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I think that's my cue to stop attempting to have rational debate in this thread.

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Also, supplying your existing gut flora with resistant starch like the potato starch Jason has mentioned will grow and rebalance your gut biome.

We only buy Bubbies pickles and sauerkraut now as it's actually fermented and not just pickled (and it's easier than fermenting your own).

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Last week, my staff nutritionist Laura Schoenfeld wrote a guest post for my blog called “Is a Low-Carb Diet Ruining Your Health”. Perhaps not surprisingly, it has caused quite a stir. For reasons I don’t fully understand, some people identify so strongly with how many carbohydrates they eat that they take offense when a suggestion is made that low-carb diets may not be appropriate for everyone, in all circumstances.

In these circles low-carb diets have become dogma (i.e. a principle or set of principles laid down by an authority as incontrovertibly true). Followers of this strange religious sect insist that everyone should be on low-carb or even ketogenic diets; that all carbohydrates, regardless of their source, are “toxic”; that most traditional hunter-gatherer (e.g. Paleolithic) societies followed a low-carb diet; and, similarly, that nutritional ketosis—which is only achievable with a very high-fat, low-carb, and low-protein diet—is our default and optimal physiological state.

Cut through the confusion and hype and learn what research can tell us about low-carb diets.

On the other hand, I’ve also observed somewhat of a backlash against low-carb diets occurring in the blogosphere of late. While I agree with many of the potential issues that have been raised about low-carb diets, and think it’s important to discuss them, I also feel it’s important not to lose sight of the fact that low-carb diets can be very effective therapeutic tools for certain conditions and in certain situations.

With this in mind, here are 7 things I think everyone should know about low-carb diets.

#1: Paleo does not equal low-carb, and very low-carb/ketogenic diets are not our “default” nutritional state, as some have claimed.

Some low-carb advocates have claimed that most traditional hunter-gatherer societies consumed diets that were very low in carbohydrates. I’ve even seem some suggestions that nutritional ketosis was “the norm” for these cultures.

These claims are false. The majority of studies have shown that traditional hunter-gatherer (HG) societies typically consume between 30–40% of their total calories from carbohydrate, though the range can vary between 3–50% depending on the population studied and the latitude at which they live. (2, 3) The only HG societies observed to eat fewer than 20% of calories as carbohydrate were those living at latitudes quite distant from the equator, often in marginalized environments where fruits, vegetables, starches, and honey were not readily available.

Yet even these cultures—such as the traditional Inuit—often made an effort to obtain carbohydrates from berries, corms, nuts, seaweed, and tubers whenever they could, as Richard Nikoley has recently detailed on his blog. What’s more, contrary to popular claims, studies have shown that it’s unlikely the Inuit spent much time—if any—in nutritional ketosis. Their high protein intake would have prevented ketosis from occurring. (5)

So, while ancestral diets were certainly lower in carbohydrate than the diet currently recommended by the USDA (45–65% of calories), they were not typically “very low” in carbohydrate (<15% of calories). With virtually no historical examples of human beings following ketogenic diets for any significant length of time, and few examples of very low-carb diets, it’s difficult to imagine how these diets could be considered our “default” nutritional state or the optimal approach for most people.

#2: Low-carb diets are incredibly effective in certain situations

Lest low-carb advocates think that I am anti-low-carb, I’d like to reiterate that both the research and my clinical experience suggest that low-carb diets can be incredibly effective therapeutic tools for certain conditions.

These conditions include (but aren’t limited to):

Overweight and obesity
High blood sugar, metabolic syndrome, diabetes (both type 1 & type 2)
Traumatic brain injury
Epilepsy
Parkinson’s disease
Alzheimer’s disease
Other neurological conditions
PCOS
I have personally witnessed some remarkable transformations using ketogenic diets therapeutically in my practice. I recall an 84 year-old woman who came to see me complaining of dementia and early-onset Alzheimer’s. She was losing her memory and cognitive abilities at an alarming rate. After just two weeks on a ketogenic diet, this progression not only halted, it reversed: her memory returned, her mind was sharper, and she was far less confused and disoriented. Her family (and her doctor) were stunned, and could hardly believe the changes they were seeing.

