Rebuttals to Fatlogic

Last update: 10 / 07 / 2019. Added more of the questions and answers.

Obligatory disclaimer: I am not a medical doctor, and the content presented in this website is intended for information purposes only. Such content should not be construed as medical advice, consultation, diagnosis or treatment.

The goal of this page is to serve as a compendium of common fatlogic claims, and to rebut them with peer-reviewed research whenever possible. As such, this page is an ongoing project, and is subject to revisions, changes, corrections, and should be considered with an open, but skeptical, mind.

To begin with, what is fatlogic? For the purposes of this page, we’ll use the definition of fatlogic that’s provided by urbandictionary.com:

[Fatlogic consists of] The astounding mental gyrations obese people use to justify their size. Fatlogic never, ever includes eating too much and exercising too little.

Funny as that is, I want to make clear what my intentions are. Firstly, I’m not interested in insulting or mocking fat people, and if you are, I recommed you take your hatred someplace else. I think it’s safe to assume that, at some point or another, we’ve all disliked our appearance and wished to change it.

Perhaps it wasn’t a matter of appeareance, but one of achieving and maintaining a different lifestyle, one where climbing stairs is just climbing stairs, where the choice of clothing isn’t limited, and one in which our own body doesn’t impose limits to whatever activities we wish to engage in. Secondly, my background is in science, and from my experience the way science is currently presented and taught is as nothing more than a collection of results, equations, quircky experiments, and pretty graphs. However, the real power of science comes from its methods, as Carl Sagan describes in The Demon-Haunted World:

Science thrives on errors, cutting them away one by one. False conclusions are drawn all the time, but they are drawn tentatively. Hypotheses are framed so they are capable of being disproved. A succession of alternative hypotheses is confronted by experiment and observation. Science gropes and staggers toward improved understanding. Proprietary feelings are of course offended when a scientific hypothesis is disproved, but such disproofs are recognized as central to the scientific enterprise.

Pseudoscience is just the opposite. Hypotheses are often framed precisely so they are invulnerable to any experiment that offers a prospect of disproof, so even in principle they cannot be invalidated. Practitioners are defensive and wary. Sceptical scrutiny is opposed. When the pseudoscientific hypothesis fails to catch fire with scientists, conspiracies to suppress it are deduced.

As may be apparent from the previous quotes, my view is that fatlogic behaves just like any other pseudoscience, and must be challenged as such.

Having said all that, let us begin: individual links to each fatlogic claim may be found at the end of this section. If you would rather read the whole thing at your own leisure here’s a link to the whole enchilada.

Quick links to general information and fatlogic claims

The whole enchilada

What is metabolism

Metabolism is the set of life-sustaining chemical reactions in organisms. The main purposes of metabolism are: the conversion of food to energy to run cellular processes; the conversion of food/fuel to building blocks for proteins, lipids, nucleic acids, and some carbohydrates; and the elimination of nitrogenous wastes.

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What is the basal metabolic rate (BMR)?

Straight from Wikipedia:

The basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at rest. It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule per hour per kg body mass J/(h·kg). Proper measurement requires a strict set of criteria be met. These criteria include being in a physically and psychologically undisturbed state, in a thermally neutral environment, while in the post-absorptive state (i.e., not actively digesting food).

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What is metabolic damage?

The term metabolic damage is thrown around with the intent that engaging in caloric restriction brings metabolism to a halt and weight gains are inevitable. In other words, that dieting kills your metabolism and, because of that slow metabolism, gaining weight is easier. Let’s see how accurate this is.

According to Leonie K Heilbronn, Eric Ravussin; Calorie restriction and aging: review of the literature and implications for studies in humans, The American Journal of Clinical Nutrition, Volume 78, Issue 3, 1 September 2003, Pages 361–369:

CR [caloric restriction] is hypothesized to lessen oxidative damage by reducing energy flux and metabolism, or the “rate of living,” thereby influencing the aging process. We know that CR results in a loss of weight and tissues and a reduction in the rate of metabolism. A portion of this decline is the result of reduced energy intake and the consequent decrease in the thermic effect of food, whereas another portion is due to the reduced size of the metabolizing mass. However, whether there is also a “metabolic adaptation,” defined here as a reduction in the metabolic rate that is out of proportion to the decreased size of the respiring mass, is a subject of continued debate. In their investigation of the biology of semistarvation, Keys et al defined metabolic adaptation as “a useful adjustment to altered circumstances.” More recently, a 1985 FAO/WHO/UNU report proposed a definition of adaptation as “a process by which a new or different steady state is reached in response to a change or difference in the intake of food or nutrients”. In this context, the adaptation can be genetic, metabolic, social, or behavioral. The important question is whether CR reduces energy expenditure (EE) more than would be expected to result from the changes observed in FM [fat mass] and fat-free mass (FFM).

