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What Is Hunger, and Why Are We Hungry?
J. Stanton’s AHS 2012 Presentation, Including Slides

The response to the written version of my 2013 AHS presentation has been overwhelmingly positive. Based on page views, the number of people willing to read my work greatly exceeds the number of people willing to watch it in video form!

Therefore, I present to you the full text of my presentation to the 2012 Ancestral Health Symposium—including slides. (The original video can be found here.)

This is some of my finest work. It provides a theoretical and practical framework for understanding hunger—an understanding sadly obscured by oversimplification and moralizing, from both scientists and policymakers. This is doubly unfortunate because the science of hunger is well-established, uncomplicated, and consonant with real-world experience.

I’ll leave you with the “Learning Objectives” from the program:

Upon completion of the session, participants will be able to:

  • Enumerate and understand the mental and physical processes which interact to produce hunger.
  • Describe how evolutionarily discordant diet and behavior can cause inappropriate hunger signals.
  • Address some of their own hunger issues, and/or further investigate the subject in their own research.

Note: You may wish to bring up the bibliography in another browser window in order to follow along with the references.


Introduction

Hello. I’m J. Stanton, gnolls.org.

People aren’t obese because they enjoy being obese, and diets don’t fail because people dislike being slim and healthy! Diets fail because hunger overrides our other motivations.

There is an inflection point somewhere around 1980. What happened? The standard explanation is that fat people are just gluttonous and lazy, so:

Well…maybe not.

It’s also popular to blame junk food…

So much for that idea.

Lately it’s become popular to blame fast food…

But the data doesn’t support that either. (The blue line is food eaten away from home, the red line is fast food…and we can see that the increase in fast food actually slowed down in the mid-1970s, just before obesity began skyrocketing.)

Note from JS: I have been specifically accused of misrepresenting this data. This is a very serious charge—so let me demonstrate that my interpretation is correct. Let’s compare the time periods from 1962 (the first year for which we have obesity data) to 1979, and from 1980 to 2008 (the last year for which we have obesity data).

1962-1979

  • 0.51% per year increase in fast food, as % of total food dollars
  • 0.09% per year increase in adult obesity
  • 0.03% per year increase in extreme obesity
  • 0.08% per year increase in child obesity
        (Child data begins in 1966, and is adjusted for the shorter timespan.)

1980-2008

  • 0.23% per year increase in fast food as % of total food dollars—less than half the rate during 1962-1979
  • 0.67% per year increase in adult obesity—7.4x the rate during 1962-1979
  • 0.16% per year increase in extreme obesity—5.3x the rate during 1962-1979
  • 0.39% per year increase in child obesity—4.9x the rate during 1962-1979

My interpretation of the data stands.

Why We Can’t Just Blame “Palatability” or “Reward”

Now before I explain the science of hunger, there is a very simple and seductive model which is wrong—and if we fall into it, we’ve made a logical error from which we can never, ever recover. That error is: food has a property called “palatability”, or “reward”, which causes us to eat it. So if a food has too much palatability—it’s “hyperpalatable”—we overeat it and get fat.

First, as we’ve already discussed, this hypothesis doesn’t fit the data.

The second problem is that palatability is like pornography. We all know it when we see it—but we just can’t seem to give it a rigorous definition.

For instance, why do different people like different foods? Hundreds of millions of people around the world find these foods delicious. Why can I get twelve different sauces for my chicken wings? 31 flavors of ice cream? And that is because, just like pornography, palatability is subjective. It is a property we assign to food.

The second problem is: why do we ever stop eating? All Oreos taste exactly the same…yet at some point, we don’t want any more. The Oreo didn’t change: we did.

The third problem is that the foods we overeat often aren’t the foods that taste the best—the classic conundrum being “I like prime rib much more than I like Pringles…but I can’t stop eating the Pringles. Why not?” Low-carbers get this all the time: “Your food isn’t really rewarding…it just tastes like it.”

So: what happens now is that the naive model does a little shuffle step. It redefines palatability as “that which we can’t stop eating”. (Or, it substitutes the generic term “rewarding”.)

