Disclaimer
• Your life and health are your own responsibility.
• Your decisions to act (or not act) based on information or advice anyone provides you—including me—are your own responsibility.
My series-in-progress, Why Are We Hungry? (part II, part III), will return after the Ancestral Health Symposium. I’m anxious to continue, because we’re just starting to dig into the meat of the problems with Part III)—but due to conference preparations and unexpected workspace issues, I simply don’t have the time to do it justice right now.
I’ll be signing copies of The Gnoll Credo at the Friday evening author event—so if you’re attending AHS, make sure to stop by and introduce yourself!
Also, if you don’t see me update next Tuesday, rest assured I’m on a mountain somewhere in the Eastern Sierra.
For reasons I’ve explained at length in What Is The Paleo Diet, Anyway?, I believe the term “paleo” is sufficient to encompass the entire online and print community. The foundation of a paleo diet is our multi-million year evolutionary history as hunters and foragers, and we all understand that humans are poorly adapted to a diet of grass seeds—which we’ve been eating for perhaps a few thousand years.
However, though we as individuals can choose any point on the continuum, the print and online literature divides itself reasonably cleanly into two schools of thought. The traditionalists emphasize re-enactment of their perception of Paleolithic foods, make very specific claims about Paleolithic nutritional composition, and stress avoidance of all foods they view as Neolithic. In contrast, the new school claims that re-enactment is impossible, many claims of Paleolithic nutritional composition are either unsupported or implausible, and that we must evaluate foods, even clearly Neolithic foods, on their nutritional merits to present-day humans—though within our evolutionary context.
I believe we need a simple, descriptive term that distinguishes the pro-fat, dairy- and potato-tolerant “new school” of Paleo from the lean-meats-nuts-and-veggies traditionalists, without being pejorative to either.
To that end, I propose the term “functional paleo” to describe the new school.
Eating foods that best support the biochemistry of human animals with a multi-million year history of hunting and foraging, primarily on the African savanna.
Avoiding foods, such as grains, grain oils, and refined sweeteners, that actively disrupt the biochemistry of these human animals.
In other words, “functional paleo” is based on the biochemical function of food within the human body. It is informed by evolutionary context, but not limited by it. (Or, most likely, a contested interpretation of it.)
This functional definition carries its own risk: we can mistakenly see “food” as a collection of nutrients, an approach that ignores the many constituents of Real Food (meat, eggs, vegetables, root starches, fruit and nuts) that haven’t yet been isolated, recognized, or classified as nutritional. That way lies “meal replacement shakes” and madness—and that is why we must keep our evolutionary context in sight.
Questions like “What would Grok do?” and “Imagine yourself in the woods, or by the ocean or on some fertile plain, with nothing but your own wit. What would you be able to eat?” are mental shortcuts to evolutionary context.
However, the functional definition allows us to avoid silly arguments like “Paleolithic humans regularly ate rotten meat, so why don’t you?” and “An archeologist found starch residue in one cave in Africa, so that means cavemen ate bread and grains are paleo.” It also allows us to understand that though nuts and honey were certainly consumed in the Paleolithic, that fact alone doesn’t make them healthy to eat—especially in large quantities. I find this to be a worthy tradeoff, and I hope others agree.
Functional Paleo: Who’s In?
Here is a non-exhaustive list of sources I consider to be “functional paleo”.Please let me know if I’ve missed you or miscategorized you, or anyone else: I’ve erred on the side of caution by not mentioning any source I’m not reasonably sure of. (Leave a comment, or contact me directly.)
Mark’s Daily Apple/The Primal Blueprint – The first book to take what I consider a functional paleo approach, and still a classic. And they update every day!
The Perfect Health Diet – The purest example of functional paleo in print. Dr. Jaminet has been doing solid original research.
That Paleo Guy – Functional paleo from the perspective of a trained athlete.
PrimalMedEd – Anastasia is now Dr. Anastasia…congratulations!
I’ll be using the term “functional paleo” at the AHS and beyond, I assert no rights over it, and I encourage its use. I hope you find it both useful and descriptive!
Live in freedom, live in beauty.
JS
What do you think? Are you a functional paleo eater? Does the term speak to you? Leave a comment!
Since this is a short article, here’s a bonus video for you!
Sometimes MMA is a subtle, skillful game of strategy: a wrestler’s top game vs. submissions from the bottom, strikes vs. takedowns, two kickboxers snapping insect-quick kicks and punches…
…and sometimes it’s two giants playing the real-life version of Rock ‘Em Sock ‘Em Robots.