Yet as impressive as very low-carb (VLC) and ketogenic diets can be in certain situations, that does not mean that these diets may not have some undesirable side effects over the long term—some of which we’re only beginning to understand. For example, as I discussed with Jeff Leach from the American Gut project in a recent podcast, some preliminary research suggests that long-term ketogenic/VLC diets may cause adverse changes to the gut microbiota. (6) In addition, a new paper soon to be published in the journal Cell by two Stanford microbiologists indicates that diets low in “microbiota-accessible carbohydrates (MACs)” contribute to modern, inflammatory disease. (7)

The phrase “microbiota-accessible carbohydrates” refers to the various fibers found in fruits, vegetables, starchy plants, nuts, seeds, legumes, and other foods that are poorly absorbed by us, but can be utilized as a food source by our intestinal bacteria. It’s worth noting that many of these fibers are found in foods with moderate to high carbohydrate content—foods that would typically be excluded on very low-carb diets.

It’s important to note, however, that the beneficial bacteria-starving effects of ketogenic/VLC diets can be at least partially offset by consuming non-digestible, fermentable fibers like resistant starch and non-starch polysaccharides that don’t count toward daily carbohydrate intake. This is something I recommend to all of my patients following low-carb diets)

#3: The fact that ketogenic/VLC diets work therapeutically for certain conditions does not make them appropriate in all circumstances, for all people

This assumption is a basic failure of logic, but it’s remarkable to see how often it happens. A person has a life-changing experience with a VLC diet, so they assume that their friend will have a similar experience. Or a clinician that works primarily with people suffering from neurological conditions has great success with ketogenic diets, and then makes the assumption that all people (regardless of their health complaints) will benefit from them.

This is akin to saying that since people with hemochromatosis (a genetic condition that causes iron overload) need to limit their iron intake, everyone should consume foods that are low in iron.

The belief that “everyone” will benefit from one particular dietary approach—no matter what it is—ignores the important differences that determine what is optimal for each person. These include variations in genes, gene expression, the microbiome, health status, activity levels, geography (e.g. latitude and climate), and more.

When it comes to diet, there is no one-size-fits-all approach.

#4: Some people do better with low-carb diets than others

If you understand #3 above, then this should not come as a surprise.

Some people may thrive on a long-term, low-carb diet. I have patients and even a family member in this category. And maybe you’re one of them too. But that doesn’t mean everyone will have this experience. If you talk to practicing clinicians who work with patients on a daily basis, or spend any amount of time in internet forums or the comments sections of nutrition blogs, you’ll find numerous reports from people who either experienced no benefit from or were even harmed by following a low-carb diet.

What blows my mind is that the “low-carb zealots” seem completely incapable of accepting these reports at face value. Instead, they’ll argue that anyone who doesn’t succeed with low-carb is either doing it wrong, cheating, or somehow imagining their symptoms.

What’s the more likely explanation here? That everyone who gets worse with a low-carb diet is either incapable of following directions, weak-willed, or delusional? Or that a low-carb diet simply does not work for everyone? You be the judge.

#5: If a low-carb diet works as a therapy in a given condition, that doesn’t mean too many carbs caused that condition in the first place

This is another error of logic that is often made. Here’s an example:

“A low-carb diet is effective for treating type 2 diabetes. Therefore, eating too many carbohydrates led to this condition in the first place.”

This is like saying:

Restricting iron is helpful in hemochromatosis patients. Therefore, consuming too much iron is what caused hemochromatosis in the first place.
A low-FODMAP diet helps patients with Irritable Bowel Syndrome (IBS). Therefore, eating FODMAPs caused IBS in the first place.
A low-histamine diet alleviates the symptoms of histamine intolerance. Therefore, histamine intolerance is caused by eating too many histamine containing foods.
Or, more ridiculously, since wearing a cast on your arm will help the broken bone heal, the reason you broke your arm in the first place is because you weren’t wearing a cast.

