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There Is No Such Thing As A “Calorie” (To Your Body)

Caution: contains SCIENCE!

A friend of mine once said “The problem with explaining complicated systems to the layman is this: it’s easy to simplify a concept to the point that that it’s no longer true.

To that end, I submit the following hypothesis:

The concept of the “calorie”, as applied to nutrition, is an oversimplification so extreme as to be untrue in practice.

What Is A “Calorie”, Anyway?

The dietary calorie is defined as “the amount of energy required to increase the temperature of 1 kilogram of water by 1 degree Kelvin.”

The dietary calorie is actually a “kilocalorie” = 1000 calories, which is why you’ll occasionally see it abbreviated as “kcal”.

It’s an obsolete unit: the “joule” is the modern unit of energy. There are 4.184 joules in a calorie, and 4184 in a dietary calorie (kilocalorie).

Problem: Our Bodies Don’t Use “Calories”

You may already see the problem here: a “calorie” is a unit of energy transfer. We determine the number of “calories” in a food by, quite literally, burning it and measuring how much heat it generates.

A bomb calorimeter

This is a bomb calorimeter. Note: not equivalent to the human digestive and metabolic system.

Unfortunately, our bodies are not steam engines! They do not burn the food we eat in a fire and convert the heat into mechanical work. Thus:

There is no biochemical system in our bodies whose input is a “calorie”.

Every metabolic pathway in our body starts with a specific molecule (or family of molecules), and converts it into another molecule—usually consuming energy in the process, not producing it.

This is why we must eat food in order to stay alive. The chemical reactions that build and repair each one of the trillions of cells in our bodies, from brain to toe, from eye to pancreas, require both energy and raw materials. The chemical reactions that allow our cells to perform their necessary functions, from transporting oxygen to parsing visual input to generating muscular force to manufacturing mucus and bile and stomach acid and insulin and leptin and T3, require both energy and raw materials. And the chemical reactions that allow our cells to communicate, via hormones and neurotransmitters, require both energy and raw materials.

In summary, the food we eat has many possible fates. Here are the major ones:

  • Food can be used to build and repair our tissues, both cellular (e.g. muscles, skin, nerves) and acellular (e.g. hair, collagen, bone mineral).
  • It can be used to build enzymes, cofactors, hormones, and other molecules necessary for cellular function and communication.
  • It can be used to build bile, stomach acid, mucus, and other necessary secretions, both internal and external.
  • It can be used by gut bacteria to keep themselves alive, and the waste products of its metabolism can meet any of the other fates listed here.
  • It can fail to be digested or absorbed, and be excreted partially or completely unused.
  • It can be converted to a form in which it can be stored for future use, such as glycogen or fat.
  • It can be transported to an individual cell that takes it in, and converts it to energy, in order to perform the above tasks.

Note that only the last of these fates—immediate conversion to energy—even approximates the definition of a dietary “calorie”.

Why “Calories In, Calories Out” Is A Radical Oversimplification

By now, the problem with “calories in, calories out” should be obvious:

The fate of a “calorie” of food depends completely on its specific molecular composition, the composition of the foods accompanying it, and how those molecules interact with our current metabolic and nutritional state.

Note that “our current metabolic and nutritional state” is the definition of satiety, as I explain in my ongoing article series “Why Are We Hungry?”, and in my 2012 AHS presentation.

Did you just have an epiphany? I hope so.

So What Matters, If Not “Calories”?

Of the possible fates I listed above, only one is wholly undesirable…storage as fat.

I speak from the modern, First World point of view, in which obesity and the metabolic syndrome are more common health problems than starvation.

And while space does not permit a full exploration of all the possible fates of an ingested “calorie” (it’s called a “biochemistry textbook”), I will give a few examples.

A Few Possible Fates Of A “Calorie”: Protein

Imagine a molecule of “protein”.

Proteins are made up of chains of amino acids. (Learn more about proteins and their structure here.) Some proteins, such as meat, are readily digested and absorbed. Some are poorly digestible, such as the prolamins found in grains like wheat and corn, and part of them will either feed gut bacteria or be excreted. Then, once protein is absorbed, its composition of amino acids determines how much of the protein we can use to build and repair (the first three fates in the list above), and how much must be burned for energy or excreted.

