Disclaimer
• Your life and health are your own responsibility.
• Your decisions to act (or not act) based on information or advice anyone provides you—including me—are your own responsibility.
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.
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.
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
Did you find this article enlightening? Wonderful! Share it with your friends using the widget below…
I’ve been working on several projects during the weeks I haven’t updated, and here’s the first. Epipheo—the people who make all those 3-minute cartoon visualizations of interesting ideas—contacted me some time ago, and asked if I was willing to help them create one based on an article of mine.
Usually when someone offers you something for “free”, they’re trying to sell you a timeshare. However, after a couple long recording sessions, some script wrangling, and several weeks, they’ve just sent me a link to their newest video visualization—based in part on my classic article “Why You’re Addicted To Bread”, and featuring narration by me!
It’s intended for a general audience, so it’s a bit of an oversimplification—but it’s a great start for when your Uncle Ned asks you “So why won’t you eat bread anymore?” So I encourage my readers to visit the Youtube page, drop a “Like” and/or a favorable comment, and spread it amongst your bread-eating friends. (Hint: share it on Facebook using the widget below.)
Bonus Video: Nose To Tail Eating With Big Primal and Primal North
A feast of heart, liver, sweetbreads, marrow, and more ‘odd bits’ from Big Primal—and some product placement, courtesy of Danny Albers from Primal North. (Youtube link.)
While I disagree with Gyorgy Scrinis (and the popularizer of the concept, Michael Pollan) on their proposed solution, I believe Scrinis’ concept of “nutritionism” as an error in dietary thinking has merit—and I doubt anyone in the paleo community would disagree.
“Reducing food to its nutrient components could be called “nutritionism”, and it has probably become the dominant way of thinking about food and health, and of constructing healthy diets.
The nutrition industry has implicitly, if not explicitly, promoted nutritionism by continually framing most research studies and dietary advice in terms of these chemical-nutrient categories.
The rise of nutritionism is clear in one of the well-known sayings promoted by the food industry and some nutritionists: “There is no such thing as good and bad foods, only good and bad diets.” According to this argument, all types of foods, including junk food, have a place in a “balanced” diet.
…
Marketing foods and diets on the basis of their nutritional composition tends to take attention away from the quality and the type of foods being promoted.
Processed foods, for example, are often fortified with vitamins and minerals, or stripped of some of their fat, to enable such nutrient-content claims to be made. Nutrient claims on the labels of processed foods and drinks conceal the fact these foods are typically high in added fat, sugar, salt, chemical additives and reconstituted ingredients, and have often been stripped of a range of beneficial micro-nutrients and food components.”
We already know all the important nutrients and their functions.
The function of an isolated nutrient (even in a synthetic form not occurring in nature, e.g. folic acid) is exactly the same as its function in food, because…
There are no competitive or synergistic effects between the thousands of chemical compounds found in one bite of real food.
The effect of a food on health is reducible to its effects on the numbers obtained from cheap, easy tests like “BMI” and “total cholesterol”.
Therefore, so long as our diet contains the proper “nutrients”, we will be healthy and happy.
I doubt anyone in the paleo community disagrees with Scrinis (and Pollan) that nutritionism, in its modern form, is bunk. A diet of chicken nuggets, Twinkies, and Diet Coke is not nutritionally equivalent to a diet of fresh meat, fruits, and vegetables no matter how many supplements we take.
What Is Anti-Nutritionism?
Unfortunately it’s possible to fall into an analogous trap when pursuing a paleo way of life…a trap I call “anti-nutritionism”. Anti-nutritionism also makes several unspoken assumptions:
We already know all the important anti-nutrients and their functions.
The function of an isolated anti-nutrient is exactly the same as its function in food, because…
There are no competitive or synergistic effects between the thousands of chemical compounds found in one seed, sprout, fruit, or bite of plant or animal tissue.
Herbivorous, seed-eating mice—especially genetic knockout mice—are metabolically and biochemically the same as humans, and are excellent models for human digestion and metabolism.