In Part I and Part II of this series, I established the following:
(Skip to Part IV.)
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.
In other words, we shouldn’t have to be hungry all the time in order to stay healthy and fit.
Yet this is clearly not the case. Most diets depend on restraint…and most diets fail.
“The authors review studies of the long-term outcomes of calorie-restricting diets to assess whether dieting is an effective treatment for obesity. These studies show that one third to two thirds of dieters regain more weight than they lost on their diets, and these studies likely underestimate the extent to which dieting is counterproductive because of several methodological problems, all of which bias the studies toward showing successful weight loss maintenance.
In addition, the studies do not provide consistent evidence that dieting results in significant health improvements, regardless of weight change. In sum, there is little support for the notion that diets lead to lasting weight loss or health benefits.”
“…Both a history of weight loss dieting and weight suppression (discrepancy between highest weight ever and current weight) predicted greater weight gain, and these effects appeared to be largely independent of one another.”
Why is this?
The flip answer, of course, is “because they’re not eating a paleo diet“. But both the evidence and common sense support a more fundamental conclusion: most diets depend on restraint—known colloquially as “willpower”.
What Is “Willpower”?
Just like the four hunger drives, “willpower” is a provably distinct mental and physical process.
This is your prefrontal cortex.
“…The prefrontal cortex is more developed and extensive in humans than any other primate, and it is responsible for what is called “executive function.” That is, the PFC helps us predict outcomes, prioritize, modulate our emotions to socially acceptable norms, and helps us sort out the best options given conflicting data (reasoning, basically). It is a bit like a policeman for your brain…”
–Dr. Emily Deans
The prefrontal cortex is responsible for what we call “willpower”—our ability to do something we don’t want to do. Willpower is the confounding factor in analyzing hunger motivations, because it can override them…to a degree.
When Willpower Fails (And Diets Fail)
When our wants overcome our will, we call them “needs”.
As anyone who’s tried to learn to play a musical instrument knows, our prefrontal cortex, our “rational mind”, is not fully in charge. All we have to do is put our fingers here, then here, then here…what’s so hard about that? Yet it takes endless hours of practice, because our PFC isn’t even in full control of our fingers—let alone our hunger drives. Similarly, when our wants overcome our will to avoid unhealthy food (or too much food), we will eat regardless.
Unfortunately, most mainstream diets require substantial willpower—huge inputs from the prefrontal cortex—to maintain. This is why the majority of people regain more weight than they lose on a diet: the diet does not bring the four drives of liking, wanting, satiation, and satiety back into balance. It simply depends on an increase in willpower…
…an increase that is, in the long run, not sustainable. The PFC can only influence behavior so much and so often, which is to say that we only have so much willpower.
Stated in plain English:
Most diets fail because they rely on willpower to override our other drives.
Willpower Requires Energy
Skeptical? Here’s the proof: exerting willpower takes a measurable amount of energy!
Laboratory tests of self-control (i.e., the Stroop task, thought suppression, emotion regulation, attention control) and of social behaviors (i.e., helping behavior, coping with thoughts of death, stifling prejudice during an interracial interaction) showed that (a) acts of self-control reduced blood glucose levels, (b) low levels of blood glucose after an initial self-control task predicted poor performance on a subsequent self-control task, and (c) initial acts of self-control impaired performance on subsequent self-control tasks, but consuming a glucose drink eliminated these impairments. Self-control requires a certain amount of glucose to operate unimpaired. A single act of self-control causes glucose to drop below optimal levels, thereby impairing subsequent attempts at self-control.
Right away we can see a problem: impaired blood glucose control, such as we see in diabetes and prediabetes, would exacerbate this effect…so the more we impair our metabolic flexibility by continually stuffing ourselves with carbohydrate, the more trouble we’ll have sticking to our dietary decisions!
Unless (as the study shows) we drink a 120-calorie glass of Kool-Aid, which helps us restrain ourselves from…ingesting sugary junk. Is anyone seeing another problem here?
Why Dieting Makes You Fat: You’re Depending On Willpower
All this seems like an obvious, common-sense result. We know intuitively that willpower is a limited resource: we only have so much tolerance for denying our own wants. Furthermore, life is far more pleasant when we’re not living in a constant state of self-denial (or self-flagellation).
But there are even more reasons to minimize the role of willpower in a diet. These titles say it all, and I don’t even have to quote abstracts:
Psychosom Med. 2010 May; 72(4): 357–364. Low Calorie Dieting Increases Cortisol
A. Janet Tomiyama, Ph.D.,a Traci Mann, Ph.D.,b Danielle Vinas, B.A.,c Jeffrey M. Hunger, B.A.,b Jill DeJager, MPH., RD,d and Shelley E. Taylor, Ph.D.c
In other words, restraint—using our willpower—doesn’t just use energy. It causes stress.
