• 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.


When Satiation Fails: Calorie Density, Oral Processing Time, and Rice Cakes vs. Prime Rib (Why Are We Hungry? Part V)

Caution: contains SCIENCE!

(Part V of a series. Go back to Part I, Part II, Part III, or Part IV—or skip to Part VI.)

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 vs. Satiety, Satiated vs. Sated: Understanding The Differences

In common use, “satiation” and “satiety” are basically synonyms. Even the scientific literature does not always maintain or respect the difference, so it’s important to understand and distinguish exactly what’s being discussed.

Satiety is your body’s response to the availability of nutrients from food that you’ve already digested and processed. (We discussed satiety at length in Part IV.)

Satiation is your immediate reaction to the ingestion of food—the drive that causes you to stop eating. It is your body’s attempt to estimate future satiety via sensory input: smell, taste, texture, and stomach distention.

I’ve quoted this passage before, but I’ll quote it again, because it’s important:

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

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.

It’s difficult to draw a sharp line between satiation and satiety: some foods digest very quickly, and their nutrients are available quickly enough for satiety to affect the satiation response. (Example: simple sugars and carbohydrates, whey protein isolate.) And there is strong support for the idea that taking longer to eat results in lower food intake, probably because the satiety response begins to come into play.

Satiation Is Relative To Satiety

Since satiation is an attempt to predict (via sensory input) future satiety (i.e. nutrient absorption), it should be obvious that our current state of satiety affects what foods we find satiating—or not satiating. Here’s an interesting example of this effect:

J. Nutr. January 1, 1998 vol. 128 no. 1 61-67
Prior Day’s Intake Has Macronutrient-Specific Delayed Negative Feedback Effects on the Spontaneous Food Intake of Free-Living Humans
John M. de Castro

Food energy intake during a day was found to only mildly affect intake on the subsequent day (mean r = −0.07, P < 0.001), but was more strongly negatively related to intake occurring on the second (mean r = −0.18, P < 0.001) and third day (mean r = −0.10, P < 0.001) afterward.

Each macronutrient was shown to have a maximal negative relationship with subsequent intake of that same macronutrient, with 2-d lag mean autocorrelations equal to −0.11, P < 0.001 for carbohydrate, equal to −0.18, P < 0.001 for fat, and equal to −0.13, P < 0.001 for protein. These effects on daily intake were found to result from separate negative feedback effects on meal size and frequency.

Stated plainly: not only does eating more food cause you to eat less food 2-3 days afterward—eating more protein, fat, or carbohydrate causes you to eat less of the same 2-3 days afterward. Here are the graphs:

The effect is not large, but it is consistent and significant.

And though deCastro didn’t graph meal size and frequency, they were also compensated for with a 2-3 day time lag.

There are some studies that claim to show macronutrient compensation doesn’t exist—but they examine only the next meal eaten on the same day, or perhaps the morning after.

This is only one example of satiety affecting satiation, but I think it proves the point: satiation is relative to your current state of satiety. (For another real-world example of the effects of previous meals on satiety, see the study referenced in my classic article How “Heart-Healthy Whole Grains” Make Us Fat.)

We’re all familiar with the manifestations of this effect. For instance, after two weeks of living primarily on bento boxes and bowls of ramen while in Japan, my friend and I found ourselves absolutely craving red meat—and we proceeded to draw a crowd of spectators at an all-you-can-eat yakiniku restaurant, by eating more than any of them had probably seen consumed at once by anyone but a sumo wrestler.

Yakiniku = grill your own meat, at your own table. Basically Korean BBQ without the kimchi.

How Satiation Fails: Bypassing Sensory Input

Since satiation is dependent on sensory input, it seems logical that we can break satiation by bypassing or attenuating the sensory experience of eating.

This is, in fact, the case.

It has been known for a long time that the obese eat more quickly than the non-obese:

Int J Obes. 1977;1(1):89-101.
Eating in public places: a review of reports of the direct observation of eating behavior.
Stunkard A, Kaplan D.

…Two measures showed promise in discriminating obese from non-obese persons. The first was food choice: obese persons chose more food than non-obese persons (and men chose more than women and tall persons more than short ones). The second measure was rate of eating: obese persons consumed more food per minute than non-obese persons.

