Rebuttals to Fatlogic

Last update: 15 / 08 / 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

[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.

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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?

Proteins are probably the closest thing we have to unobtanium, a material with extraordinary, almost magical, properties. See, proteins can be found in most of our tissues, like our muscles, organs, skin, and blood. Protein’s importance is due to it being made up of amino acids (organic molecules made up of an acid group, an amine group, and a specific side chain group), which our body requires to manufacture its own proteins and other molecules that support life. We’ll follow the classification of proteins provided by Gropper and Smith, which is based on their biological functions.

Biological functions of proteins

  • As catalysts. A catalyst is any substance that increases the rate at which a chemical reaction occurs, and enzymes are proteins that act as catalysts. In our body, such reactions are necessary to sustain life, and they take place within our cells. Examples of the processes in which enzymes take part are digestion, energy production, neuromuscular contraction and blood coagulation. Sometimes, in order for the reaction to take place, a cofactor (also known as coenzime) is needed, minerals like copper, iron, and zinc are examples of cofactors.
  • As messengers. Hormones are our organism’s chemical messengers, and some proteins are hormones. In our case, hormones are made in endocrine glands and released into the bloodstream, which then transports them to their target organs. Hormones tend to be regulators of metabolic processes, either by modifying enzymatic activity or the synthesis of enzymes themselves.
  • As structural elements. This is the function that you probably already know. As expected, proteins can be found in cardiac, skeletal (voluntary), and smooth (involuntary) muscles. However, there are other proteins, like collagen, elastin, and keratin that can be found in other tissues, like hair, bone, teeth, skin, tendons, cartilage, blood vessels and nails.
  • As immunoprotectors. Part of our organism’s immune system uses immunoproteins (also known as immunoglobulins or antibodies), and the way they work is by sticking to antigens (foreign substances, like viruses or bacteria) and inactivating them. What follows is that the immunoglobulin and antigen structure is identified and destroyed through chemical reactions involving other proteins or cytokines.
  • As transporters. Proteins that act as transporters combine with the substances they transport (like nutrients, vitamins and minerals) and then provides a mean of transportation within a given cell, into or out of cells or by carrying the substances in the bloodstream. There are several examples of transport proteins, but I think the clearest one is hemoglobin, which helps transport oxygen and carbon dioxide in red blood cells.
  • As buffers. As we covered before, proteins contain an acid group in their structure, and so they can help in maintaining acid-base balance as buffers. Buffers are substances that reduce the impact of a pH change due to the addition of an alkali (basic) or an acid into a given solution. Different tissues and organs of our body must be kept within different pH values, and the presence of proteins in those tissues helps maintain the proper pH balance within them.
  • As fluid balancers. The idea is that the presence of proteins in the bloodstream or within cells helps to attract water and maintain the correct osmotic pressure (so that our cells don’t shrink or swell). Because of this, the proper concentration of proteins must be kept in blood and in cells.

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How are proteins digested?

Unlike what happens with carbohydrates, there is no appreciable digestion of proteins either in the mouth or in the esophagus, and real protein digestion does not begin until reaching the stomach. Due to the presence of hydrochloric acid in the stomach, proteins are broken down, leaving polypeptides (a long chain formed by more than 20 amino acids), oligopeptides (chains between 2 to 20 amino acids), and free amino acids as products. The compounds are then transported to the small intestine for their further digestion.

Once in the small intestine, the release of regulatory hormones and peptides signals the secretion of digestive proenzymes which will aid during digestion. Those proenzymes are secreted by the pancreas and once they reach the small intestine they are converted into their respective enzymes. The different enzymes produced are responsible for the hydrolization of polypeptides into oligopeptides and tripeptides, as well as the release of individual amino acids from the polypeptides. As this process goes on, the end result of protein digestion is the production of peptides (mostly dipeptides and tripeptides) and free amino acids. Most of these substances are then absorbed across the intestinal wall in order for the organism to use them. Of those amino acids that are not absorbed, they are used by intestinal cells to synthesize proteins and other compounds.