Therefore, if I eat a food for six months and I don’t get any fatter or suffer obvious health problems, I can recommend it to others as healthy—and perhaps even paleo-compatible.
Food Doesn’t Want To Be Eaten
It’s tempting to believe that if a food we like doesn’t contain gluten, excessive omega-6 fats, or excessive fructose, that it’s fine to eat. However, all food has defenses against being eaten—because any plant or animal that was eaten before it reproduced failed to leave descendants!
This leads us to a tautological but astonishing conclusion. Every living thing on this Earth is the descendant of millions of generations of successful ancestors—not a single one of which was eaten, trampled, gored, poisoned, burned, drowned, starved, fell from a tree, killed by parasites or infection, or otherwise died before it managed to reproduce at least once.
“Being eaten” certainly qualifies as a reproduction-limiting event. Animals can hide, run away, or counter-attack—but plants cannot. Therefore, we might expect their defenses to involve being disgusting, poisonous, or indigestible—particularly for seeds, their agents of reproduction.
Fruit is the exception to the rule, but there’s an unspoken bargain involved: “eat this delicious, sweet fruit, but don’t digest the seeds…poop them out somewhere else.” As we’d expect, the seeds of most sweet fruits range from bitter to frankly poisonous.
Many books, websites, and scientific papers explore the biochemistry of anti-nutrients like gluten and gliadin (found in wheat and its relatives) and lectins (found in just about every plant seed), and I won’t rehash the biochemistry here. But just as our knowledge of the nutrients in food and their function is incomplete, our knowledge of anti-nutrients is, if anything, far more incomplete.
To illustrate the limitations of the paleo community’s understanding of anti-nutrients, here’s an example I’ve never seen mentioned by any paleo source: L-canavanine.
(Update: Though it makes no appearance in the literature, apparently Dr. Loren Cordain has indeed been discussing L-canavanine in his speeches and presentations. Thanks to Pedro Bastos for the correction.)
“L-canavanine is a common non-protein amino acid found naturally in alfalfa sprouts, broad beans [also known as "fava beans"], jack beans, and a number of other legume foods [including sword beans] and animal feed ingredients [1] at up to 2.4% of food dry matter. This analog of arginine (Figure 1.) can also block NO synthesis [2-5], interfere with normal ammonia disposal [6,7], charge tRNAarg, cause the synthesis of canavanyl proteins [8], as well as prevent normal reproduction in arthropods [9] and rodents [10].
Canavanine has also been reported to induce a condition that mimics systemic lupus erythematosus (SLE) in primates [11,12], to increase antibodies to nuclear components and promote SLE-like lesions in auto immune-susceptible (e.g., (NZB X NZW)F1) mice [13].” (Brown 2005)
Stated plainly: canavanine “looks” like arginine, and is incorporated into our tissues like arginine…but the resulting proteins don’t function properly. And did I hear someone say “lupus”?
“Alfalfa sprouts can induce systemic lupus erythematosus (SLE) in monkeys. This property of alfalfa sprouts has been attributed to their non-protein amino acid constituent, L-canavanine. Occurrence of autoimmune hemolytic anemia and exacerbation of SLE have been linked to ingestion of alfalfa tablets containing L-canavanine. In this report we show that L-canavanine has dose-related effects in vitro on human immunoregulatory cells, which could explain its lupus-inducing potential.”
Rheum Dis Clin North Am. 1991 May;17(2):323-32. Dietary amino acid-induced systemic lupus erythematosus.
Montanaro A, Bardana EJ Jr.
“In this article, we detail our experience with a human subject who developed autoimmune hemolytic anemia while participating in a research study that required the ingestion of alfalfa seeds. Subsequent experimental studies in primates ingesting alfalfa sprout seeds and L-canavanine (a prominent amino acid constituent of alfalfa) is presented. The results of these studies indicate a potential toxic and immunoregulatory role of L-canavanine in the induction of a systemic lupus-like disease in primates.”
