(This is a multi-part series: click here for the index.)

It is the 21st century. We have telephones that fit in a watch pocket, we can sequence the genetic code of life itself, and we can sift the accumulated knowledge of centuries in fractions of a second using Internet search engines. Yet we still don’t understand enough about human biochemistry to create a pill that stops us from eating without causing heart valve defects or uncontrollable diarrhea.

Diet pill’s icky side effects keep users honest, msnbc.com, 7/6/2007

“I’ve pooped my pants 3 times today, and sorry to get descriptive but it even leaked onto the couch at one point!”

“Ya know how when you start moving around in the morning ya pass a little gas. Well, I did and then went into the bathroom and to my horror I had an orange river of grease running down my leg.”

Do Diet Drugs Work?, The Telegraph, 4 May 2009

“I’ve done it. I figured out the secret behind the Alli pills. It’s fear…It’s amazing how the thought of suffering faecal incontinence can create rock solid will-power.”

Clearly I’m in the wrong business: writing life-changing books and articles about how to stay fit and healthy is far less profitable than selling drugs that make people crap their pants.

Meanwhile, in the absence of the magical anti-hunger pill, everyone seems to have their own concept of how to defeat hunger—and thousands of diet books published every year claim that we are simply deficient in everything from acai berry extract to “resistant starch” to the urine of pregnant women. Obviously this is all baloney, because we’re fatter and sicker than ever…

…so let’s back up a few steps and ask ourselves a simple question: “Why are we hungry?”

To answer this, we need an answer to an even simpler question:

“What is hunger?”

Disassembling Hunger and Appetite

To most dieters, hunger is a crafty, insidious demon whispering sweet nothings in our ears.

"Pringles are delicious, and you can stop eating them any time you want."

Yet much of the published research, and most of the popular discourse, simply dismisses hunger as an annoying inconvenience—an atavistic, mildly embarrassing instinct that we must rise above in order to maintain our health.

This is completely untrue. Hunger is a normal and necessary human drive, and it serves a very important function: to cause us to find and ingest the nutrients we need to survive. Yet to understand hunger, we must break it down into its components, because:

Until we understand this, we are doomed to perpetual confusion over our own motivations and desires—let alone others’ writings and recommendations on how to successfully deal with them.

I’ve addressed this subject before, in my very popular article Why Snack Food Is Addictive, which (among other things) explains the concept of “food reward”. What I’m doing here is creating a theoretical framework that allows us to go even farther—by understanding the concept of hunger.

Components of Hunger: Liking Vs. Wanting

We know that liking something and wanting something are not the same thing. I like prime rib, but I don’t want any right now, because I just ate.

Miraculously, the scientific literature often uses helpful and descriptive English words when describing components of hunger. “Liking” and “wanting” are part of the official scientific lexicon: “liking” is a measurement of the pleasure we experience upon eating, i.e. palatability, and “wanting” is a measurement of the relative motivation to acquire and ingest a food.

It turns out that “liking” and “wanting” produce specific patterns of activity in the human brain!

Pharmacology Biochemistry and Behavior
Volume 97, Issue 1, November 2010, Pages 34-46
Hedonic and motivational roles of opioids in food reward: Implications for overeating disorders
Susana Peciña and Kyle S. Smith

Food reward can be driven by separable mechanisms of hedonic impact (food ‘liking’) and incentive motivation (food ‘wanting’). Brain mu-opioid systems contribute crucially to both forms of food reward. Yet, opioid signals for food ‘liking’ and ‘wanting’ diverge in anatomical substrates, in pathways connecting these sites, and in the firing profiles of single neurons.

Brain Research Volume 1350, 2 September 2010, Pages 43-64
The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders
Kent C. Berridge, Chao-Yi Ho, Jocelyn M. Richard and Alexandra G. DiFeliceantonio

“Liking” mechanisms include hedonic circuits that connect together cubic-millimeter hotspots in forebrain limbic structures such as nucleus accumbens and ventral pallidum (where opioid/endocannabinoid/orexin signals can amplify sensory pleasure). “Wanting” mechanisms include larger opioid networks in nucleus accumbens, striatum, and amygdala that extend beyond the hedonic hotspots, as well as mesolimbic dopamine systems, and corticolimbic glutamate signals that interact with those systems.