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What are fats / lipids?

Lipids are substances that are defined due to their solubility in organic solvents like ether, chloroform, and acetone. Because of that definition, there are more chemical compunds that qualify as “lipids” than just the dietary sources of energy that we usually call fats. In other words, if you’re used to only thinking of lipids as fats, then you’re in for some learning.

Just like happened in our post on proteins, we’ll follow the categorization provided Gropper and Smith, which is based on the physiological function of the different kinds of lipids.

Biological functions of lipids

As fatty acids. In terms of structure, fatty acids are the simplest form lipids come in, and this is because they consist of a hydrocarbon chain with a carboxylic acid group on one of its ends. They also serve as building blocks for more complex kinds of lipids. When it comes to physiological function, fatty acids are responsible for most of the calories that come from dietary fat. The hydrocarbon chain that makes up a fatty acid can be between 4 and 24 carbon atoms, and they can be saturated, monosaturated or polyunsaturated. What does that mean? Well, I hope you remember a little from your chemistry classes, especially when it comes to double bonds:

  • Saturated fatty acids: having no carbon double bonds. They tend to come from animal sources.
  • Monosaturated fatty acids: having at least one carbon double bond. They tend to come from plant sources.
  • Polyunsaturated fatty acids: having several carbon double bonds. They also come from plant sources.

Why do we even bother with this sub-categorization? It turns out that the degree of saturation of a fatty acid is related to its geometry, and a less saturated fatty acid (one with more double carbon bonds) can bend and kink more than a saturated one. Whether the molecule bends or not is then related to it having a cis or trans isomerism (same chemical formula, but different geometric structure). You’ve probably heard of trans fats, and how they may be related to adverse nutritional effects. We’ll deal with them on a later post though.

As triacylglycerols (aka triglycerides). Once our body stores fat, it does so in the form of triglycerides. By the way, I hope you don’t mind me calling triglycerides TGs, it’s just that i keep messing up the spelling. TGs are formed by three fatty acids bonded to glycerol. Depending on the acid groups, TGs can be simple (the three fatty acids are the same) or mixed (the three fatty acids are different). TGs can be found in solid (called fats) or liquid (called oils) form at room temperature, and this depends on their constituent fatty acids: the more saturated fatty acids, and the longer their hydrocarbon chains, a TG possesses, the higher its melting point.

As sterols and steroids. Both sterols and steroids have a core structure composed of four rings which is often refered to as a steroid. Sterols build up on a steroid core by adding an alcohol group to it. You may already be familiar with one example of a sterol: cholesterol. While cholesterol can only be found in animal cells, sterols are also found in plant cells. Despite its bad reputation, cholesterol is a key component of cell membranes, and it also is a precursor for other steroids produced in our body, like bile acids, the sex hormones (estrogens, androgens and progesterone), and adrenocortical hormones. Compared to other lipids, sterols and steroids make up a tiny amount of our dietary intake at around 5%.

As phospholipids. As the name implies, phospholipids contain phosphate as well as fatty acids, and they come in two kinds: glycerophosphatides (if their core constituent is glycerol) and sphingophosphatides (if their core constituent is sphingosine, an amino alcohol). In general terms, phospholipids are important components of cellular membranes, and they’re also a source of other physologically important compounds.

As glycolipids. Just like phospholipids have phosphate in their structure, glycolipids have glucose in theirs. This doesn’t mean that their main function is as an energy source, but rather as a structural component of the nervous system. Glycolipids come in two flavours: cerebrosides and gangliosides.

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How are lipids digested?

Most of the lipids in our diet come in the form of triglycerides, phospholipids, and sterols. The ordering of those lipids isn’t casual, as triglycerides make up the bulk of our lipid intake while sterols the least. Upon ingestion, digestive enzymes begin breaking down lipids in the gastrointestinal tract. Different enzymes are responsible for breaking down each kind of lipid. As there are different digestive processes that take place depending on the kind of lipid, we’ll first deal with triglycerides, and then with phospholipids and sterols.