Further reading: Psychosom Med Vol. 42, No. 6
Eating Style of Obese and Nonobese Males
Kaplan D

And under controlled conditions, people eat more when they are allowed to eat quickly than when their eating rate is restricted:

Am J Clin Nutr August 2009 vol. 90 no. 2 269-275
Effect of bite size and oral processing time of a semisolid food on satiation
Nicolien Zijlstra, René de Wijk, Monica Mars, Annette Stafleu, and Cees de Graaf

Results: Subjects consumed significantly more when bite sizes were large than when they were small (bite size effect: P < 0.0001) and when OPT [oral processing time] was 3 s rather than 9 s (OPT effect: P = 0.008). Under small bite size conditions, mean (±SD) ad libitum intakes were 382 ± 197 g (3-s OPT) and 313 ± 170 g (9-s OPT). Under large bite size conditions, ad libitum intakes were much higher: 476 ± 176 g (3-s OPT) and 432 ± 163 g (9-s OPT). Intakes during the free bite size conditions were 462 ± 211 g (free OPT), 455 ± 197 g (3-s OPT), and 443 ± 202 g (9-s OPT). 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, significantly decreases food intake.

Many food choices can increase our rate of eating. We can eat liquid foods more quickly than solid foods, soft foods more quickly than hard foods, tender foods more quickly than tough foods.

For instance, “meal replacement shakes”, being liquid, don’t produce the same satiation response as eating real food:

Journal of Comparative and Physiological Psychology Volume 68, Issue 3, July 1969, Pages 327-333 doi:10.1037/h0027518
Preloading and the regulation of food intake in man
Barbara C. Walikea, Henry A. Jordan and Eliot Stellar

“17 human Ss [Ss = subjects] ate 20-min meals of Metrecal through a straw connected to a hidden reservoir. Oral preloads of Metrecal were administered before the meals, and these varied 20-120% of the amount of the base-line meal intake and were given 1-120 min. before the meal. Test-meal intake was depressed as a function of the size of the preload; however, the Ss did not take the preload fully into account and they overate.

Note: Metrecal started the 1960s craze for meal replacement shakes. Its ingredients: “A mix of skim-milk powder, soybean flour, corn oil, minerals and vitamins.” (More information here.) It is also claimed that Metrecal tasted absolutely terrible—though since it hasn’t been produced since the 1970s, there’s no way to know for sure.

And people eat more yogurt when they can suck it through a straw than when they have to use a spoon:

Am J Clin Nutr April 2010 vol. 91 no. 4 841-847
Intake during repeated exposure to low- and high-energy-dense yogurts by different means of consumption
Pleunie S Hogenkamp, Monica Mars, Annette Stafleu, and Cees de Graaf

Results: Intakes (P = 0.01) and eating rates (P = 0.01) were highest in the liquid/straw group. Average intakes over 10 exposures were 575 ± 260 g for liquid/straw, 475 ± 192 g for liquid/spoon, and 470 ± 223 g for semisolid/spoon; average eating rates were 132 ± 83 g/min for liquid/straw, 106 ± 53 g/min for liquid/spoon, and 105 ± 88 g/min for semisolid/spoon.

Conclusions: We observed no energy intake compensation after repeated exposure to yogurt products. Differences in ad libitum yogurt intake could be explained by eating rate, which was affected by the different means of consumption.

From this, we can see that it’s easy to bypass our satiation response by eating highly processed foods. Processing (and cooking) basically pre-digests food for us, which increases both the speed at which we can eat it and the speed at which we can absorb it.

Even the toughest, stringiest cut of modern beef is from an animal that has never had to run from predators…and it’s been ‘aged’ for at least two weeks, which is to say that it’s been left to slowly rot in its own digestive enzymes in order to make it softer and more tender.

Thought experiment: consider the rate at which you could hack meat and fat off of a fresh bison carcass using sharp rocks, and the rate at which you could chew and swallow that raw meat—versus the speed at which you can gobble down medium-rare hamburger or prime rib.

Finally, I’ll note that an increasing cultural tendency to “eat on the run” increases our rate of food ingestion. Gobbling down food in a hurry because we need to get back to work, or pick up the kids, or get our shopping done, seems likely to cause us to eat more regardless of what we’re eating—and taking the time to savor our food and enjoy the process of eating is likely to cause us to eat less, again independently of what we’re eating.

Not an environment that encourages savoring food.

It's called 'fast food' for excellent reasons.

It is also most likely the case that eating while distracted—watching TV, working, driving—attenuates the sensory experience of eating, and thereby the satiation response. (Hat tip to alert commenter JKC.) There is much more to investigate here.

Stomach Distention: Necessary But Not Sufficient

Finally we turn to stomach distention: the sensation of being “full”.

I’ve saved the best part for last…so keep reading!