(…)

In summary, there is evidence that a metabolic adaptation develops in response to CR and loss of weight in humans. The reason for the apparently paradoxical difference between rodents and humans with regard to an adaptation in EE in response to CR may be related to the erroneous way in which physiologists express rodent energy metabolism data (60) or to differences in metabolism between rodents and humans. Other possible reasons are that the methods for measuring human EE are more sensitive than are those for measuring rodent EE, and investigators can obtain the full cooperation of the subjects.

Put simply, there is a reduction in metabolic rate because of caloric restriction, and such a reduction is due to

  • the lesser intake of energy and the associated reduction in the thermic effect of food
  • a lesser amount of body mass involved in energy consumption, which is caused by weight loss
  • lower hormone concentrations in the thyroid

From the second of those three factors it’s clear that if the weight loss is maintained constant, then the reduction in metabolic rate will also remain constant, all else being equal. This would be akin to hiking a given distance without a backpack and with a 100 Kg weight, carrying the larger weight requires more energy.

This latter point was confirmed by the second phase of of the CALERIE studies (Redman, L. M., Smith, S. R., Burton, J. H., Martin, C. K., Il’yasova, D., & Ravussin, E. (2018). Metabolic slowing and reduced oxidative damage with sustained caloric restriction support the rate of living and oxidative damage theories of aging. Cell metabolism27(4), 805-815):

Phase 1 CALERIE or the Comprehensive Assessment of the Long-Term Effects of Reducing Intake of Energy studies were the first randomized controlled trials to test the metabolic effects of CR in non-obese humans. Then, the phase 2 CALERIE study, a 2-year 25% CR prescription in non-obese volunteers, was shown to be safe and without any untoward effects on quality of life. Importantly, the study confirmed the presence of a CR-induced decrease in total daily energy expenditure (EE) measured by doubly labeled water after 12 and 24 months (measured CR was 12% on average), indicating a decrease in physical activity and/or a metabolic adaptation. However, in the CR group compared with the control group, resting metabolic rate adjusted for loss of fat-free and fat masses was only lower during the weight loss phase, i.e., at 12 months of intervention, but not a year later.

So this metabolic damage doesn’t seem so damaging, unless you are willing to say that a reduction in the metabolic rate, whatever its magnitude, constitutes metabolic damage.

Now let us consider what would happen if the caloric restriction were to be halted and the individual were to return to their original dietary habits. Given the quote from the first paper, this would mean an increased metabolic rate, since some energy would be required to digest the ingested food, and, because the individual would return to their original weight, a greater body mass would require greater amounts of energy to function.

In other words, even if the term metabolic damage were accurate, then the process could be reversed by simply stopping what caused it in the first place.

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What is fasting?

According to Wang, Tobias; Hung, Carrie; Randall, David (2006). “The Comparative Physiology of Food Deprivation: From Feast to Famine”. Annual Review of Physiology68 (1): 223–251:

In humans, fasting often refers to abstinence from food, whereas starvation is used for a state of extreme hunger resulting from a prolonged lack of essential nutrients. In other words, starving is a state in which an animal, having depleted energy stores, normally would feed to continue normal physiological processes.

In other words, a fasting mammal will voluntarily forgo food, but a starving one will feed or attempt to do so in order to keep normal physiological processes going on. As an example of fasting, consider how migratory birds can travel vast distances, sometimes non-stop, and feed after reaching their destination.

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What is starvation?

According to Wang, Tobias; Hung, Carrie; Randall, David (2006). “The Comparative Physiology of Food Deprivation: From Feast to Famine”. Annual Review of Physiology68 (1): 223–251:

In humans, fasting often refers to abstinence from food, whereas starvation is used for a state of extreme hunger resulting from a prolonged lack of essential nutrients. In other words, starving is a state in which an animal, having depleted energy stores, normally would feed to continue normal physiological processes.

In other words, a fasting mammal will voluntarily forgo food, but a starving one will feed or attempt to do so in order to keep normal physiological processes going on. As an example of fasting, consider how migratory birds can travel vast distances, sometimes non-stop, and feed after reaching their destination.