  • Triglyceride digestion: TG digestion begins in the stomach, as the digestive enzymes involved are secreted by the chief cells of the stomach and by the serous gland under the tongue. It is important to note that fats are hydrophobic, while digestive enzymes are hydrophilic, and so TGs must be emulsified in order for them to be digested. Part of the emulsification process is done through muscle contractions of the stomach, but the reality is that only a tiny percentage of the TGs present in the stomach will be fully digested, and digestion will truly take place in the small intestine. However, there is an upside to the presence of undigested TGs in the stomach: their presence delays the rate at which stomach contents empty, so it can be said that TGs have a high satiety value. TGs are completely digested in the small intestine due to the less acidic environment, the presence of more digestive enzymes and emulsifying agents (like bile), and the fact that absorptive cells are also present. The end result of TG digestion is a mix of diaglycerols, monoaglycerols, and free fatty acids.
  • Phospholipid and sterol digestion: In this case the process is very similar to the previous one, with the production of free fatty acids and cholesterol. The difference lies in that, during digestion, polymolecular aggregates called micelles are produced. Micelles are composed of monoacylglycerols, lysolecithin, cholesterol, and fatty acids. During the last stage of digestion, those micelles are broken down into free fatty acids and cholesterol.

As was the case with carbohydrates and proteins, the products of lipid digestion are then trasported to the appropriate cells so that more complex compounds can be produced.

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What is alcohol?

As may be obvious, alcohols are neither proteins, carbohydrates or lipids. They are also, unsurprisingly, not macronutrients, but they do make up an important part of the average diet, so we might as well become acquainted them. Ethanol’s structure most closely resembles that of carbohydrates, and its digestion is similar to that of fatty acids. To keep things simple, ethanol’s chemical structure is that of a short hydrocarbon chain with a hydroxyl group on one of its ends. Unsurprisingly then, it is a source of calories although it carries no additional nutritional contents, and is therefore said that those are “empty calories”.

Biological “functions” of lipids

Even though alcohol doesn’t have any nutritional value, its moderate consumption has been linked to an elevation of high-density lipoprotein (HDL) and a decrease of serum lipoprotein, both of which are related to a decrease in cardiovascular disease risk.

By the same token, though, excessive alcohol intake may lead to alcoholism and its ugly consequences: fatty liver, hepatic disease (cirrhosis), metabolic tolerance and lactic acidosis.

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How is alcohol digested?

Once ingested, alcohol is absorbed through the entire gastrointestinal tract, although most of the absorption occurs in the smaller intestine. After that, it is transported through the entire bloodstream without any form of processing. As alcohol is transported through different tissues and organs, it is then oxidized, first producing acetaldehyde and then acetate. As you’re surely aware of, the liver is the organ primarily responsible for alcohol degradation, and it, alongside peripheral organs, then continues the metallization of acetate through several different enzyme systems.

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What are micronutrients?

Just like macronutrients, micronutrients are dietary nutrients. Unlike macronutrients, micronutrients are required in smaller doses (hence the micro prefix), and although they don’t provide us with energy, they allow our body to produce enzymes, hormones and other substances required to keep our metabolic processes going. Most micronutrients are essential nutrients, meaning they cannot be produced by our body, and must come from our diet. This also means that their deficiency or absence is a serious health concern.

Just like macronutrients can be categorized into carbohydrates, proteins, lipids, and alcohols, so too can micronutrients be categorized into two groups: vitamins and minerals.


The word vitamin comes comes from vitamine, and it came about because the first vitamin to be discovered was necesary for life and an amine. As more and more vitamins were discovered, it turned out that not all of them were amines, but the name has stuck regardless.

A given vitamin may fulfill several regulatory functions, so its deficiency is associated with a syndrome (a group of signs and symptoms). Furthermore, different vitamins will have different physiological roles like electron transfer reactions, CO2 transfer, cell division, energy production, and as antioxidants, among others. Finally, they can come in two forms: water-soluble and fat-soluble, and the way that the body handles each type is different.