In other words, “We overeat that which we overeat…because it’s overeatable.”

Of course, if we’re writing a grant proposal, we’ll use the term “obesogenic”. And with that little shuffle step, we’ve just bypassed the entire science of hunger.

Now. I’m beating this dead horse for a very good reason, which is that like phlogiston, spontaneous generation, and the luminiferous ether, this very simple and very seductive error absolutely prevents us from understanding hunger. Once again:

Palatability and reward are subjective properties we assign to food based on our past experience, and our current nutritional and metabolic state.

What Is Hunger?

So: what is hunger?

It turns out there is a large body of established science. I could easily teach a semester-long class, I asked for forty minutes, and they gave me twenty—so I’ll do my best.

Hunger is not a singular motivation. It is the interaction of four different clinically measurable, provably distinct biochemical processes:

  • Satiety: Our body’s nutritional and metabolic state. It includes both our biochemical response to the absorption of nutrients, and our access to stored nutrients.
  • Satiation: An estimate of future satiety, based on the sensory and cognitive experience of eating.
  • Hedonic impact (“likes”): The pleasure we experience from an action. “Palatability” is the hedonic impact of food.
  • Incentive salience (“wants”): Our actual motivation to obtain something we “like”. It is largely, but not exclusively, a product of the other three motivations.

Two more factors interact with hunger to modulate our food intake:

  • Availability: How difficult it is to get something we want.
  • Willpower: The conscious overriding action of the forebrain, known as “executive function”.

Availability and Willpower

Let’s talk about availability for a moment. Even though we might want prime rib much more than leftovers, we eat the leftovers because they’re what’s available to us. If I want prime rib, that’s three hours and a trip to the store, or 40 dollars and a trip to the restaurant. In contrast, we don’t have to want processed snack foods much at all, because all we have to do is open the bag.

They’re not hyperpalatable — they’re hyperavailable.

The Reward System—Hedonic Impact (“Likes”) and Incentive Salience (“Wants”)

Time doesn’t permit me to explore the biochemistry and neuroscience of the reward system—so for the details, I’ll point you to the pioneering work of Dr. Kent Berridge, whose work I was proud to introduce to the community last July. [In this article series, starting with the very first installment. References are also linked in my bibliography. -JS] A couple quick notes:

It’s important to note that likes and wants are not limited to food. Any experience we “like” — that has hedonic impact—is capable of producing a “want” for more—incentive salience.

It is also very important to note that what is colloquially called “reward” is a mashing together of hedonic impact and incentive salience. Both vary independently, and both are subjective properties—so the term “food reward”, which implies a singular property of the food itself, is intrinsically misleading—because it drops us right back into the cognitive trap of the naive model.

But if liking and wanting are subjective, what determines them? Yes, taste is one part of it, but the interesting question isn’t why we eat: it’s why we can’t stop eating.

And so we move on to satiation and satiety.

Satiation and Satiety

Two quick examples: You’ve just left the all-you-can-eat Brazilian steakhouse. What tastes good to you right now?

Almost nothing.

Now: you’ve just hiked seventeen miles over three mountain passes with a 40-pound pack, and that dehydrated lasagna is the best thing you’ve ever tasted.

Again, the food didn’t change—but somehow its hedonic impact, how much we like it — and, therefore, its incentive salience, how much we want it—did change.

Now. Satiation and satiety are synonyms in common usage: so why do we distinguish them? The answer lies in gastrointestinal transit time: it takes hours for the nutrients in food to be digested and absorbed, which means that the satiety response is not a useful signal to stop eating.

(I deleted this passage from the speech as given, because I was concerned about running out of time. However, I think the concepts are valuable, so I’ll reprint it here.)

Furthermore, we must distinguish two types of satiation: positive and negative. When we eat real food, we are rewarded twice: once by the pleasure of eating, and again by the pleasures of positive satiation and satiety.

In contrast, negative satiation is that sick feeling we get when we’ve eaten too many empty calories. It’s our body’s way of telling us “We can’t dispose of any more of that.” So we receive that quick hit of pleasure, or hedonic impact, from eating tasty but nutritionally empty non-food—but it’s over the moment that candy slides down our throat, and we never receive the hedonic impact of positive satiation and satiety that tells us “You’re done, you can stop eating now.”