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What is starvation mode?

The term starvation mode is intended to mean that when engaging in caloric restriction our body sort of freaks out and slows down metabolism, and somehow turns everything we eat into fat, since it doesn’t know when we might eat again. Let’s see how truthful this is, following Wang, Tobias; Hung, Carrie; Randall, David (2006). “The Comparative Physiology of Food Deprivation: From Feast to Famine”. Annual Review of Physiology68 (1): 223–251:

When faced with absolute food deprivation, mammals go through three distinct metabolic phases. These are characterized on the primary fuel available and the associated changes in overall body mass. Fasting occurs during the first two phases, while starvation happens during the third one. The three phases are as follows:

  • Phase I: This phase follows immediately after the last meal has been absorbed from the gastrointestinal tract. During this phase glycogenolysis (the breakdown of glycogen) maintains blood sugar levels constant and keeps metabolism going. Glycogen is mostly stored in the liver, with a lower amount stored in the muscles. This phase can last for hours.
  • Phase II: This phase begins when the liver’s glycogen stores are depleted. As some organs, like the brain, require glucose to function, gluconeogenesis becomes necessary to keep things running. Although there is a contribution of amino acids from proteolysis of muscle protein (in english: breaking down of muscle protein to get amino acids), adipose tissue provides the bulk of the material for the synthesis of glucose by providing glycerol. This phase can be maintained during weeks in humans.
  • Phase III: Should starvation proceed as fat stores are depleted, gluconeogenesis is carried on at the expense of muscle. This process eventually kills the animal.

So to summarize, after our last meal is absorbed from the gastrointestinal tract our body keeps functioning on the glycogen that’s stored in our liver. After some hours, that glycogen storage runs dry and our body needs to generate glucose. That glucose comes mainly from our fat and a little from our muscles. After some weeks of this, our fat deposits dry up and only muscles remain to be consumed. Death follows.

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What is thermogenesis?

Thermogenesis is the generation of heat by organisms, and the main purpose of such heat generation is to maintain a stable body temerature. As you may expect, thermogenesis is common to warm-blooded (endothermic) organisms, and it occurs due to the burning of calories.

Some examples of thermogenesis are the thermic effect of food, running a fever, shivering, exercising, and all the things that you or your body does while not enjoying a nice fever, eating, exercising, shivering or sleeping.

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What is the thermic effect of food?

Let’s have a couple of reminders. Firstly, metabolism encompasses all the chemical reactions that sustain an organism’s life, and some of those reactions deal with how food is converted into our body’s energy. Secondly, we have seen that decreasing our caloric intake impacts our metabolism, so it stands to reason that eating also impacts our metabolism. To see how this is the case, we’ll use the following reference: Secor, S. M. (2009). Specific dynamic action: a review of the postprandial metabolic response. Journal of Comparative Physiology B179(1), 1-56.

There have been many investigations into the changes in metabolic rate after eating a meal, and because of this the Thermic Effect of Food has amassed a large number of names. Among them we find Specific Dynamic Action (SDA), Heat Increment of Feeding (HIF), Diet Induced Thermogenesis (DIT), and the Thermic Effect of Feeding (TEF). This is because different researchers focused on different aspects or mechanisms of the same thing, and so came up with several names. We’ll just refer to the Thermic Effect of Food as the Thermic Effect of Food. After all, how many people will look for Specific Dynamic Action?

Alright, so what is the Thermic Effect of Food? According to our chosen reference,

[the Thermic Effect of Food] is the accumulated energy expended (or heat produced) from the ingestion, digestion, absorption, and assimilation of a meal.

In other words, the Thermic Effect of Food is just all the energy required to process whatever it is that we have eaten.

There have been several studies on how the Thermic Effect of Food is impacted due to exercise, pregnancy, stage of the menstrual cycle, stress, age. Even the effect of watching horror vs romantic films has been studied!

Anyway, from what Secor says, the Thermic Effect of Food in humans is modest, as the metabolic rate shows a 25% increase above fasting rate that lasts between 3 to 6 hours. However, one would expect that meal size, meal energy content, body composition, and body size would have an effect on the Thermic Effect of Food , right?