Water-soluble vitamins

Unlike fat-soluble vitamins, water-soluble ones are absorbed into the blood and they tend not to be retained in the body for long, as they are excreted in our urine. You already know some of the water-soluble vitamins, even if not by name, because all B-complex vitamins are water soluble, and so is vitamin C.

Fat-soluble vitamins

Fat-soluble vitamins are absorbed, transported, and stored just like lipids are. This means that, even though different fat-soluble vitamins are stored in different amounts, they are not excreted like water-soluble ones are. Fat-soluble vitamins are made up of vitamins A, D, E, K and the carotenoids.


Minerals make up a tiny percentage of our body weight, but they have several important functions, like strenghtening our bones and teeth, being cofactors to metalloenzymes, and determine the osmotic properties of body fluids. Even though they are micronutrients, minerals can be macro or micro depending on how much they make up of our body, although we won’t get into specific numbers.


This group of minerals is important because they help maintain electrolytic balance, are structural components of bones and teeth, are enzyme cofactors and they help our muscles contract. Among them we find calcium, chloride, magnesium, phosphorus, potassium, sodium, and sulfur.


These trace minerals are also required for one or several specific functions, although the quantities requires are less than for macrominerals.  Among them we find iron, zinc, copper, iodine, selenium, molybdenum, fluoride, manganese, chromium.

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

We have talked about how carbohydrates come in two different groups: simple (meaning one or two saccharide molecules) and complex (containing three saccharide molecules or more). We also learned that carbohydrate digestion can be summarized as “break complex carbs down into simple carbs, then absorb them into the bloodstream”. However, would this mean that simple carbohydrates are digested quicker than complex ones? The simple answer is “yes”, but let’s stick around a little longer to learn what else this means.

Glycemic response

Since complex and simple carbohydrates are digested at different rates, they differ in how they impact blood glucose concentration. By glycemic response, we refer to the effect that food which contains carbohydrates has on blood glucose levels. For example, food that causes a rapid rise and fall in blood glucose levels has a different glycemic response than food which has a more gradual increase in blood glucose, has a lower peak level and also falls at a slower rate. It would be very nice to have some way to classify foods based on its effect on blood glucose levels, perhaps this could be done with some sort of numeric index?

Glycemic index

The glycemic index is the numerical value that represents the impact that specific food has on blood glucose levels. According to Gropper and Smith (Advanced nutrition and human metabolism), the glycemic index is determined as follows:

Glycemic index is defined as the increase in blood glucose level over the baseline level during a 2-hour period following the consumption of a defined amount of carbohydrate (usually 50 g) compared with the same amount of carbohydrate in a reference food.

However, they also tell us how the glycemic index is actually determined:

(…) the glycemic index is measured by determining the elevation of blood glucose for 2 hours following ingestion. The area under the curve after plotting the blood glucose level following ingestion of the reference food is divided by the area under the curve for the reference food times 100. If glucose is used as the reference food, it is arbitrarily assigned a glycemic index of 100. With glucose as the reference food white bread has a glycemic index of about 71. The use of white bread as the reference assigns the glycemic index of white bread of 100.

To simplify, the glycemic index tells you how much of a “sugar hit” some food will give you relative to either glucose or white bread. Unsurprisingly, some foods have a greater effect on blood glucose levels than white bread, so their glycemic index is higher than 100 when using white bread as a reference.

The way the glycemic index is measured isn’t perfect, as methodological differences (the way food is prepared or the ingredients used), and even the food’s temperature have an impact on its numerical value. There is another problem: we rarely eat a single food, but rather meals composed of several foods. In order to deal with this issue, the idea of glycemic load was introduced.

