonic impact of fat and salt—increasing the probability that we’ll consume it in the form of junk food instead of eggs, fatty meat, coconut milk, and other nutritious foods.
Getting Tired Of Food: “Sensory-Specific Satiety”
Space does not permit a full discussion of sensory-specific satiety. To summarize quickly, it’s the effect by which both our “liking” and our “wanting” for a food decrease as we eat it, irrespective of its other characteristics. For example:
Appetite. 2009 Feb;52(1):222-5. Epub 2008 Oct 4.
Food liking, food wanting, and sensory-specific satiety.
Havermans RC, Janssen T, Giesen JC, Roefs A, Jansen A.
Participants had to consume a certain amount of chocolate milk and afterwards approximately half of the participants played a game to obtain more chocolate milk, whereas the other half played a game to obtain crisps. Participants showed a decline in subjective liking of taste and smell of the chocolate milk in comparison to crisps. Furthermore, they showed less motivation (i.e. wanting) to obtain more chocolate milk. It is concluded that sensory-specific satiety in humans reflects a decrease in both food liking and food wanting.
[Note that “satiety” is somewhat of a misnomer. Depending on the time between consumption and testing, the satiation response is often still in play—and since this effect is dependent on taste, I believe “sensory-specific satiation” is a more appropriate name. But “sensory-specific satiety” is the accepted scientific terminology, so I’ll continue to use it.]
In the vernacular, we call this “getting tired” of a food, as in “I don’t even want to LOOK at another guava right now.” This effect is very well-established, and points to the idea that variety may be a greater motivator of consumption than palatability. I may explore this issue in more detail if there is demand.
Palatability Affects Satiation But Not Satiety (That’s A Quote)
Even if we consume more food at a sitting, this does not automatically mean we’ll consume more calories throughout the day. A metabolically functional person who eats more food will simply be sated for longer, because hedonic reward doesn’t affect satiety:
Physiol Behav. 1999 Jun;66(4):681-8.
Palatability affects satiation but not satiety.
De Graaf C, De Jong LS, Lambers AC.
The results showed that the ad lib intakes of the less pleasant and unpleasant soups were about 65 and 40% of the intake of the pleasant soup. Subjects ingested about 20% more soup when the subjects had to wait for the test meal about 90 min, compared to the 15 min IMI condition. The availability of other foods had no effect on the effect of pleasantness on ad lib intake. There was also no effect of the pleasantness on subsequent satiety: hunger ratings and test meal intake were similar after the three standardized soups. One conclusion is that pleasantness of foods has an effect on satiation but not on subsequent satiety.
These are common-sense results: eating a palatable food doesn’t magically decrease its nutritive value. And given equal satiating power, we may eat more of the palatable food—but having eaten more, we’ll also experience greater satiety.
(Do note that tomato soup is extremely non-satiating under the best of circumstances: the standardized soups contained 350g for women and 500g for men. This translates to 105 and 150 kcal (“calories”), respectively, with essentially zero fat or protein, and of which the majority is sugar. In other words, nutritively, they’re candy plus a bit of starch and a few vitamins…and the reason anyone stops eating it is most likely due to the effect of sensory-specific satiety.)
Most importantly, we might eat less of unpalatable foods—but having eaten less, we’ll be more hungry afterward.
J Nutr. 2011 Mar;141(3):482-8. Epub 2011 Jan 26.
Staggered meal consumption facilitates appetite control without affecting postprandial energy intake.
Lemmens SG, Martens EA, Born JM, Martens MJ, Westerterp-Plantenga MS.
Participants (n = 38, age = 24 ± 6 y, BMI = 25.0 ± 3.1 kg/m(2)) came to the university twice for consumption of a 4-course lunch (40% of the daily energy requirements) in 0.5 h (nonstaggered) or in 2 h with 3 within-meal pauses (staggered) followed by ad libitum food intake.
However, this [staggered meal consumption] was not translated into lower energy intake.
In other words, eating the same food over a longer period of time doesn’t cause anyone to eat any less…
…assuming we’ve eaten real food. Consuming junk food will always leave us hungry: candy has no satiating power, and will not produce satiety, no matter what circumstances we consume it under. (Recall again that satiation is an estimate of future satiety, and satiety is nutritionally driven.)
Wrapping Up: Just What Is Incentive Salience, Anyway?