A lot of noise has been made about how “energy density” is the key to dieting—usually by low-fat apostles who never fail to recite the fact that protein and carbohydrate have roughly four calories per gram, whereas fat has about nine. The same theory lies behind the Volumetrics Diet, which pushes high-bulk, low-fat foods as the key to weight loss—and it drives our medical establishment to perform tens of thousands of lap-band surgeries and gastric bypasses every year.

Unfortunately, feeling “full” is not the entire story, as we can demonstrate by one simple fact: if it were, all anyone would need to lose weight is a giant jar of sugar-free Metamucil. Now that we’ve solved the obesity problem, we can all go home, right?

Well, no. As I explained back in Part II, you can fake satiation, but you can’t fake satiety. Eating extremely energy-dense foods can indeed cause us to overeat…but if we’re not getting the energy and nutrients we need, consuming more water and eating more indigestible fiber does not magically make us feel satiated or sated.

In support of this, note the long-term results from stomach stapling (VBG, or “vertical banded gastroplasty”) and lap-band surgery:

J Gastrointest Surg. 2000 Nov-Dec;4(6):598-605.
Ten and more years after vertical banded gastroplasty as primary operation for morbid obesity.
Balsiger BM, Poggio JL, Mai J, Kelly KA, Sarr MG.

“Weight (mean +/- standard error of the mean) preoperatively was 138 +/- 3 kg and decreased to 108 +/- 2 kg 10 or more years postoperatively. Body mass index decreased from 49 +/-1 to 39 +/- 1. Only 14 (20%) of 70 patients lost and maintained the loss of at least half of their excess body weight with the VBG anatomy. Vomiting one or more times per week continues to occur in 21% and heartburn in 16%.

Note that the long-term results of lap-band surgery (“gastric banding”) are very similar: “no significant difference in weight loss was registered between the 2 study groups” (Miller et.al.)

While the average patient maintained a 30 kg weight loss, this didn’t get them even halfway to normal weight: only one in five patients managed to maintain this milestone.

Energy Density: It’s Not The Fat, It’s The Water

Clearly low energy density isn’t a panacea—but it does make some difference to satiation. Let’s take a look at the data!

Besides protein, fat, and carbohydrate, foods typically contain “fiber” (indigestible carbohydrate) and water. While the anti-meat, anti-fat brigade concentrates on 9 vs. 4 calories per gram, we need to take into account the fact that meat is comprised primarily of water.

I’ll handicap the comparison by choosing an extra-fatty USDA Prime grade of prime rib, which contains 367 calories per 100 grams, or about 3.7 calories per gram. (Link.)

In contrast, rice cakes contain 392 calories per 100 grams, or almost 4 calories per gram. (Link.) That’s right: rice cakes are a denser source of calories than prime rib!

That’s because rice cakes, like all shelf-stable foods, have most of the water removed in order to preserve them and retard bacterial growth. As a rule, anything you’ll find in a box on the shelf will be dehydrated—and, in consequence, extremely calorie-dense.

Dehydration and Preservation

We’re all familiar with the phenomenon of stored food getting wet and rotting, or going moldy. Since life requires water, one of the best ways to keep food from spoiling is to remove all the water, and seal it to stop water from getting in—thus preventing bacteria from growing on or in it.

For instance, pemmican is just meat with all the water removed: the fat is separated from the meat and boiled to remove the water, while the meat is air or oven-dried and ground into bits.

Here are some “calories per 100 grams” readings for common “healthy” packaged foods—

—all of which are more calorically dense than prime rib!

In contrast, here are some statistics for whole paleo foods commonly derided as “rich”, “heavy”, and “fattening”:

Furthermore, as long as we’re talking about water, we must take into account the water we consume along with the food we eat. Some studies claim that oatmeal is the most satiating food in the world—but if you don’t allow people to drink, a food made with mostly water will be more ‘filling’ than a drier food, even if the real-world result would be equal bulk due to the drier food making you more thirsty.

A Speculative Hypothesis About Water Intake

Since we require water in order to process salt, it might very well be that a low-salt diet causes decreased water consumption and a parallel decrease in satiation during real-world meal consumption. A similar situation might also occur with bland vs. spicy food: increased water intake with spicy food might result in greater satiation.

If anyone knows any research that addresses this issue, please let me know. Most studies don’t allow or record ad lib water consumption, and therefore aren’t much help.

(It is also the case that it takes more time to chew and eat a less calorically dense food than a more calorically dense food…so density most likely affects eating rate as well as gastric distention. And how much do you have to chew a steak, versus breakfast cereal?)