Glycemic load

The idea behind the glycemic load is that it’s both the quality (related to the glycemic index), and the quantity of carbohydrates in a meal. Fortunately, its definition is rather simple, as the glycemic load (GL) equals the glycemic index times the grams of carbohydrate in a serving of the meal. As may be expected from its definition, a higher GL means a higher blood glucose level, and a long-term diet with a high GL is associated with greater risk of type 2 diabetes and coronary heart disease. In other words, the higher blood glucose levels rise and the longer such increased blood glucose lasts, the higher is our risk for diabetes and heart disease.

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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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What is the Body Mass Index (BMI)?

The Body Mass Index (BMI) is defined as a person’s weight in kilograms, divided by their height in meters squared, namely (and copied from Wikipedia because I can’t write math in WordPress):

\mathrm {BMI} ={\frac {{\text{mass}}_{\text{kg}}}{{\text{height}}_{\text{m}}^{2}}}={\frac {{\text{mass}}_{\text{lb}}}{{\text{height}}_{\text{in}}^{2}}}\times 703

Now, let’s try to interpret that definition. To begin with, BMI’s units are of mass over surface area, so it’s analogous to surface mass density. Secondly, this surface mass density is made up of a person’s weight is distributed uniformly in a square whose sides are equal to that person’s height.

Let’s refer to the square representation of a person’s height with the term “square-person”. Hopefully in this way, you can understand BMI as a measurement of a given square-person’s mass density. Intuitively, two square-people of the same height but different weights will have to spread those different weights throughout the same surface, and two people of the same weight but different heights will have to spread that same weight over different surfaces. Simple, right?

BMI categories

Let’s get something out of the way, BMI is useful when it comes to populations, as it provides a quick and easy way to check wether an individual is underweight, of normal weight, overweight, or obese within that population. This does not mean, however, that it is the be all and end all criterion for establishing someone’s weight-status, although it provides a quick reference for that. This is something which fatlogicians don’t seem particularly interested in understanding, and appear to be more focused in throwing away the concept of BMI altogether.

I won’t cite specific BMI values, but it is worth noting some of the categories they reference: underweight, normal weight, overweight, and obese. It is also worth mentioning that each of those categories encompasses a whole range of BMI values, and thus there is a whole spectrum for an individual’s weight-status within a given population. This is another thing fatlogicians seem to forget: although the cutoff BMI values between one category and another might appear harsh and arbitrary, the reality is that there are ranges of BMI values that are compatible with having a normal weight or being overweight or obese, so focusing on whether one is a decimal above or belove a given cutoff is missing the forest for the trees.

BMI’s applicability and limitations

It would be senseless to assume a definition for BMI like the one given above would suit everyone. Clearly, extremely tall or short people would have issues fitting into the “correct” weight category. Likewise, muscular people tend to be bumped into the overweight or obese categories. However, unless you are some sort of outlier, or can handily lift a small car, chances are that BMI and its weight-categories are well suited to you.

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BMI doesn’t work!

Through a quick Google search I found the following claims of how BMI is useless. They are in no particular order, and I have limited the number of claims to respond to so that this post doesn’t become repetitive, boring, or a dissertation.

  • BMI doesn’t work for athletes/short people/tall people/, so it’s useless!
  • BMI doesn’t take into account my activity level!
  • BMI doesn’t tell me about problem areas!
  • BMI gets body fat/muscle mass wrong!
  • BMI is lying by scientific authority!
  • BMI is a tool of the insurance industry so that they can charge higher premiums!
  • There are better tools than BMI!