A Brief Note On Cortisol
Cortisol is a glucocorticoid—a class of necessary regulatory hormones whose functions and interactions are far too complicated to discuss here. However, we know that persistently high cortisol levels are strongly associated with increased stress, and that administration of exogenous glucocorticoids (the fancy term for “giving them as drugs”) actually produces increased stress, along with a litany of terrible side effects.
“Side effects of oral corticosteroids that are used on a short-term basis include: an increase in appetite, weight gain, insomnia, fluid retention, and mood changes, such as feeling irritable, or anxious.
Side effects of oral corticosteroids used on a long-term basis (longer than three months) include: osteoporosis (fragile bones), hypertension (high blood pressure), diabetes, weight gain, increased vulnerability to infection, cataracts and glaucoma (eye disorders), thinning of the skin, bruising easily, and muscle weakness.”
–UK National Health Service
Persistently high cortisol not only makes you feel stressed, with all the nervousness, sleep disruption, and ugly side effects that entails…
“Low dose CRH [corticotropin-releasing hormone] administration significantly increased food intake compared to a placebo injection in healthy, non-obese adults, as measured by both calories and total grams consumed. The magnitude of the peak cortisol response to CRH was a strong predictor of subsequent food intake.
These data extend growing evidence of a link between stress response systems and human eating behavior, by suggesting that activity within the HPA axis – our central, neuroendocrine stress response system – is neurobiologically linked to food consumption.”
Note that George et. al. is an actual controlled study, not an associative population study…so we can conclude that there is a causal relationship, not just an association. Cortisol makes you eat, as do the other corticosteroids…as anyone who has taken prednisone for an extended period of time can tell you.
And since this paper does such a great job of summarizing the literature on glucocorticoids, I’ll simply quote it here:
Glucocorticoids also influence behavior and may further influence energy availability by altering food intake. In humans, chronic GC administration increases ad libitum food intake (Tataranni et al., 1996). In animal models, GCs appear to impact caloric intake through direct neuropharmacological effects (Dallman et al., 2007), and corticosterone has been shown to dose-dependently increase intake of palatable foods such as sucrose, saccharin (Bhatnagar et al., 2000), and lard (la Fleur et al., 2004). These findings may have relevance to the modern obesity epidemic – repeated stress-related GC release could cause excess intake of high calorie foods and contribute to weight gain. Indeed, animals prone to obesity have been shown to need circulating glucocorticoids in order for it to occur (Bray 1985) and GC receptor antagonism prevents or reverses weight gain in these animals (Okada et al., 1992). Interestingly, in humans, there is also a link between heightened HPA axis response to stress and abdominal obesity (Epel et al., 1999; Epel et al., 2000; Pasquali et al., 1993; Pasquali et al., 1999).
–Ibid.
Here’s a tidbit they missed, from a study on cortisol inhibitors in humans that found completely negative results from medicating cortisol levels downward…
…thus proving, once again, that these chemicals are metabolic markers, not control levers we can pull to produce a desired result. Artificially medicating one element of a complex homeostatic system doesn’t always fix a disequilibrium. In other words, you can’t fix your car by removing the “Check Engine” light.
“…There was a positive correlation between urinary free cortisol and fat intake in obese men during placebo periods when the product chosen was consumed.”
Conclusion: A Successful Diet Must Minimize The Role Of Willpower
The problem here should be obvious:
Restrained eating causes stress. Continually exercising your willpower in order to eat less food than you want—or different food than you want—is stressful.
Stress makes you eat more.
Unfortunately, in a world of supernormal stimuli, we can never completely disconnect our prefrontal cortex—because we’ll end up with a long roll of lottery tickets, as well as a shopping cart full of Cheez-Its and Mountain Dew…
…but it’s clear that we need to minimize its role, by bringing our two hunger drives (likes and wants) and our two satisfaction drives (satiation and satiety) as close as we can to their natural evolutionary state of balance and accord.
I’ll continue this series next week with an examination of several different pathological states of hunger, and how they can be explained by the interaction of these four motivations. Click here to continue!
Part I of this series clearly establishes the following, which I hope is non-controversial:
Hunger is not a singular motivation: it is the interaction of several different clinically measurable, provably distinct mental and physical processes.
This is intuitively obvious to everyone: hunger is not a generic drive, satisfiable by shoving a generic substance called “food” into our mouths. The fantasy of “food pills” remains squarely in the Future That Never Was, along with flying cars and nuclear power too cheap to meter.