And with each bite of empty calories, we not only receive less and less pleasure—we make it more and more difficult to achieve the pleasures of positive satiation and satiety.

Furthermore, because satiation is the sensory experience of eating, it can be fooled. It’s well known that:

  • People eat more in groups than when eating alone
  • People eat more when they’re able to eat more quickly
  • Hidden calorie preloads are never completely compensated for

However, the failure of dietary fiber to affect body weight or fat mass in controlled interventions (Papathanasopoulos 2010) suggests that faking satiation with indigestible bulk is not a useful long-term strategy for weight loss. You can fool satiation, but you can’t fool satiety.

Satiety

And satiety is the key to understanding hunger, because, as we’ve seen:

  • Satiation is just an estimate of future satiety based on the sensory and cognitive experience of eating.
  • Both our likes and our wants are very strongly modulated by satiation and satiety.

If we do an experiment where we sit teenagers down at the mall food court and let them have all the food they want for an hour, we find that the lean kids eat a huge amount of food—nearly as much as the obese kids. (Ebbeling 2004) In other words, both groups want the same amount of food. The difference is that the lean kids compensate for that over the rest of the day, but the obese kids do not. And this strongly suggests that obesity is primarily a failure of satiety.

So: we are clearly converging on a primarily nutritional model of hunger, because that’s the definition of satiety. Let’s explore some of the evidence.

We can begin by asking the obvious question: “What else could hunger possibly be for?” Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would have been strongly selected against.

Moving on to the science: taste receptors are not just located on our tongues—they’re located throughout our bodies. (Steinert 2011, Iwatsuki 2012) In our intestines, they modulate the release of satiety hormones like CCK, NPY, VIP, and GLP-1. In the pancreas, they modulate the release of insulin, among other systems…and these effects are so powerful that:

“…The postabsorptive effects of glucose are sufficient for the postingestive behavioral and dopaminergic reward-related responses that result from sugar consumption.” (Oliveira-Maia 2011)

[In other words, you can inject sugar into a rat and get the “food reward” response…even though the rat never tasted the sugar. Also see de Araujo 2008, Ren 2010, Oliveira-Maia 2012. -JS]

Yes, satiety is rewarding in itself…so by eating food that doesn’t produce satiety, you’re chasing a reward that never comes. Does this sound familiar?

Our taste buds both produce and respond to satiety hormones (Shin 2010)…which directly alter the perception of taste. So it might not be your imagination that food doesn’t taste as good when you’re sated.

There are opioid receptors in the walls of your portal vein (Duraffourd 2012)…and they’re not there because your liver wants to get high. They’re a protein sensor—they bond to freshly digested protein fragments.

So, now that I’ve convinced you a nutrient-driven model of satiety and hunger is both biologically and evolutionarily plausible, let’s review some of the experimental evidence.

  • The obese tend to be deficient in many different micronutrients: iron, calcium, zinc, vitamin A, vitamin C, vitamin D, vitamin E, vitamin K, B1, B2, B12, folate. (Leão 2012, García 2009, Xanthakos 2009, Kaidar-Person 2009)

But that’s associative data, so let’s talk about some interventions:

  • Protein leverage. Animals from rats to people tend to eat until they’ve ingested a sufficient amount of complete protein to meet their daily needs.
  • Women given multivitamins lose weight and fat mass: women given placebo do not. (Li 2010)
  • If calories are held constant, weight and fat remain the same, but the placebo group experiences greater hunger than the multivitamin group. (Major 2008)
  • Calcium and vitamin D supplementation alone can decrease body weight and fat mass, but ONLY if you are calcium-deficient. (Major 2009)

And here’s the blockbuster, courtesy of nutrition pioneers Dr. Donald Davis and Dr. Roger Williams:

Feed rats a plausible human diet. Not the “cafeteria diet”, not a “high-fat” diet, a real food diet. Meat, flour, eggs, vegetables, and fruit, all ground up together so it’s uniform. Split them in two groups, supplement one group with a very comprehensive list of vitamins, minerals, and other micronutrients, and let them feed freely.