Finally, we address the standard bulking agent: “fiber”. Most of the controlled studies on fiber address the “heart-healthy” claims and focus on blood lipoprotein levels, but this review conveniently summarizes the available literature relating to weight loss:

Gastroenterology. 2010 January; 138(1): 65–72.e1-2.
Dietary Fiber Supplements: Effects in Obesity and Metabolic Syndrome and Relationship to Gastrointestinal Functions
Athanasios Papathanasopoulos, M.D. and Michael Camilleri, M.D.

Recent meta-analyses of randomized controlled studies (RCTs) suggest only minor effects on weight loss for commonly used DF supplements.

Conveniently, Table 3 lists the studies and their findings—and a quick reading shows that the studies whose only intervention was additional fiber resulted in zero or insignificant weight loss, whereas the studies that resulted in significant weight loss were compound interventions of which fiber was only one small component.

Conclusion: How We Break Satiation

  • Since satiation is an estimate of future satiety based on sensory input, much of satiation is driven by our body’s nutritional needs, and the factors that affect satiety will also affect satiation.
  • Therefore, we can fail to achieve satiation by eating nutritionally incomplete foods, with no protein (or incomplete protein) and few nutrients.
  • Since satiation is dependent on sensory input, we can fool satiation by decreasing sensory exposure to our food—or otherwise attenuating the sensory experience of eating.
  • We can do this by eating quickly, which we usually accomplish by eating food in liquid or other highly processed (and, therefore, pre-digested) forms. It is also likely that caloric density enables quicker eating to some degree.
  • Cultural factors may also play a role in satiation. A culture that treats eating as an inconvenient obstacle to accomplishment, rather than an experience to be savored, seems likely to decrease our sensory exposure to food by eating quickly (“on the run”) or while distracted, thereby reducing satiation and encouraging overconsumption.
  • Decreased caloric density also increases satiation, to a degree—but it is primarily driven by water content, not by calories per gram of macronutrient. Packaged foods are typically far more calorie-dense than whole, fresh foods due to dehydration.
  • Dietary fiber may increase satiation—but since it has no significant effect on long-term weight loss, it clearly has no effect on satiety.

Continue to Part VI: Hedonic Impact (“Liking”), Incentive Salience (“Wanting”), and “Food Reward”: Why Are We Hungry? Part VI

Live in freedom, live in beauty.


(Part V of a series. Go back to Part I, Part II, Part III, or Part IV.)

Did you find this article surprising or illuminating? Yes, you did, because you didn’t know that prime rib is less calorically dense than rice cakes.

You can support my continued efforts to inform, educate, and amuse you by buying a copy of my “Funny, provocative, entertaining, fun, insightful” novel The Gnoll Credo. US residents can buy signed copies directly from my publisher, Barnes and Noble offers free shipping to the USA, and it’s available worldwide, with free shipping, through (EDIT: link fixed) The Book Depository.

(Yes, you can still buy it through Amazon.com, but they’re taking at least a week to ship.)

When Satiety Fails: Why Are We Hungry? Part IV

Caution: contains SCIENCE!

(Part IV of a series. Go back to Part I, Part II, or Part III, or skip to Part V.)

This is a long and detailed article, but it’s very important. I believe the conclusions justify the length: we’re done laying groundwork, and we’re finally starting to build some answers to the original question: “Why are we hungry?”

I must emphasize that I have no stake in any of the current controversies. I have no diet books for sale and no research thesis to defend, and I began this series long before the AHS. My concern is (as always) to organize and present the facts as I understand them to you, my readers, so you can draw useful conclusions about your own diet and life.

Furthermore, my diet at the moment contains roughly a Perfect Health Diet-compliant 15% of carbohydrate, plus whatever I need for intense physical activity (though I don’t count or track my intake), so I don’t believe I belong to either the high-carb or low-carb camps.

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.

Now we can examine some of the ways that our hunger signals fail us.

It is important to remember that, by definition, all our hunger drives are in balance with our willpower at any moment in time! Otherwise we would be eating more or less than we are. The issue is that for many of us, this balance is only reached at an unhealthy weight or body composition—or it involves an excessively stressful amount of willpower. Part III explores this subject in detail.

Why Are We Ever Sated?

The desired result of eating is satiety: our body’s signal that it is replete with nutrients. But first, let’s ask a question: why are we ever sated? Since starvation is an animal’s primary concern, why didn’t Paleolithic humans simply eat themselves into obesity whenever possible?