L-canavanine, being an amino acid, is not deactivated by heat or cooking. So when we hear statements like “Beans are fine so long as you soak or sprout them”, it’s worth reminding ourselves that this isn’t even true according to the tiny fraction of legume biochemistry we understand—let alone the overwhelming majority we don’t.
“Much more needs to be learned of the biological activity, the relative toxicities of these compounds to different organisms, and their nutritional value if we are to make the best use of them and the plants in which they are synthesized.”
Am J Clin Nutr November 1995 vol. 62 no. 5 1027-1028 Reply to NR Farnsworth
Victor Herbert
Also note that you’ll find a much-copied reference on the Internet claiming that canavanine toxicity is irrelevant to humans. Don’t be misled: it’s an article from a 1995 vegetarian journal which makes a host of blatantly false claims, such as “There is NO canavanine at all in other legumes that are commonly used as human food.”
Favism: A Postscript to the Fava Bean/Broad Bean Issue
Canavanine toxicity is distinct from vicine toxicity. Vicine (and its analogs covicin and isouramil) is a poison in fava beans that causes hemolytic anemia in susceptible people—a sometimes-fatal condition known as favism. Favism is caused by G6PDH deficiencies, common X-linked mutations which affect over 400 million people worldwide, mostly in Africa, the Middle East, and southern Asia.
Intermission
The Limitations Of Self-Experimentation and N=1
Self-experimentation is very important, and we can learn much that is useful from it. For instance, trying to dial in carbohydrate intake can be a balancing act between weight loss, mood, and physical performance. People have found solutions to their own individual health issues via anything from egg yolks to beef liver to coconut oil to magnesium supplementation. And just coming up with a new repertoire of healthy, paleo-compatible foods to replace the pantry full of junk we used to eat involves extensive N=1 with new recipes—with immediate success not guaranteed.
However, there are limits to the knowledge we can accumulate. Stated plainly:
N=1 self-experimentation can tell us what works best for ourselves—within the limits of healthy eating, as defined by biochemistry and evolutionary context.
However, self-experimentation alone cannot tell us which foods are healthy to eat, because even a dramatic increase in lifetime risk is vanishingly unlikely to manifest itself during a few months of self-experimentation.
For instance, here’s a seemingly reasonable statement:
1. “I ate corn for six months, and I didn’t gain weight or feel worse. Therefore corn is healthy to eat.”
It’s certainly tempting to make these sorts of statements—but I find that temptation is best resisted. To illustrate why, here’s an equivalent statement that we can all agree isn’t reasonable:
2. “I started smoking six months ago, and I feel fine. Therefore smoking is healthy.”
Permit me to drive the point home with force:
3. “I started eating strontium-90 six months ago, and I haven’t got cancer yet. Therefore radiation exposure is healthy.”
4. “I started shooting heroin six months ago. It’s solved all my anxiety issues, and I’ve lost twenty pounds! Therefore shooting heroin is healthy.”
5. “I started having unprotected sex with Tanzanian hookers six months ago, and I feel great! Therefore unprotected sex with high-risk strangers is healthy.”
The reason we can identify the second through fifth statements as false is because we don’t trust the results of our own self-experimentation. We know that long-term observations show that smoking greatly increases our risk of several forms of cancer and heart disease; each Sievert of radiation exposure causes a 5-10% increase in cancer deaths (Strom 2003); heroin addiction is almost never a controllable vice; and HIV infection takes longer than six months to produce symptoms of AIDS—no matter how we feel in the short term.
No, I’m not directly comparing eating corn to smoking or unprotected sex with high-risk strangers! I’m demonstrating that even a substantial increase in lifetime risk is vanishingly unlikely to manifest itself within any period of self-experimentation. This is why anecdotes are useless when evaluating risk.