Then, after several weeks, give both groups free access to granulated sugar for an entire day.

The non-supplemented rats—eating a plausible whole-foods diet of meat, flour, eggs, vegetables, and fruit—consumed 67% more sugar than the supplemented rats. (Davis 1976)

Wow.

And this is something we absolutely cannot explain via the palatability model. The sugar didn’t change…the diet didn’t change. The only difference is micronutrient content.

So: satiety modulates reward

…and junk food is self-reinforcing. The more empty calories you eat, the more you’ll crave empty calories.

Why It’s Critically Important To Understand Hunger

The problem with popularizing for mass consumption is that it’s easy to simplify a concept until it’s no longer true. In the process of oversimplification, concepts also become politicized—and the naive model, in which palatability is a property of food that causes obesity, is being used to resurrect the diet-heart hypothesis.

The story goes like this:

You have not become fat, sick, and diabetic because we’ve been telling you to eat the wrong foods for 35 years! These massive surpluses of corn, soy, and wheat we’ve created by an agricultural policy that subsidizes the destructive chemically-based monocropping of genetically modified birdseed by giant multinational corporations are completely a coincidence. And our dietary edicts, from the original Dietary Guidelines for Americans to the Food Pyramid to the Food Plate are not just excuses to turn you into passively compliant grain disposal units—which consequently require heroic doses of highly profitable, patented pharmaceuticals to keep you alive. No, no, no.

That is NOT the problem. Pay no attention to the 500 billion dollar income stream behind the curtain.

You are the problem, because YOU DID IT WRONG.

You didn’t eat those hard, dense, bitter whole grain breads we told you to. You’ve been putting salt and butter on your vegetables. You’ve been putting dressing on your salad. You’ve been eating food that tastes good, not the dry, tasteless, low-fat whole grains we told you to.

But that’s okay. It’s not really your fault. We know you’re weak and stupid and can’t be trusted to make your own decisions. The fault lies with those evil corporations who have been making food that tastes too darn good, and you just can’t resist it. So we’re going to save you.

We’re going to tax sugar! Because just like liquor taxes have stopped us from drinking, sugar taxes will stop us from drinking soda and eating candy.

That is the new narrative. And there are people here playing footsie with it.

And THAT is why we must understand the real science of hunger.

First, because we quite literally can’t afford not to. 35 more years of the obesity epidemic will bankrupt Medicare, our government, our health care system, and us.

But far more important is that the cost in human lives and human suffering will be incalculable. Millions will suffer terribly and die needlessly. Been to a cheap nursing home lately? It’s an ugly reality.

However! There is good news, which is that the real science of hunger is not complicated—and if I’ve done my job here, you now have enough of a handle on the concepts to figure out for yourself how the science of hunger applies to your own research, and your own issues around food. And I challenge each one of you—individually and collectively—to follow the path of science, not the path of politics.

So I’ll close with some takeaways.

Takeaways

  • Hunger does not exist to make us fat. It exists to keep us alive.
  • Hunger is the interaction of four biochemically and neurologically distinct motivations: likes, wants, satiation, and satiety.
  • Our resulting desire to consume is modulated by availability and willpower.
  • Cells and organs throughout our bodies are full of taste and nutrient receptors that sense their external and internal environment. In response, they issue hormonal and neural signals in order to maintain an environment which keeps them alive and functional. These homeostases define our current nutritional and metabolic state—our “satiety”.
  • “Palatability” and “reward” are not properties of food. Our likes and wants are subjective properties we assign to food based on our past experiences, and our current state of satiation and satiety. (Remember the rats.)
  • Our food consumption is primarily determined by its ability to produce satiation and satiety, not its hedonic impact.

Conclusions

  • Obesity is primarily a failure of satiety.
  • Your mother was right. The problem isn’t “hyperpalatability”: it’s empty calories.

I’m J. Stanton, gnolls.org. Thank you.

(My bibliography is available at this link.)