We all know what happens if we eat a big meal just before intense exercise: at best, our performance suffers greatly, and at worst, we vomit. This is because digestion requires a meaningful amount of energy. Clearly it would be counterproductive to go hunting when our mental and physical performance is greatly impaired. Even foraging would be impaired, as gathering in the wild requires a keen eye and close attention, and the brain uses perhaps 20% of our energy at rest.

So it’s clear that we must wait until our body has either used or stored the energy and nutrients from our previous meal before we perform at our best. The fact that ghrelin is neurotrophic makes this clear: our brains only kick into high gear when it would be both possible and beneficial to acquire more food.

This suggests an obvious consequence: energy retrieval from storage is an important part of satiety. We don’t eat via a constant intravenous infusion of exactly the nutrients we need, at exactly the rate we are using them: we digest them and store them for use as needed. I’ll explore this in detail below.

Polar Bears Playing

Not so well suited to the African savanna.

A secondary motivation is that stored fat both traps heat and slows us down. Since humans evolved as diurnal (daytime-active) hunters and foragers on the African savanna, heat dissipation was often our limiting factor in procuring food. (This is most likely why we are hairless and have sweat glands, as opposed to the inches-thick layer of fat surrounding, say, a polar bear.) And, of course, fat adds weight: consider how much slower you’d run with an extra 20 pounds attached to you. (Put on some two-pound wrist and ankle weights, a vest with twelve pounds of sand in the pockets, and see how fast you run the 400-meter.) So while some fat accumulation would have been beneficial as a buffer against bad times, there was clearly a point beyond which fat accumulation would have impaired our ability to hunt and forage.

Everything Flows Downhill From Satiety

As we previously established, satiety is our body’s signal that it is replete with nutrients. Therefore, it should be obvious that nothing can make up for a lack of satiety: no amount of tricks to achieve temporary satiation will make up for a nutritional deficiency.

Satiety Is Not Generic

As stated back in Part II, “hunger” is not a generic drive, satisfiable by a generic substance called “food”. A properly functioning animal is hungry for different foods, depending on its nutritional status: even butterfiles—insects!—are smart enough to lick water off of mineralized rocks, and every animal, from aardvark to zebra, is capable of finding and ingesting the myriad nutrients it needs to survive.

The Salt-Mining Elephants of Kitum Cave

There are caves in Mount Elgon National Park, Kenya, partway up the shield of the extinct volcano Mount Elgon. (The best-known is called Kitum Cave.) The soil in the park is of recent volcanic origin, and the high rainfall washes away many of its minerals, leaving animals throughout the reserve deficient in many things—most critically, sodium.

Kitum Cave reaches over 700 feet into the side of Mount Elgon, and the cave complex of which it is a part contains the only known salt deposits in the region. Consequently, nearly every herbivore in the park must make periodic pilgrimages to the cave—up the side of the mountain, and over a long, narrow, dangerous path with no escape—in order to lick sodium sulfate from the rocks of Kitum Cave. In fact, it is plausibly argued that Kitum Cave was primarily created by the mining actions of elephants scraping salt from its walls and floor!

Joyce Lundberg and Donald A. McFarlane
Speleogenesis of the Mount Elgon elephant caves, Kenya
GSA Special Papers 2006, v. 404, p. 51-63
(fulltext, includes pictures and figures)

From Lundberg and McFarlane’s overview article, “Mount Elgon’s Elephant Caves”:

“The caves, of which Kitum and Makingeny are the best known, have long been known to attract elephants and other animals. The herbivores enter the dark cave interiors to consume salts, mainly mirabalite and sodium sulphate (Glauber’s salt) that effloresce from the cave walls. The crystals are gouged out by elephant trunks and bushbuck teeth and licked off wall by buffalo.”

Elephants in Kitum Cave

Elephants in Kitum Cave.

BBC 2 once aired an amazing documentary called “Elephant Cave”, which shows just how dangerous the round-trip to and from the cave is. Unfortunately it’s not available to watch online, but the enterprising web searcher can probably find a torrent of it.

Note that Kitum Cave is not the only example of a salt ingestion cave, just the largest known:

Lundquist Charles A., Varnedoe Jr. William W.
Salt ingestion caves
International Journal of Speleology, vol 35, issue 1, pp. 13-18, 2006.
(Note: containts link to fulltext PDF)

In conclusion, even small, skittish herbivores like bushbucks have instinctive hunger drives of sufficient discernment to motivate them to make a dangerous pilgrimage up a volcano to obtain just one of the many nutrients—sodium—they need to live.