Well, indeed! For instance, the greater the amount of energy in food, the greater the Thermic Effect of Food will be. This makes perfect sense, it takes more energy to process a meal that has more energy. On the other hand, meal composition is also important,††

[TEF] is affected by the interactions among the relative amounts of proteins, carbohydrates and lipids

Wikipedia cites some numbers corroborating this, but Wiki’s references are older than the paper I’m using, so take them as you will:

  • Carbohydrates: 5 to 15% of the energy consumed
  • Protein: 20 to 35%
  • Fats: at most 5 to 15%

What if energy content remains the same, but meal size differs (like eating a chocolate bar vs eating a ton of lettuce)? Well, meal size is also a factor to consider since the greater the size of the meal, the greater the TEF will be as well. It is important to note that this occurs not only by having a greater TEF peak, but by its duration increasing as well.

One factor that I wasn’t expecting to see is meal temperature. For endotherms (remember, warm-blooded animals), food tends to be at a lower temperature than their body, so some energy is expended in heating the meal upon ingestion. Of course, warming a large-cold meal involves a greater amount of energy than warming up a small-already-warm meal.

Finally, a greater body size increases BMR. This makes sense, since there is more mass that requires energy to keep alive. This also means, however, that TEF is also greater with a larger body size. As to body composition, it’s not clear whether it actually has an impact on TEF; some studies have evidence that it does, others show that it doesn’t.

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How is the Thermic Effect of Food determined?

If the Thermic Effect of Food corresponds to the energy needed to process what we’ve eaten, then the problem is measuring that energy. Because of the additional work our body must perform to digest, absorb, and assimilate a meal, then there is an increase in our metabolic rate that can be measured and related to the Thermic Effect of Food. In order to determine the Thermic Effect of Food, we keep track of changes in the metabolic rate in the following way:

  1. Establish what the metabolic rate before the meal was. In the lab what is actually measured is the Baseline Metabolic Rate. For warm-blooded animals, endotherms, the Basal Metabolilc Rate (BMR) is that Baseline Metabolic Rate.
  2. The animal is then fed a meal to satiety or so that the meal is a set percentage of body mass.
  3. After feeding, the metabolic rate is measured continuously or periodically. The results of such measurements are plotted on an xy graph, where x is the time after feeding, and y stands for the metabolic rate.

Secor, S. M. (2009). Specific dynamic action: a review of the postprandial metabolic response. Journal of Comparative Physiology B179(1), 1-56 has an amazing image of the sorts of graphs that can be obtained with the previous method. I think that image is so good at helping understand what TEF is that I’ll post it as well.

SDA peak
Metabolic rate vs Time postfeeding. From Secor, S. M. (2009). Specific dynamic action: a review of the postprandial metabolic response. Journal of Comparative Physiology B179(1), 1-56

If that graph confuses you, don’t fret, because its rather simple to explain. Prior to meal ingestion, the metabolic rate corresponds to the BMR, which explains why its value is so low and taken as the baseline. After meal ingestion, the metabolic rate rises in order to process the meal itself. Such increase in metabolic rate reaches a peak and then slowly declines until the metabolic rate returns to its BMR value. So how does that graph tell us the Thermic Effect of Food? Well, the Thermic Effect of Food, which is called SDA in the graph, corresponds to the area under the curve. If you’re into calculus, that last statement must have made your heart beat with joy.

So from that graph several variables can be identified: BMR, the value of the postprandial (after meal) peak, the time that it takes to reach the peak, the duration of the Thermic Effect of Food, and the Thermic Effect of Food itself.

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What are macronutrients?

Macronutrients are the dietary nutrients that supply energy to an organism. And nutrients are substances that are required by organisms in order to remain alive, grow, and reproduce. We’ve all heard examples of macronutrients before, as they come up any time discussion about diet and food happens. Namely they are carbohydrates, proteins, fats (lipids), and alcohol.

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What are carbohydrates?

Carbohydrates are substances made up of carbon, hydrogen and oxygen atoms in a proportion that resembles “hydrates of carbon”, Cx(H2O)y, where x and y may be different numbers.

Carbohydrates can be classified into two main groups: complex and simple carbohydrates. Simple carbs are made up of one or two saccharid molecules, and are known respectively as monosaccharides and disaccharides. Complex carbs are further divided into oligosaccarides (between three to ten saccharide molecules) and polysaccharides (anything beyond ten saccharide molecules).

As may be apparent from the classification of carbohydrates, monosaccharides are the simplest form carbohydrates come in and polysaccharides are the most complex. Chances are you know examples of  each one of them: glucose is a monosaccharide and glycogen is a polysaccharide. As we’ve covered before, glycogen stored in the liver is broken down into glucose through glycogenolysis, which means that complex and simple carbohydrates are metabolized in different ways by the organism.