For example, my grandfather smoked two packs of cigarettes a day for over sixty years, dying in his 80s of a non-smoking-related illness…but that doesn’t change the fact that smokers contract lung cancer 15-20x more often than non-smokers (Thun et.al. 2008), and also suffer from all types of heart disease, many other cancers, renal damage, and impotence at a far greater rate than non-smokers. And while I’ve spent plenty of time making fun of weak associations extracted from known-bad data, I do find the evidence for negative health effects from regular smoking reasonably convincing—though perhaps of smaller magnitude than claimed by typical sound-bites.
In conclusion, it’s clear that anti-nutritionism makes it easy to fall into the trap of extrapolating N=1 beyond its limits. By assuming that we already know all the important anti-nutrients, we can easily convince ourselves that a clearly Neolithic food is healthy (or, at least, harmless) just because we don’t feel any obvious harmful effects from consuming it in the short term.
To answer such questions, we need to apply science, not N=1…
…and it is very likely that the answer will not be authoritative. Scientific answers are much more likely to be of the form “There are a lot of potential toxins, but we don’t know how bad they are for humans, either singly or in combination” or “It’s analogous to something that quickly causes pancreatic cancer in rats—at 10 times a realistic dietary dose.”
That’s where evolutionary context comes in, and where I use my general rule of thumb, previously seen here:
Eat foods you could pick, dig, or spear. Mostly spear.
The Takeaways: Now What?
My intent is not to encourage anyone to become overly fearful about eating the occasional bowl of ice cream or tarka dal! I understand that even functional paleo can feel somewhat limiting at times, and that nothing will make a fresh, hot Krispy Kreme not taste delicious.
What I’m doing is cautioning my readers that no interesting or useful information comes from arguments about whose N=1 is more authoritative; I’m reiterating my own commitment to careful, rational inquiry; and, most importantly, I’m hoping to communicate my own respect, humility, and awe as one infinitesimal part of our huge, beautiful and dizzyingly complex world and the multi-billion year history of life upon it. As I said nearly a year ago:
“There is an important difference between “We don’t know all the answers yet” and “Do what feels right, man.” These questions have answers, because humans have biochemistry, and we should do our best to find them and live by the results.”
Meanwhile, I will continue to do my best to find interesting and useful information at the intersection of biochemistry and evolutionary context, and I will continue to explain it as best I can to you, my readers, here at gnolls.org.
And since I like to leave my readers with a few practical takeaways, here are some useful thoughts for when you start finding even functional paleo limiting or monotonous.
Consider what you’ve gained, not just what you’ve lost. Sure, you can’t just binge on half a dozen crullers anymore…but you can eat all the prime rib you want without any form of guilt. How cool is that?
If you’re stuck in a rut of monotonous food, try some new recipes. Yes, it’ll take some time and several tries to find and perfect a new dish you like as much as your current favorites. Here’s an endless source to get you started.
Cheat proudly. For the most part, the dose makes the poison…so unless cheating will start you on a binge, it’s better to say “I am going to eat these street tacos because they’re delicious and I want some” than to try to convince yourself that corn is paleo.
Cheat intelligently. Think of a cheat as dessert: once you’ve satisfied yourself with a complete meal, you can think about a Coke or a Reese’s. Otherwise you run the risk of your cheat replacing an entire meal—and once you’ve been paleo for a while, 1200 calories worth of Krispy Kremes will most likely make you feel like you’ve contracted Ebola Zaire.
Live in your body. The pleasure of junk food lasts until it slides down your throat: the pleasure of good health manifests itself 24/7 in better sleep, less pain, greater mental clarity and capacity, and greater physical ability. The strong, sleek, healthy body of an apex predator is a great place to be. Instead of medicating it into passivity or becoming a sessile peripheral to your computer and television, go outside. Climb a tree, kick balls, shoot baskets. Learn a new skill. Explore somewhere you’ve never been.
There’s a big, bright, beautiful world out there: what are you waiting for?
Live in freedom, live in beauty.
JS
Yes, this one turned into another epic! Spread it like pollen with the new social clicky-popup-thing…and please support my continued efforts by making your Amazon purchases through my referral link. Did I mention that T-shirts are back in stock, in all sizes?
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