I miss the future that never was.
While a bewildering variety of “meal replacement drinks” exists, walking down any commercial street in the world reveals restaurants—not kiosks with a row of Slurpee machines filled with flavors of Ensure, Slim-Fast, and Muscle Milk. And even the most dispiriting accretion of fast-food dispensaries around a freeway exit features everything from hamburgers to burritos to chicken salads to tuna sandwiches.
Fortunately, it’s possible to cut through the fog of conflicting motivations by analyzing these four drives in detail: “liking” and “wanting”, which make us eat, and “satiation” and “satiety”, which make us stop eating.
First, let’s define the four drives. I’ll start with the end of the process, for reasons that will become clear.
What Is Satiety? What Does “Sated” Mean?
“Satiety” is our body’s response to the absorption of nutrients through the intestine.
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.
The important takeaway here is twofold. First, satiety is not a conscious response over which we have any control.Satiety is our body’s direct measurement of actual nutrient intake—a system honed over hundreds of millions of years of evolution. It answers the question “Should I seek out food now—or can I do something else, like seek a mate, play with my children, or take a nap?”
Second, since satiety is based on actual nutrient absorption, which occurs through the small intestine, it takes a long time to receive any satiety cues from the food we eat. As I describe in this article, it takes 2.5-3 hours before half of a mixed meal has even left the stomach, much less been absorbed through the intestine! GI transit times vary dramatically, and are shorter for highly processed, fat-free foods—but it’s clear that satiety takes far too long for it to be a useful signal to stop eating.
Most likely this is why satiation is a separate biochemical process.
What Is Satiation? What Does “Satiated” Mean?
Satiation occurs when the value we place on another bite of food drops below zero. It is our estimate of the marginal utility of eating the next piece of food.
For those not familiar with the economic term, “marginal utility” refers to the value we place on acquiring one more of something. “Marginal” means that we may already have some of it, i.e. we may not be starting from zero. Furthermore, the concept of “diminishing marginal utility” is often useful, because the value we place on something usually decreases as we accumulate more of it. (There are exceptions, which we’ll discuss later.)
This is easy to demonstrate: imagine that we’re at a big outdoor concert, like Coachella. It’s very hot outside, we’re thirsty from standing in the sun and shouting along to bands we like, it would take us a long time to get out to the car and back in, and we don’t want to miss the next band. A cold bottle of water might be worth $5 to us at that point, or even more…so we willingly pay the extortionate $4 from the kiosk. Once we drink it, though, we’re no longer as thirsty as we were, so the value we place on a second bottle might be only $2. However, since the venue still charges $4, we don’t buy a second bottle. In other words, a transaction only occurs if the value we place on something is greater than or equal to the price at which it’s available.
It’s easy to understand satiation by going to an all-you-can-eat buffet: the value we place on each additional plate of food decreases until we decide it’s not even worth getting up from the table to take more—though we could have it for free!
Satiation is not the same thing as being full, or being sated. If all we have in the house is a jar of sweet pickles and a bag of Twizzlers, we might quickly become satiated, since we don’t want to eat any more of either. However, this does not leave us sated: our body knows that pickles and Twizzlers do not contain the nutrients we need to live.
The important distinction here is that satiation is an estimate, based on the sensory experience of eating. Ideally, satiation would accurately predict future satiety—but while satiety is a direct measurement of nutrient intake, and cannot be easily fooled, satiation is dependent on our perceptions.
You Can Fake Satiation, But You Can’t Fake Satiety
Satiation is affected by our senses of taste, smell, texture, and stomach distention; it’s affected by our perception of a food’s caloric and nutritional value; and it’s even affected by mundane considerations like serving size. Not only can satiation be overridden by sufficiently powerful wants, our perceptions of satiation (= future satiety) can easily be influenced or fooled entirely.
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. –Ibid.
Many different experiments prove that satiation can be manipulated: here are a couple I found interesting. Let me know if you find others!
“In the presence of visible fats, energy intake was lower than in the presence of hidden fats, suggesting that hidden fats may contribute to overconsumption.”
The effect was minor but significant: 8-9%. Our perceptions do not perfectly estimate the nutritive content of foods.
“Conclusion: This study shows that greater oral sensory exposure to a product, by eating with small bite sizes rather than with large bite sizes and increasing OPT [oral processing time], significantly decreases food intake.”
The effect was striking: people ate up to 50% more when able to eat freely vs. when limited to small bites every nine seconds! Therefore, satiation is also affected by how fast we eat and how big of a bite we take. The old advice to “eat slowly and mindfully” and “take small bites” does have some scientific support.