The amino acid composition of grains is different than what our bodies need, since the metabolic needs of a grass seed are very different than the metabolic needs of a human being. That’s why grains score so low on measures of protein quality, such as the PDCAAS, compared to meat and eggs. (Grains score 0.25-0.4, versus approximately 1.0 for all animal-source proteins.)

But even if the protein is perfectly digested, absorbed, and of high quality, that is no guarantee of its fate! If we’ve already absorbed enough complete protein for our body’s needs, additional protein will still be converted to glucose, burned for energy, or excreted, no matter how high its quality. (Our bodies have no dedicated storage reservoir for protein…the process of muscle-building is very slow, and only occurs when stimulated by the right kinds of exercise.)

So, right away we can see that a “calorie” of meat protein that is digested, absorbed, and used to build or repair our bodies is not equal to a “calorie” of meat protein surplus to our needs. Nor is it equal to a “calorie” of wheat protein that is only partially digested, poorly absorbed, and disruptive to the digestive tract itself! (e.g. Fasano 2011)

A Few Possible Fates Of A “Calorie”: Fructose

(Again, space does not permit a full exploration of all possible fates of all possible types of “calories”, so these explanations will be somewhat simplified.)

Imagine a molecule of fructose.

Under ideal conditions, fructose is shunted immediately to the liver, where it is converted into glycogen and stored for future use. However, fructose has many other possible fates, all bad. It can fail to be absorbed, whereupon it will feed gut bacteria—a process that can cause SIBO, and consequent acid reflux, when continued to excess. If our liver is already full of glycogen, fructose is converted to fat—a process strongly implicated in NAFLD and visceral obesity. And when our liver is overloaded with fructose (or alcohol, which uses part of the same metabolic pathway), it can remain in circulation, where it can react with proteins or fats to form AGEs (advanced glycation endproducts), useless and/or toxic pro-inflammatory molecules which must be filtered out by the liver.

A typical Big Gulp contains over 100 grams of HFCS. Even the typical “healthy” fruit smoothie contains over 90 grams of high-fructose fruit sugar!

An adult liver can only store, at most, 100-120g of glycogen…and our bodies never let it become deeply depleted.

The problem here should be obvious.

Now ask yourself: which of the above fates has any meaning relative to the definition of a “calorie”?

A Few Possible Fates Of A “Calorie”: Starch

I can’t possibly explore all the fates of starch, but here are some common ones.

Starch is made of glucose molecules chained together. Upon digestion, it’s broken down into these individual glucose molecules, and absorbed—usually reasonably well, unlike fructose (though certain forms, called “resistant starch”, are indigestible and end up being used for energy by our gut bacteria).

Once glucose enters our bloodstream, its fate depends on a host of metabolic and nutritional factors. Ideally, because high blood glucose is toxic, our muscles and liver are not already full of glycogen, and insulin will quickly force it into one of them, whereupon it will be stored as glycogen and used as needed. Our brain and red blood cells also need glucose, since they can’t run on fat, and if they’re low on energy they can burn it too.

Unfortunately, as we’ve seen, our liver has a very small storage capacity, and the capacity of our muscles isn’t very large either—1-2% of muscle mass.

A 155 pound (70 kilo) adult at 14% bodyfat will contain about 66 pounds (30 kg) of muscle, leaving him with 300-600 grams of glycogen storage, depending on his level of training. (Source.)

Note that only reasonably intense exercise (> 50% VO2max) significantly depletes muscle glycogen, and only from the muscles used to perform the effort. Also note that the mainstream recommendation of 50-60% of daily “calories” from carbohydrate equals 300g-360g for a 2400 “calorie” diet.

Again, the problem here should be obvious.

Then, our cells will try to switch over to burning the surplus of available glucose, instead of burning fat for energy.

People with impaired metabolic flexibility have a problem switching between glucose and fat metabolism, for reasons that are still being investigated.

This is yet another example of how our nutritional and metabolic state affects the fate of a “calorie”; why a “calorie” of fat and a “calorie” of sugar are not equivalent in any sane sense of the word; and why different people respond differently to the same number and composition of “calories”.

Next, our body will try to “rev up” our basal metabolic rate in order to burn off the excess glucose…if sufficient cofactors such as T3 are available, and if our metabolic flexibility isn’t impaired. And a continued surplus will be (slowly) converted to fat in either the liver or in fat cells…but if it remains in circulation, it can react with proteins or fats to form AGEs (though more slowly than fructose).