We should not expect any worse from the hunger drives of a properly functioning human animal.

How Satiety Fails

Now we are ready to dig into the meat of this essay.

Satiety can fail in three ways:

  • We fail to ingest the energy and/or nutrients our body requires.
  • We fail to absorb the energy and/or nutrients our body requires.
  • We cannot retrieve the energy and/or nutrients our bodies have stored.

Satiety Failure #1: Failing To Eat The Real Food We Require

We know from experience that no matter how many calories worth of Skittles or Oreos we eat, we won’t satisfy our hunger. Our stomachs might be full to bursting—but as soon as we have room to digest it, we’ll be hungry again, because Skittles and Oreos don’t give us the nutrients we need to live. And as I’ve explained above, satiety is not generic: if we’re short on any one of the hundreds of nutrients our body needs, we’ll keep eating until we get it.

I’ve linked this study before (hat tip to Fat Fiction), but since it’s so illustrative, I’ll link it again:

Y Li, C Wang, K Zhu, R N Feng and C H Sun
Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women
International Journal of Obesity (2010) 34, 1070–1077

“After 26 weeks, compared with the placebo group, the MMS group had significantly lower BW [body weight], BMI, FM [fat mass], TC and LDL-C, significantly higher REE [resting energy expenditure] and HDL-C, as well as a borderline significant trend of lower RQ [respiratory quotient] (P=0.053) and WC [waist circumference] (P=0.071). The calcium group also had significantly higher HDL-C and lower LDL-C levels compared with the placebo group.”

How much is “significant”? From the summary:

“…The multivitamin and mineral group lost an average of 3.6 kg (8 pounds) of body weight, compared to 0.9 kg (2 pounds) and 0.2 kg (0.44 pound) for the calcium and placebo groups, respectively.

Protein targeting is another very important issue (previously discussed here.) Our bodies have an absolute requirement for complete protein—but unlike carbohydrate or fat, we have no storage depots for it. So if we don’t get complete protein in our diet, we must disassemble our own tissues to get it. (Previously discussed here.)

“Protein” is just chains of amino acids. “Complete protein” is protein containing all the essential amino acids—the ones we must eat because our bodies can’t make them—roughly in the proportions our body needs them.

On the other hand, if we eat too much complete protein, our bodies have a limited capacity to convert it into glucose…so we tend to desire neither too much nor too little complete protein. For more on protein targeting, including links to the scientific literature, read Dr. Paul Jaminet’s excellent summary, “Protein, Satiety, and Body Composition.”

(This satiety mechanism can be extended to other essential nutrients—but this article is already far too long!)

In closing, I’ll note that a can of Pringles has the same number of calories as a dozen large hard-boiled eggs. Which will leave you sated hours later: 32 Pringles (300 calories), made of seed oil and potato slurry—or four hard-boiled eggs (300 calories), containing 12g of complete protein and a host of vitamins, minerals, and essential nutrients like choline and lutein?

Satiety Failure #2: Failing To Absorb Nutrients

It doesn’t matter if we eat real food if we can’t absorb its nutrients.

Unfortunately, covering the various gut malabsorptions and dysbioses, such as celiac, IBS, Crohn’s, and SIBO, is well beyond the scope of this series. However, I must stop to point out that a diet low in simple sugars and high-GI simple starches, and that eliminates the antinutrients, enzyme inhibitors, and gut irritants found in grains and (to a lesser extent) beans and many nuts, is beneficial for almost all such issues.

Yes, I’m talking about a functional paleo diet.

(Those interested in digging more deeply into the subject might want to watch Dr. BG’s presentation at AHS 2011. Here’s the video, and here are the slides.)

Satiety Failure #3: Energy Stuck In Storage

We use energy continually throughout the day. And depending on how active we are, our energy usage can go from ‘minimal’ (sitting on couch watching TV) to ‘moderate’ (walking, intense mental activity) to ‘huge’ (sprinting at top speed, lifting heavy objects).

Yet we do not eat a constant stream of calories that corresponds exactly to our current degree of physical and mental effort. Our bodies must store the energy we eat for later usage. And as our storage capacity for glucose (as glycogen) is very limited, our body’s long-term energy storage is…fat.

Glycogen: A Short Explanation

A glycogen hairball.

