(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.

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.

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:

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?”

Conclusion

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.

JS

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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