Note that these proteins and fats can be part of living tissues: neuropathy, blindness, and all the complications of diabetes are consequences of excessively high blood sugar over the long term.

Are you starting to understand why the concept of a “calorie” is so oversimplified as to be effectively meaningless?

A Few Possible Fates Of A “Calorie”: Fat

Explaining all possible fates of all possible fats, even cursorily, would require an even longer section than the above two! However, I trust my point is clear: the fate of dietary linoleic acid differs from the the fate of DHA, the fate of palmitic acid, or the fate of butyrate, and their effects on our nutritional and metabolic state will also differ.

But Wait, There’s More

I also don’t have time or space to explore the following important factors:

  • Energy loss when food is converted to different forms of storage (e.g. gluconeogenesis, glycogenesis, lipogenesis) or retrieved from storage
  • How different types and quantities of dietary protein, fat, and carbohydrate affect our hormonal and metabolic environment
  • How the fate of a “calorie” depends on the composition of the other foods it’s eaten with
  • How different types and quantities of food, as well as our nutritional and metabolic state (our satiety), affect our perception of hunger
  • The host of known, measurable differences between individuals, such as MTHFR genes, the respiratory quotient, and the bewildering variety of hormones on the HPTA axis.

Conclusion: The Concept Of A “Calorie” Is So Oversimplified As To Be Meaningless

Let’s recap some of the possible fates of a “calorie”:

  • Food can be used to build and repair our tissues, both cellular (e.g. muscles, skin, nerves) and acellular (e.g. hair, collagen, bone mineral).
  • It can be used to build enzymes, cofactors, hormones, and other molecules necessary for cellular function and communication.
  • It can be used to build bile, stomach acid, mucus, and other necessary secretions, both internal and external.
  • It can be used by gut bacteria to keep themselves alive, and the waste products of its metabolism can meet any of the other fates listed here.
  • It can fail to be digested or absorbed, and be excreted partially or completely unused.
  • It can be converted to a form in which it can be stored for future use, such as glycogen or fat.
  • It can be transported to an individual cell that takes it in, and converts it to energy, in order to perform the above tasks.

Note that only the last of these fates—immediate conversion to energy—even approximates the definition of a dietary “calorie”.

I hope it is now clear that the fate of a “calorie” depends on a bewildering host of factors, including our current nutritional and metabolic state (our satiety), the composition of the other foods it’s eaten with; our biochemical individuality, both genetic and environmental; and much more.

Takeaways

  • There is no biochemical system in our bodies whose input is a “calorie”.
  • The food we eat has many possible fates, only one of which approximates the definition of a dietary “calorie”.
  • The fate of a “calorie” of food depends completely on its specific molecular composition, the composition of the foods accompanying it, and how those molecules interact with our current metabolic and nutritional state—our satiety.
  • Therefore, the concept of the “calorie”, as applied to nutrition, is an oversimplification so extreme as to be untrue in practice.
  • Therefore, the concept of “calories in, calories out”, or CICO, is also unhelpful in practice.

  • The health-supporting fates of food involve being used as raw materials to build and repair tissues; to build enzymes, cofactors, and hormones; to build bile, mucus, and other necessary secretions; to support “good” gut bacteria, while discouraging “bad” bacteria; and, once all those needs are taken care of, providing energy sufficient to perform those tasks (but no more).
  • Therefore, we should eat foods which are made of the raw materials we need to perform and support the above functions.
  • Biochemical individuality means that the optimum diet for different people will differ—as will their tolerance for suboptimal diets.
  • However, eating like a predator—a diet based on meat, fish, shellfish, vegetables and fruit in season, and just enough starch to support your level of physical activity—is an excellent starting point.

Live in freedom, live in beauty.

JS

This is a multi-part series. Continue reading Part II, “Did Four Rice Chex Make America Fat?”

ATTENTION! Before reflexively commenting that “A CALORIE IS A CALORIE BECAUSE SCIENCE!!11!!!1!”, you are required to read both the comments below (in which I address many such questions)—

and, more importantly, the peer-reviewed research contained in Part II, Part III, Part IV, Part V, Part VI, Part VII, and Part VIII. (And there’s more to come.)

Yes, metabolism is complicated. Deal with it.


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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?”

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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