Glycogen is a big hairball of glucose molecules connected to a protein called glycogenin, and it’s how our body prefers to store glucose. However, our body’s glycogen reserves are small: perhaps 70g in the liver and 200g in all our skeletal muscles, combined.* (The second capacity increases with muscle mass and training: a large, muscular, trained athlete can store perhaps 400g.) Furthermore, glycogen cannot be shuttled out of or between muscles: it’s only available to the muscle containing it.**

This isn’t very much energy: about 1100 calories’ worth, of which only 240 are available to the brain via the liver. So our bodies store most excess energy as fat, which is more energy-dense (approximately 9 calories/gram vs. 4), and for which we have a basically infinite storage capacity in our adipose tissue (‘fat cells’).

* Figures cited for muscle glycogen storage vary widely, and I haven’t found an authoritative source. Furthermore, it’s not clear how deeply storage is or can be depleted by exercise: even running to exhaustion only depletes specific muscles by perhaps 40-60%.
** This study (hat tip to alert commenter Franco) appears to show that glycogen can move slowly between muscles (over the course of hours), but only after exercise and only when fasted. Transfer doesn’t appear to be significant during exercise.

But what if we had trouble using fat for energy—or using energy at all? Clearly we’d have a problem: we would eat food, and as soon as the energy was either used or stored, we’d be hungry again—even though we were gaining weight!

This is exactly what happens to many people.

I’ve previously discussed metabolic flexibility and the RER (“Respiratory Exchange Ratio”), also known as the RQ (“Respiratory Quotient”), at length in this article. Metabolic flexibility (“met flex”) is the ability of our cells (specifically, our mitochondria) to switch back and forth between glucose oxidation and fat oxidation for energy, and the RER/RQ is how we measure what proportion of glucose vs. fat we’re burning.

It turns out that:

  • The obese have impaired metabolic flexibility.
  • The obese have impaired mitochondrial capacity to turn nutrients into energy in the muscles.
  • The obese have an impaired ability to oxidize fat for energy, which we can objectively measure.
  • Both the formerly obese and the soon-to-be-obese also suffer these impairments.

Linda Bakkman, Maria Fernström, Peter Loogna, Olav Rooyackers, Lena Brandt, Ylva Trolle Lagerros
Reduced Respiratory Capacity in Muscle Mitochondria of Obese Subjects
Obes Facts 2010;3:371-375
(fulltext available as PDF)

“Obese subjects had a decreased respiratory capacity per mitochondrial volume compared to the reference groups: this was evident in state 4 (65% and 35% of reference group A and B, respectively) and state 3 (53% and 29% of A and B, respectively) (p < 0.05)."

In other words, obese people have a greatly decreased ability to create energy from the nutrients they ingest.

The ability to oxidize fat is also impaired. How great is this impairment?

Ranneries, C., Bulow, J., Buemann, B., Christensen, N. J.,
Madsen, J., & Astrup, A.
Fat metabolism in formerly obese women.
AJP – Endo January 1998 vol. 274 no. 1 E155-E161

“…Fat mobilization both at rest and during exercise is intact in FO [formerly obese], whereas fat oxidation is subnormal despite higher circulation NEFA levels. The lower resting EE [energy expenditure] and the failure to use fat as fuel contribute to a positive fat balance and weight gain in FO subjects.”

The difference is remarkable. From Table 2 of Ranneries et.al., we find these startling facts:

  • Normal subjects are burning 30% more calories at rest than the formerly obese.
  • Normal subjects are burning 7% carbs and 78% fat at rest, whereas formerly obese subjects are burning 49% carbs and 34% fat at rest!

Let that sink in for a moment. These aren’t even the obese: they’re the formerly obese. So the theory that some people become “metabolically broken” has factual support.

Here’s the graph of fat oxidation before, during, and after an hour-long bout of exercise. The triangles are controls, the circles are the formerly obese:

Fat oxidation in the normal vs. formerly obese

Fraction of energy expenditure covered by fat oxidation (E%) during rest (t = 0 min), exercise (t = 0–60 min), and recovery (t = 75 min) in formerly obese subjects (FO, •) and matched controls (C, ▿). Values are means ± SD.

We can easily see that normal subjects have metabolic flexibility—the ability to switch back and forth between carb and fat oxidation—whereas the formerly obese are impaired. (Though exercise does increase metabolic flexibility, as I’ve previously noted.)

Continuing, we see that RER (= RQ) is predictive of future obesity:

F. Zurlo, S. Lillioja, A. Esposito-Del Puente, B. L. Nyomba, I. Raz, M. F. Saad, B. A. Swinburn, W. C. Knowler, C. Bogardus, and E. Ravussin
Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ
AJP – Endo November 1990 vol. 259 no. 5 E650-E657

“Subjects with higher 24-h RQ (90th percentile) independent of 24-h energy expenditure were at 2.5 times higher risk of gaining greater than or equal to 5 kg body weight than those with lower 24-h RQ (10th percentile).”