As we’d expect, “liking” tends to stay more stable over time, whereas “wanting” tends to change dynamically, being a measure of one’s desires at that moment:

Physiology & Behavior Volume 90, Issue 1, 30 January 2007, Pages 36-42
Is it possible to dissociate ‘liking’ and ‘wanting’ for foods in humans? A novel experimental procedure
Graham Finlayson, Neil King and John E. Blundell

Findings indicate a state (hungry–satiated)-dependent, partial dissociation between ‘liking’ and ‘wanting’ for generic food categories. In the hungry state, participants ‘wanted’ high-fat savoury > low-fat savoury with no corresponding difference in ‘liking’, and ‘liked’ high-fat sweet > low-fat sweet but did not differ in ‘wanting’ for these foods. In the satiated state, participants ‘liked’, but did not ‘want’, high-fat savoury > low-fat savoury, and ‘wanted’ but did not ‘like’ low-fat sweet > high-fat sweet. More differences in ‘liking’ and ‘wanting’ were observed when hungry than when satiated.

This would indeed seem to be the common-sense result, but it’s important to understand that liking vs. wanting are not just theoretical constructs: they are distinct biochemical processes.

These motivations don’t just apply to food: any experience we “like” is capable of producing a “want” for more. I discuss this at length in Part VIII.

Components of Hunger: Satiation Vs. Satiety

We also know that the factors which make us stop eating (satiation) are different than the factors that cause us to feel hungry or not hungry (satiety). If all I have available to eat is cotton candy, I’ll soon be satiated, with no desire to eat more—but I won’t experience satiety, because I’ll still be hungry for real food.

Like the terms “liking” and “wanting”, “satiation” and “satiety” have specific meanings in the scientific literature, though according to the dictionary they are synonyms.

Interestingly, French distinguishes them in the same way scientists do: “rassasiement” = satiation, “satiété” = satiety.

Also like the terms “liking” and “wanting”, “satiation” and “satiety” are distinct and reproducible drives:

Nutrition Bulletin Volume 34, Issue 2, pages 126–173, June 2009
Satiation, satiety and their effects on eating behaviour
B. Benelam

Satiation and satiety are controlled by a cascade of factors that begin when a food or drink is consumed and continues as it enters the gastrointestinal tract and is digested and absorbed. Signals about the ingestion of energy feed into specific areas of the brain that are involved in the regulation of energy intake, in response to the sensory and cognitive perceptions of the food or drink consumed, and distension of the stomach. These signals are integrated by the brain, and satiation is stimulated. When nutrients reach the intestine and are absorbed, a number of hormonal signals that are again integrated in the brain to induce satiety are released.

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.

This is another common-sense result: we might eat less of unpalatable foods, but having eaten less, we’re more hungry afterward. And once again, we find that the motivation to stop eating (satiation) is a distinct biochemical process from the satiety (or lack thereof) we feel later on.

Conclusion

Hunger is the interaction of several different clinically measurable, provably distinct biochemical processes—each with its own effects on our brains and bodies. Until we understand this, we are doomed to confusion: fragmentary understanding and incomplete solutions that address only one component of hunger while ignoring the others.

Fortunately, we don’t have to understand the biochemical cascades involved in liking, wanting, satiation, and satiety—because no one does. (These are “active research areas”, which means “we’re still trying to figure all this stuff out”.) Simply understanding these drives on a conceptual level—and why they were selected for in our evolution as humans—can help us navigate the dangerous shoals of dietary advice.

I’ll explore some of these questions in more detail in the upcoming weeks.

Live in freedom, live in beauty.

JS

Continue to Part II, “Hunger Is the Product Of Multiple Perceptions And Motivations, Sometimes Conflicting.”

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