Answering the criticisms

  • As BMI is determined by considering the weight and the height of an individual, what happens when an individual’s height or weight are out of the norm? Remember, BMI is useful when it comes to populations, so some individuals will be outliers and their BMI will make little sense. An example of this are strength athletes who will be categorized as overweight or obese due to their large muscular mass, which makes no sense. The same goes for shorter than average or taller than average people, the former tend to find themselves in the overweight category despite being healthy while the latter tend to find themselves in the underweight category despite, again, being healty. Is this reason enough to do away with BMI? The quick answer would be to ask yourself if you truly are more athletic than the average person, or if you’re taller or shorter than average. Chances are that the average person is, well, average, and BMI will work well for them.
  • By its very definition, BMI doesn’t account for anyone’s activity level. What the problem with this is, I still can’t figure out. It’s clear that this particular criticism is aimed towards saying that even if a person is classified as overweight or obese, BMI is wrong because that person may lead an active lifestyle and they’re healthy. Again, BMI works well for populations, and the farther an individual strays from being average in terms of weight or height, the less reliable BMI becomes. However, this activity level issue shouldn’t be a problem unless you are as active as an athlete, and you have the extra muscle mass to show it.
  • Why would BMI tell you about problem areas? Is there anything in its definition that even considers them? What is a problem area to begin with? See, this criticism seems to come from the same school of thought that claims that spot reduction is a thing. For those who may not know, spot reduction is the idea that we can target specific places in our body and only lose the fat located in them. The reality is that fat is put on and lost by our body in a manner that is beyond our control beyond what we put into our mouths. In other words, this criticism is rather nonsense.
  • BMI cannot get muscle mass or body fat wrong because BMI doesn’t even account for them. Take a look at BMI’s definition, do you see a variable that specificly accounts for muscle mass or body fat? On the contrary, both are being implicitly accounted for in a person’s weight. As stated previously, if you’re an athlete then BMI won’t even be a thing you take into account, but if you’re smack down average, then BMI will work well.
  • I don’t even know what lying by scientific authority means. Do we use Einstein’s field equations because Einstein came up with them? No, we use them because they work, just like we use quantum mechanics where applicable and Newt0n’s Law of Gravitation where it gives the right results. That’s where science’s authority comes from. Perhaps what this criticism is trying to say is that BMI is flawed but it’s been given an air of authority, which would be an appropriate criticism, especially considering athletes, tall and short people. If the meaning of this criticism is a different one, then I’ve no idea what it is.
  • I would be surprised if BMI wasn’t taken into account when setting insurance premiums. However, going from there to the conspiratorial side is a little extreme, since it’s not insurance companies that have established the different classifications due to BMI.
  • This last one is a perfect criticism because it’s true. There are indeed better tools than BMI, but the question then is: better at what? If you want a quick and cheap way to classify populations based on height and weigh, BMI works fine. If you want to take a more careful look into an individuals body fat levels or muscle mass then yes, BMI won’t give you any information about that. The task determines the tool, and for the average person BMI is good enough.

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What is ghrelin?

A quick Google search will tell you that ghrelin is the hunger hormone. Cool, so what does that mean? As we’ve covered before, hormones are substances that serve as chemical messengers. They are transported through the circulatory system to organs so that their phisiology and behavior can be regulated. In particular, ghrelin is a peptide secreted mainly by endochrine cells in the stomach and small intestine, and it stimulates food intake.

What is ghrelin for?

Once ghrelin is released by your stomach and small intestine, our feeling of hunger increases. In fact, ghrelin concentration in the blood rises when we fast (check this post for a definition on fasting), and it decreases right after eating, especially if we’ve ingested carbohydrates.

In addition to that, ghrelin also causes the release of Neuropeptide Y, which also stimulates hunger. Ghrelin, neuropeptide Y and leptin are hormones that are constantly duking it out to give you hunger or to make you feel satisfied. In a later post we’ll talk about leptin, but suffice to say that whenever leptin hangs out in your blood, neuropeptide Y doesn’t have any effect.

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What is leptin?

Leptin is a hormone, primarily produced in the adipocytes (fast cells), that helps regulate our metabolism by inhibiting appetite, and making us feel sated. Although leptin is used by our body in a variety of ways, we’ll just stick to those related to metabolic rates, food intake, and obesity.

Leptin and genetics

I know very little of genetics, so please bear with my misuse of the terminology or my misunderstanding of it. In our organism, the gene LEP contains the instructions to produce leptin, so mutations in that gene will have an effect on the production of leptin and our overall metabolism.