Let me be clear. This is the best theoretical and empirical framework we currently have for understanding hunger. Any concept or phenomenon we’re having difficulty with can be reduced to its effect on the four motivations (likes, wants, satiation, and satiety) and two modifying factors (availability and willpower)…and any hypotheses that conflate, bypass, or oversimplify them (e.g. treating “reward” as a property of food) will inevitably produce contradiction, confusion, and a lack of progress towards our goal of better health.

I invite my readers to analyze their own observations about hunger using this framework!

Live in freedom, live in beauty.

JS


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It’s Just Like Drug Addiction EVERYONE FREAK OUT: The Role And Limits Of Reward (Why Are We Hungry, Part VIII)

It’s good that we’re learning more and more about the brain’s reward systems. I’ve spent months dissecting their role in hunger—and indeed, hunger is the subject of my upcoming AHS 2012 presentation!

(This is part VII of a series. Go back to Part I, Part II, Part III, Part IV, Part V, Part VI, or Part VII.)

Unfortunately, one side-effect of more brain science is more breathlessly ominous news releases claiming that the Vice of the Moment—whatever it is this week—is mediated by the same brain circuits that mediate drug addiction! EVERYONE FREAK OUT

“After a month of sugar binging and increased dopamine levels, the rats’ brains developed fewer dopamine receptors and more opioid receptors—changes similar to those observed in mice on cocaine and heroine.”
Move Over, Heroin: “Sugar Addiction” May Be a Reality

“In a new study of mouse brains, scientists show that the patterns of gene regulation stimulated by salt cravings are the same gene patterns regulated by drug addiction.”
Cocaine Addiction Uses Same Brain Paths as Salt Cravings

“People who frequently use tanning beds experience changes in brain activity during their tanning sessions that mimic the patterns of drug addiction, new research shows.”
How Tanning Changes The Brain

    “Oh, no!” we think. “Eating sugar, or getting a tan, is just like being a junkie! Who will rescue us from the evil clutches of Toucan Sam and Cap’n Crunch? Or the siren song of the tanning bed?”
    “Oh, yes!” the regulators think. “We can politicize this issue by stigmatizing people as ‘addicts’, taxing and criminalizing their behavior, and using the profits to finance the same efficient and effective tactics* we’re using to fight the War on Drugs!”

(* = sarcasm)

Anyway, I don’t want to turn this into a political rant. OK, maybe I do, a little, having just paid my taxes, and having seen this incredible sentence in a peer-reviewed scientific paper:

Arch Dermatol vol 141, Aug 2005 pp. 963-966
UV Light Tanning as a Type of Substance-Related Disorder
Molly M. Warthan, MD; Tatsuo Uchida, MS; Richard F. Wagner, Jr, MD

“…Even if the issue of indoor UVL exposure is successfully addressed, the successful regulation of outdoor tanning with natural sunlight, a major source of UV exposure, would remain problematic.”

Yes, our self-appointed guardians of public health are sincerely disappointed that they haven’t yet found a way to make the sun illegal.

OK, I’m done.

The Role And Limits Of Reward

Given the fearmongering in the popular press, and the ongoing confusion in the paleo community, I want to emphasize two important points about the role and limits of reward. The first I’ve mentioned before, but I’ll mention it again, because it’s important:

The brain’s reward system underlies all our motivations—not just the bad or “addictive” ones.
  • Any time we experience pleasure—any time we “like” something—that’s hedonic impact. (And it doesn’t require conscious appreciation of the fact.)
  • Any experience we “like” is capable of producing a “want” for more—incentive salience.

Organizing the refrigerator. Petting a dog. A long shower after hard physical work. Greeting a friend or a lover. Being complimented. Successfully finishing a long, difficult task. Seeing wildlife outside your window. It doesn’t matter whether that pleasure is from a physical thrill, positive social interaction, the satisfaction of a job well done, or direct chemical stimulation—it’s all mediated by (gasp!) the same circuits that mediate drug addiction.

This is why drugs that act on the reward system are so addicting: they can directly stimulate the feeling of having done something pleasurable without the user having to actually do anything.