The study also contains this hidden gem: “The subjects had to be healthy, be aged 18–30 y, be of normal weight [body mass index (in kg/m2): 18.5–25.0], and like chocolate custard.”
Liking: the actual pleasure component or hedonic impact of a reward. Pleasure comprises two levels: (1) core ‘liking’ reactions that need not necessarily be conscious; (2) conscious experiences of pleasure…
In common usage, “liking” is the reward we anticipate from future consumption. However, in scientific usage, “liking” refers to the pleasure we feel from actually eating food—its hedonic impact.
Like “satiation”, “liking” is situationally dependent, and it is only nominally under conscious control. Cultural and social conditioning can affect our likes, particularly as children: for instance, most non-Japanese people find natto disgusting, and most non-Filipinos have a difficult time with balut.
It reminds me of Giger's "Alien".
Yes, that's a chicken embryo.
And though we cannot simply choose to “like” something, conscious efforts to affect our preferences will sometimes have an effect over time: for instance, most children find beer disgusting, and it’s well-known that most of us must “develop a taste” for it.
It is important to note that palatability is a major component of “liking”, and “hedonic impact” is the technical term for the pleasure associated with actual consumption. However, we must be careful to distinguish the reward itself from our perception of it. When we say we “like” a food, we may also be taking conscious perceptions and biases into account.
Food reward is not simply a physical property of a taste stimulus itself…Palatability, or the hedonic component of food reward, instead results from a central integrative process that can incorporate aspects not only of the taste, but of the physiological state and the individual’s associative history.
What is “Wanting”? What Are “Wants”?
“Wanting: motivation for reward, which includes both (1) incentive salience ‘wanting’ processes that are not necessarily conscious and (2) conscious desires for incentives or cognitive goals.” –Berridge and Kringelbach
Rephrased: Wants are desires at a specific moment in time. We measure them by how motivated we are to actually go out and get whatever it is we ‘want’. Applied to food, we often use the word “appetite”.
Note that wants are partially, but not entirely, under our conscious control. I might know that cake is bad for me, but that doesn’t stop me from wanting cake. Furthermore, wants vary dramatically over time depending on the degree of satiation and satiety we are experiencing. To use my previous example, if I’ve just eaten a 20-ounce prime rib, I’m unlikely to want any more prime rib…but that doesn’t mean I like prime rib any less.
You’ll note that I’m carefully avoiding the gory biochemical details of these sensory and motivational pathways. This is intentional, and it’s for two reasons: first, we don’t completely understand them, and second, they don’t really matter. The details of ghrelin, leptin, cholecystokinin, peptide YY, and the dopamine-reward system are fascinating…but since we’ve already demonstrated that there’s no magic pill we can take that blunts our hunger without making us poop our pants, we don’t have to understand all of the details.
In short, we can understand wanting, liking, satiation, and satiety (and their interactions) on a purely functional level. We don’t have to understand the biochemistry of these drives in order to eat like a predator.
We can relate satiation and wanting in this common-sense way: satiation occurs when we don’t want any more food.
A Summary Of The Components Of Hunger
Likes (scientific usage) = the pleasures we experience from eating, known scientifically as “hedonic impact”.
Wants = desires at a specific moment. A measure of our motivation to attain a reward. Our “appetite”.
Satiation = absence of motivation to eat more. The absence of attainable wants. An estimate of future satiety, based on the sensory experience of eating.
Satiety = a signal from your body that it is replete with nutrients.
Perceptions And Motivations In Harmony And In Conflict: Evolutionary Concordance And Discordance
Ideally, if everything were functioning properly, our likes and wants would always coincide, satiation would always be an accurate predictor of satiety, and the combination of hunger signals (likes and wants) and satisfaction signals (satiation and satiety) would result in energy and nutrient balance.
Existing in this state of harmony and balance would have been strongly selected for throughout tens of millions of years of evolutionary history, all the way back to the great apes and beyond. Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would have been strongly selected against.
However, we can see that both the simple states of hunger and non-hunger, in which our motivations agree, are just two possible outcomes of the collision of these four processes—and that just as hunger isn’t necessary to make us eat, non-hunger isn’t sufficient to make us stop eating.
Furthermore, we can see that these disorderly outcomes are most likely the product of evolutionary discordance.
I’ll explore some of those issues in Part III and beyond.
Are you finding this series valuable? Does this breakdown allow you to explain hitherto confusing concepts? Leave a comment, and spread it using the buttons below!
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