Thanks to our parents, we have two copies of the LEP gene, one inherited from each parent. However, this also means that the gene can suffer from several mutations. According to Wikipedia, there are eight of those mutations, and all of them result in obesity with hyperphagia (excessive hunger or eating) in childhood. For the purposes of this post, we’ll just talk about the three possible scenarios that result from LEP mutations that are mentioned in Advanced Nutrition and Dietetics in Obesity:

  • Case 1: the LEP copies have no mutations. In this case or bodies response to leptin is the standard one. All is well, and is business as usual.
  • Case 2: one of the LEP copies contains a mutation. In this case BMI is skewed towards larger values, but no other problems are present.
  • Case 3: both LEP copies contain mutations. In this case both obesity and hyperphagia are present.

Leptin and food intake

Here we will talk about the lipostatic hypothesis. The hypothesis essentially tries to account for the perceived relationship between obesity and food intake by proposing that fat tissue is somehow involved in appetite control. There is also a glucostatic hypothesis, but we’ll talk about it in a later post.

The lipostatic hypothesis seems to make sense, right? The more fat tissue you have, the more leptin is produced. By having greater leptin levels then your appetite would be at a minumum and you would eat less since you’ve got more fat to spare. However, it turns out that the relationship between the amount of fat that we carry and the control of our food intake is neither obvious nor simple. The hypothesis works well for leaner people with more normal weights: fat acts as a regulator of appetite and further food intake is inhibited due to fat reserves. The problem is that as our fat levels increase, so does the level of leptin and, just like it happens with insulin, a resistance to leptin is developed. In other words, as one becomes fatter, leptin becomes less useful and it is more difficult to control our eating.

When it comes to weight loss (focusing specifically on fat loss), studies have shown that dieters who lose weight also have reduced levels of leptin. Such a dramatic decrease in leptin levels is associated with an increase of hunger, which may result in weight regain. If anything, all this should tell you to not get too fat.

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What is insulin?

Insulin is a hormone, produced by the beta-cells of the pancreas, that plays a key role in regulating the blood level of glucose when feeding or fasting, as it is involved in protein, glucose and lipid synthesis and storage. You can think of insulin as the hormone in charge of letting the body know when it’s in times of plenty or scarcity. In times of plenty, excess glucose in our blood is turned into glycogen or fatty-acids. In times of scarcity, the process is the other way around.

What does insulin do?

In broad terms, insulin serves to increase the activity of those enzymes that catalyze (accelerate) the synthesis of lipids, glycogen and protein while also inhibiting the expression of those enzymes that catabolyse (break down) those same substances.

When blood glucose levels are elevated, beta-cells in the pancreas produce insulin. In turn, this stimulates the absorption of glucose by muscle cells and fat cells, while also inhibiting the synthesis of glucose (gluconeogenesis) in the liver. In muscle cells, the uptake of glucose results in the production of glycogen, while the uptake of glucose in fat cells results in further fatty acid production.

Just as we learned that ghrelin and leptin fulfill antagonistic roles, insulin has a hormonal counterpart known as glucagon. Glucagon is produced by the alpha-cells in the pancreas and serves to increase the concentration of glucose and fatty acids in the bloodstream. Glucagon is produced when insulin concentration falls too low in our blood.

In this way, insulin and glucagon are supposed to keep blood levels of glucose within upper and lower bounds, neither too low nor too high. We’ve previously talked about how blood glucose concentration changes after eating a meal on our post on the glycemic index, so check it out if you are interested.

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What is glucagon?

Just as we learned that ghrelin and leptin fulfill antagonistic roles, insulin has a hormonal counterpart known as glucagon. Glucagon is produced by the alpha-cells in the pancreas and serves to increase the concentration of glucose and fatty acids in the bloodstream. Glucagon is produced when insulin concentration falls too low in our blood.

In this way, insulin and glucagon are supposed to keep blood levels of glucose within upper and lower bounds, neither too low nor too high. We’ve previously talked about how blood glucose concentration changes after eating a meal on our post on the glycemic index, so check it out if you are interested.

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