How are carbohydrates digested?

Unless our eating habits are based mainly on processed food, free monosaccharides are not present in large quantities in our diet. On the contrary, this menas that polysaccharides and disaccharides are the most important dietary carbohydrates. Although monosaccharides are absorbed into the bloodstream from the gastrointestinal tract, polysaccharides and disaccharides must first be broken into their individual monosaccharide components.

Polysaccharide digestion first begins in the mouth, as enzymes contained in saliva begin the breaking down process. As food moves into the stomach and intestines, enzymes continue this digestion until maltose (a disaccharid), isomaltose (another disaccharid) and glucose (remember, monosaccharid) are the main products.

Disaccharides, on the other hand, are not broken down either in the mouth or the stomach, and their digestion takes place in the upper small intestine. As was the case with polysaccharides, enzymes are responsible for disaccharides breaking down into their constituent monosaccharides.

Whether it’s monosaccharides, disaccharides, or polysaccharides, virtually all carbohydrates are broken down into monosaccharides and absorbed into the bloodstream by the time they reach the jejunum, which is in the upper part of the small intestine. After this, they are transported to the liver, where they are processed into, and stored, as glycogen. Some of that glycogen is then transported to the cells of different tissues to be used as a fuel source. Alternatively, the glycogen may be catabolized on the spot and used to provide energy and maintain blood level homeostasis.

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What is fiber?

Fiber is a kind of polysaccharide that cannot be completely broken down by digestive enzymes. It also makes up the structure of fruit skins, seeds, leaves, stems, and roots. Fiber can be classified into two main categories: water-soluble fiber and water insoluble-fiber. The first kind of fiber can be fermented in the colon and delays gastric emptying, resulting in feeling full for a longer time. The second kind of fiber absorbs water as it moves through the digestive system, easing the process of defecation.

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What are proteins?

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What are fats / lipids?

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What is alcohol?

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What are micronutrients?

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What is the glycemic response / glycemic index / glycemic load?

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You hate fat people!

That’s not a question, but no. This blog doesn’t hate fat people, and neither do I.

It is undeniable that there are those who hate fat people: the fatpeoplehate subreddit and similar sites are a testament to this. Such content, however, is not welcome on this blog neither as posts nor as comments. There is a clear difference between wanting to help someone, even if it’s worded harshly, and just disrespecting others. No matter who you are, regardless of your background, you deserve to be treated with respect.

I want this post to be a more thorough explanation of what the Rebuttals to Fatlogic page of this blog is intended as. From my experience, most of what that page covers is taught during elementary school and junior high school. Still, the fact is that we tend to remain ignorant when it comes to actually applying that knowledge or understanding how it relates to us in everyday life. The prevalence of fad diets, dumb things like detoxing, wraps, and cleanses show this to be the case.

It is impossible for a lone (and terrible) writer like myself to change that situation head on, so the point of the Rebuttals to Fatlogic page is to try something different. Just as we imagine monsters hiding under the bed, under the stairs and in the closet when we’re young, the gaps in our knowledge serve as fertile ground for falsehoods and misconceptions to take root. Those who believe in the gospel of fatlogic do so because they get something out of their belief: the assurance that they’ve done what they can and the problem lies somewhere beyond their control. Fatlogic then is both self-reinforcing and soothing. That is also its greatest weak spot.

The clear difference between fatlogic and science is that the former only offers excuses and keeps looking backwards while the latter gives explanations and forces us to look forwards, towards trying out new ideas and seeing if they pass muster. Fatlogic allows you to lie to yourself when it comes to how much food you actually eat and how much you exersize, but a proper tracking of those activities cannot be fooled, and will eventually be apparent.

The Rebuttals to Fatlogic page is intended to be well sourced, and to offer a greater amount of information than a quick Google search without getting bogged down in with details. It is also not interested in getting you to buy anything (except, perhaps, the sort of clothes you actually want to wear), and this project is primarily aimed at helping me get my own head around what is true and what is false in the fatlogic vs science “debate”, and it is then intended to make that information available to others who find themselves in a similar position.

If, after checking things out, your choice is to not change your lifestyle and keep doing what you’ve already have, good for you. If you, on the other hand, decide to make changes and try out a different way, then good for you too. What I find unacceptable, however, is to believe your own stories and excuses without challenging them and being convinced by the evidence. Hopefully this gives a better understanding as to the point of the Rebuttals to Fatlogic section of the blog.

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