We now know that hedonic reward (“liking”, “palatability”) does not alter a food’s power to produce satiety, because satiety is not modulated by taste. And though “sensory-specific satiety” (again, a partial misnomer: the satiation response is involved) is a well-understood phenomenon, reward’s power to affect incentive salience (“wanting”) depends strongly on circumstances and whose studies you believe.
In other words, to make any sense of the situation, incentive salience (“wanting”) must be understood as a product of hedonic impact (“liking”), satiation, and satiety—and the limit on our food consumption comes primarily from its satiating and sating power, not its hedonic impact (“palatability”).
This neatly solves the conundrum that some current theories of “food reward” face: they must claim that foods like bacon-wrapped filet mignon and pâté de foie gras lack the magical property of “food reward”, even though they’re delicious (in other words, “your food isn’t rewarding, it just tastes like it”)—and that foods like Wheat Thins and Pringles have this same magic property of “reward” in excess, even though they’re not nearly as delicious as that bacon-wrapped filet.
It also explains common observations like “There’s always room for dessert”…because dessert, being nutritionally incomplete, is not satiating.
Finally We Can Define “Hyperpalatability”
Previously the term “hyperpalatable” has been like “pornography”: we know it when we see it, but we can’t define it—or we define it circularly, as “tasty foods which we overeat”.
However, now that we understand that how much we eat is determined by the opposing forces of satiation, satiety, and incentive salience (“wanting”), we can easily understand why certain foods are hyperpalatable: they combine a meaningful amount of hedonic reward with an inability to produce satiation or satiety, resulting in incentive salience that doesn’t decrease as you eat.
To draw an analogy: hedonic impact (“liking”) is the gas pedal, satiation (and, after a delay, satiety) are the brakes, and the speed of the car is incentive salience (“wanting”). We can eat foods with high hedonic impact—but so long as they also produce satiation (and, eventually, satiety), the car will stop. However, if we eat foods that do not satiate (or sate), our car has no brakes, and it won’t stop no matter how slowly it’s moving.
And now we can see why hyperpalatable foods don’t necessarily taste as good as your favorite foods: they don’t have to! All they have to do is be made of ingredients so nutritionally empty that they never produce satiation or satiety (e.g. linoleic acid and fructose), and be so calorie-dense that they don’t fill up our stomachs until we’ve eaten pathological amounts.
This leads us to a disturbing conclusion: the worse a snack food is for us, the more difficult it usually is to stop eating. Read my article “Why Snack Food Is Addictive: The Grand Unified Theory of Snack Appeal” for a deeper exploration of this subject.
Conclusion: It’s Not Just The Taste, It’s The Nutrition (And Much More)
If we find ourselves overeating a food, we need to ask ourselves “Is this a nutritious, whole food, containing complete protein, healthy fats, and a generous helping of nutrients?” For most of us, the answer will be “No, it’s Corn Pops,” or some other nutritionally incomplete junk.
Just because a snack doesn’t contain carbohydrates or HFCS doesn’t mean it’s not junk food. Nuts, for instance, generally contain incomplete protein and large quantities of omega-6 PUFA (linoleic acid)…cake made with xylitol and nut flour is still cake, not food. Fruit is good in moderation, but in excess (especially as juice) it’s just sugar with some vitamins. And snacking is bad for many reasons, even if you’re eating “healthy” snacks.
- Reward systems drive all our behaviors, not just our food preferences.
- Liking and wanting don’t exist just to make us fat: they exist to keep us alive. They are the product of millions of years of natural selection, during which animals that didn’t have our tastes died out and were replaced by those that did.
- Liking and wanting are values we assign to food, not invariant or intrinsic properties of the food itself.
- The modulation of reward (liking and wanting) does not require taste at all.
- Incentive salience (“wanting”) is a product of hedonic reward (“liking”), satiation, and satiety.
- Eating food you like may either decrease or increase your want for more, depending on the food, the circumstances, and whose studies you believe.
- Palatability can affect satiation, either via nutritional satiation or “sensory-specific satiety”, but it does not affect satiety.
- Hyperpalatability is an unnatural amount of hedonic reward, combined with an inability to produce satiation or satiety. Therefore, the worse a snack food is for you, the more difficult it usually is to stop eating.
- Conclusion: in order to keep incentive salience (“wanting”) under control, make sure that hedonic impact (“liking”) is always accompanied by nutrition. Eat delicious but nutritionally dense foods, containing complete protein, healthy fats, and ample nutrients. Otherwise you’re eating food with no brakes.
- And when you do take the risk, eat your cheat food after you’ve already satiated yourself with a complete meal.
Live in freedom, live in beauty.
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