- 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.
American Psychologist, Vol 62(3), Apr 2007, 220-233.
Medicare’s search for effective obesity treatments: Diets are not the answer.
Mann, Traci; Tomiyama, A. Janet; Westling, Erika; Lew, Ann-Marie; Samuels, Barbra; Chatman, Jason
“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.”
Am J Clin Nutr. 2009 July; 90(1): 33–40.
Dieting, restraint, and disinhibition predict women’s weight change over 6 y
Jennifer S Savage, Lesa Hoffman, and Leann L Birch
“Women who reported dieting at study entry were heavier at study entry and gained more weight over time than did nondieters.”
Appetite. 2006 Jul;47(1):83-90. Epub 2006 May 2.
Multiple types of dieting prospectively predict weight gain during the freshman year of college.
Lowe MR, Annunziato RA, Markowitz JT, Didie E, Bellace DL, Riddell L, Maille C, McKinney S, Stice E.
“…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.
“…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!
J Pers Soc Psychol. 2007 Feb;92(2):325-36.
Self-control relies on glucose as a limited energy source: willpower is more than a metaphor.
Gailliot MT, Baumeister RF, DeWall CN, Maner JK, Plant EA, Tice DM, Brewer LE, Schmeichel BJ.
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.
And here’s the popular version, from the New York Times.
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:
Am J Clin Nutr. 2001 Jan;73(1):7-12.
Cognitive dietary restraint is associated with higher urinary cortisol excretion in healthy premenopausal women.
McLean JA, Barr SI, Prior JC.
J Gerontol A Biol Sci Med Sci. 2006 Jun;61(6):628-33.
High cognitive dietary restraint is associated with increased cortisol excretion in postmenopausal women.
Rideout CA, Linden W, Barr SI.
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…
…it makes you eat!
Psychoneuroendocrinology. 2010 May; 35(4): 607–612.
CRH-stimulated cortisol release and food intake in healthy, non-obese adults
Sophie A. George, Ph.D., Samir Khan, Ph.D., Hedieh Briggs, M.S.W., and James L. Abelson, M.D., Ph.D.
“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).
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.
Physiol Behav. 1993 Oct;54(4):717-24.
The effects of the acute administration of RU 486 on dietary fat preference in fasted lean and obese men.
Kramlik SK, Altemus M, Castonguay TW.
“…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!
Live in freedom, live in beauty.
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