And it’s very likely that we find pleasure in these actions for a reason: they were survival traits throughout evolutionary time. Stated in scientific language:

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

“Drugs causing pleasure and addiction are comparatively recent and likely reflect usurping of evolutionary ancient systems with high survival value by the gratification of contemporary hedonic indulgences.”

Therefore, saying that sugar, salt, tanning, or any other Vice Of The Moment “mimics the patterns of drug addiction” creates needless fear and distress, because it’s a tautology—it’s always true. It’s like saying “Did you know that your body is contaminated with DIHYDROGEN MONOXIDE?” Well, yes: that would be one name for ‘water’. (Read the Dihydrogen Monoxide FAQ for more information on this dangerous chemical.)

It’s also useful to remember that “addiction” is a matter of definitions and social norms. Even a behavior generally viewed as positive (e.g. cleanliness) is defined as pathological (obsessive-compulsive disorder) when practiced too frequently.

The second important point is easy to forget in the excitement of learning:

Just because a behavior we hope to change is signaled through the reward system doesn’t mean that it’s caused by a malfunction in the reward system.

I offer the following analogy: the reward system is like the dashboard of a car.

As the driver of the car, we know some basic things just by sitting in the driver’s seat: is it running? Is the engine making a strange noise? Does it respond to our use of the steering wheel, gas, and brake? However, there is a lot we can’t know from direct sensory input, and the dashboard (with its associated gauges and warning lights) is how the car lets us know important things like coolant temperature, oil level, our exact speed, and how much gas is in the tank.

Continuing the analogy, if the gas gauge reads “empty”, the problem might not be that the gas gauge is faulty. We might actually be running out of gas! Similarly, if the coolant temperature keeps reading high, we shouldn’t just blame the gauge, or the temperature sensor, and keep driving. (“You’re fat because you lack the willpower to stick to a diet”…”everyone is fat primarily because they are trying to entertain themselves with food”…does this sound familiar?) The fact that we learn of a malfunction through the dashboard does not mean that a malfunctioning dashboard is the cause of our car troubles!

Similarly, just because we have a problem (for example, excessive hunger) that manifests itself through the reward system (e.g. “wanting” so much food that we start gaining fat), that doesn’t mean that a dysfunctional reward system is the cause of our hunger! We could have any number of metabolic, endocrine, or nutritional issues to which excessive hunger is a perfectly reasonable response. (A few examples: diabetes, hypothyroidism, vitamin insufficiency, some antidepressant and antipsychotic drugs.)

It’s tempting to explain away every aspect of a mind-bogglingly complex homeostatic system, like human metabolism, in terms of the few parts we understand. The result even looks like science, because of all the footnotes! However, I’ve found the temptation is best resisted.

Conclusion

  • The brain’s reward system underlies all our motivations—not just the bad or “addictive” ones. Any choice we make that isn’t purely a rational product of our forebrain likely involves some measure of reward signaling.
  • Just because a behavior we hope to change is signaled through the reward system doesn’t mean that it’s caused by a malfunction in the reward system. The reward system is the conduit by which our wants and needs are communicated to our conscious mind: it’s not the cause of our wants and needs.

I hope this article helps clarify the role and limits of reward!

Live in freedom, live in beauty.

JS

(To be continued! Or, go back to Part I, Part II, Part III, Part IV, Part V, Part VI, or Part VII.)


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Why Do We Ever Stop Eating? Taste, Reward, and Hyperpalatability (Why Are We Hungry? Part VII)

Caution: contains SCIENCE!

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.

(This is part VII of a series. Go back to Part I, Part II, Part III, Part IV, Part V, or Part VI.)

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.

A Disclaimer

(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.

Rat response to salt and sugar water

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?

Oreo Cookies!!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.

(For more information, or to refresh your memory, I discuss satiety in Part IV, and satiation in Part V.)

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.

Intermission

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.

No carbs != healthy.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.

Continue to Part VIII, “It’s Just Like Drug Addiction EVERYONE FREAK OUT: The Role And Limits Of Reward”

Live in freedom, live in beauty.

JS


(This is part VII of a series. Go back to Part I, Part II, Part III, Part IV, Part V, or Part VI.)

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