There are many more interesting papers I could cite and quote here—but if I do so, this article will expand to an unreadable size! So, instead of bombarding you with more citations, I’ll quote this excellent research review, which contains more citations for the above facts, and even more fascinating data for which space does not permit discussion.

Mary Madeline Rogge
The Role of Impaired Mitochondrial Lipid Oxidation in Obesity
Biol Res Nurs April 2009 vol. 10 no. 4 356-373
(fulltext available as PDF)

“Figure 2. In obesity, impaired glucose tolerance, and type 2 diabetes, mitochondrial beta-oxidation is decreased in skeletal muscle cells.

[Beta-oxidation is the process by which mitochondria produce energy from fat.]

“Carnitine palmitoyltransferase 1 (CPT1) activity, necessary for the transport of long-chain fatty acids into the cell, is diminished, leading to the accumulation of fatty acyl-CoA within the cytosol. Under the influence of the enzyme acetyl-CoA carboxylase (ACC), unmetabolized fatty acyl-CoA is converted to malonyl-CoA and committed to the re-synthesis of fatty acids, which can accumulate within the cell or be transported to other tissues as triglycerides. The reduced ability to use fatty acids for ATP production increases obese individuals’ reliance on glycolysis and decreases their exercise capacity.

If you want to learn more, p. 361 of the full text and the subsection “Decreased Fat Oxidation” will be quite illuminating, and I strongly recommend reading it. For that matter, just read the whole paper, as it’s an excellent overview and summary.

These facts provide an explanation for the additional fact that some people, particularly the obese, do not find carbohydrate to be satiating:

Chambers L, Yeomans MR.
Individual differences in satiety response to carbohydrate and fat. Predictions from the Three Factor Eating Questionnaire (TFEQ).
Appetite. 2011 Apr;56(2):316-23. Epub 2011 Jan 8.

“Those scoring high on the TFEQ-disinhibition scale consumed more energy at the snack test than those with low TFEQ-disinhibition, but this was only following the high carbohydrate breakfast. … In normal-weight females the tendency to overeat may be related to insensitivity to the satiating effects of carbohydrate.”

An impaired ability to burn fat for energy means that you will no longer be sated once your blood sugar drops, leaving you hungry again—even though most of the energy has been stored and you are in positive energy balance. In other words, the combination of impaired fat oxidation and a high-carbohydrate, low-fat diet is likely to leave you both hungry and gaining weight. (See this study for a real-world instrumented comparison.)

Impaired fat oxidation also causes the “low carb flu”. You’re forcing your body to adapt to burning fat by refusing to provide it with carbohydrate—but since your mitochondria don’t burn fat very well, you’ll have very little energy until you adapt.

I conclude this section with several thoughts:

First, this is not the “greedy fat cells” theory of obesity, which posits an inability of the obese to retrieve fat from fat cells into circulation. That ability appears to be intact. What is indisputably damaged is the mitochondrial function of the obese, the formerly obese, and the soon-to-be-obese, and their ability to oxidize fat for energy.

Second, any valid theory of obesity or its treatment must take the facts of these metabolic impairments into account.

Third, satiety is indeed a primary driver of hunger, and without satiety we will always be hungry—but as important as it is, this is only one part of the answer to “Why are we hungry?”


A lack of satiety will leave us hungry no matter what else we do to compensate.

We fail to achieve satiety in the following ways:

  • By not ingesting the energy and/or nutrients our body requires.
  • By not absorbing the energy and/or nutrients our body requires.
  • By an inability to retrieve the energy and/or nutrients our bodies have stored, due to impaired metabolic flexibility caused by impaired mitochondrial function and, most importantly, impaired fat oxidation.

Thank you for reading all the way through this long but (I believe) rewarding article! The following installments explore failures of the other hunger drives—and once we understand the failures, we can finally begin to construct workable solutions.

Live in freedom, live in beauty.


Continue to Part V: When Satiation Fails…Calorie Density, Oral Processing Time, and Rice Cakes vs. Prime Rib.

This is Part IV of an ongoing series. Go back to Part I, Part II, or Part III.

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Restrained Eating: Willpower and Why Diets Fail (Why Are We Hungry? Part III)

Caution: contains SCIENCE!
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.

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.

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!

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.


Continue to Part IV: When Satiety Fails.
Or, go back to Part I or Part II.

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