It’s true that VLC/ketogenic diets are effective for improving the metabolic markers associated with type 2 diabetes. But that doesn’t mean that eating too many carbohydrates led to the condition in the first place. It is certainly possible (and indeed likely) that eating too many refined and processed carbohydrates, in the form of flour and sugar, contributes to diabetes. But I have not seen a single study suggesting that eating whole-food carbohydrates (e.g. fruit or starchy plants) leads to diabetes or other metabolic problems. On the contrary, reviews of prospective studies looking at the relationship between fruit intake and diabetes have found that those with the highest intake of fruit had the lowest incidence of diabetes. (8, 9)

It is also worth pointing out that virtually all studies performed so far showing benefits of the Paleo diet in conditions like type 2 diabetes and obesity have used moderate carbohydrate (not low or very-low carb) versions of the Paleo diet.

#6: If a low-carb diet is an effective therapy for a condition, that doesn’t mean it’s the only therapy for that condition

There’s little doubt, as I said above in #2, that low-carb diets can be remarkably effective in certain situations. For example, there are numerous studies showing that low-carb and ketogenic diets can help with weight loss and metabolic problems. (10)

However, that doesn’t mean it’s not possible to lose weight and reset your metabolism through other means. Studies have also shown that calorie-restricted diets, protein-sparing modified fasts, and even low-fat diets can also be effective treatments. (11, 12, 13)

This means that it’s not necessarily true, for example, that everyone with type 2 diabetes should be on a low-carb diet. They may be able to reverse their condition by following a high-protein, moderate-carbohydrate, moderate-fat diet (such as the Paleo diet with 32% of calories from carbohydrate in this study), or any of the methods I just mentioned.

#7: Whole-food carbohydrates do not affect the body in the same way as processed and refined carbohydrates

This should be obvious to anyone with a basic understanding of nutrition and human physiology, so I’m amazed at how often I see experts talk about all carbohydrates as if they’re the same.

In #1 above, I referenced studies indicating that most hunter-gatherer societies consumed about 30–40% of calories from carbohydrate. These carbohydrates came from starchy tubers and plants, whole fruit, and in some cases, honey. We also have evidence of specific ancestral populations—such as the Kitava, traditional Okinawans, and Tukisenta—that consumed between 70–95% of calories from whole-food carbohydrate. (14)

Yet despite this liberal consumption of carbohydrates, these people were remarkably lean, fit, and free of chronic, inflammatory diseases like diabetes, cardiovascular disease, and neurological conditions. (15) If carbohydrates cause these conditions, regardless of their source, why don’t we see such conditions in these groups?

What we do see is that these cultures acquire modern disease when they adopt a modern diet and lifestyle, complete with the highly processed and refined foods that characterize it.

When it comes to macronutrients, quality is much more important than quantity for most people.

Final thoughts

I hope this helps to clarify some of the confusion that has surrounded this issue. Low-carb diets are an effective therapeutic tool in certain situations, and one that I (and many other clinicians) use in my clinical practice. That said, it’s equally true that low-carb—and especially VLC and ketogenic—diets are not appropriate in all circumstances, and they are certainly not our “default” or optimal nutritional state.

Sadly, it doesn’t seem to matter how much scientific evidence, clinical experience, and common sense is brought to bear on this question: those who preach and follow low-carb dogma will not be swayed. Ah, well. As they say: “You can’t fight faith with facts.”

Now I’d like to hear from you. What has your experience with low-carb diets been like? Have you had success with them over the long term? Or have they caused you harm? What is your optimal intake of carbohydrate? Let us know in the comments section.

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Artificial sweeteners -- promoted as aids to weight loss and diabetes prevention -- could actually hasten the development of glucose intolerance and metabolic disease, and they do so in a surprising way: by changing the composition and function of the gut microbiota -- the substantial population of bacteria residing in our intestines. These findings, the results of experiments in mice and humans, were published September 17 in Nature. Dr. Eran Elinav of the Weizmann Institute of Science's Department of Immunology, who led this research together with Prof. Eran Segal of the Department of Computer Science and Applied Mathematics, says that the widespread use of artificial sweeteners in drinks and food, among other things, may be contributing to the obesity and diabetes epidemic that is sweeping much of the world.

For years, researchers have been puzzling over the fact that non-caloric artificial sweeteners do not seem to assist in weight loss, with some studies suggesting that they may even have an opposite effect. Graduate student Jotham Suez in Dr. Elinav's lab, who led the study, collaborated with lab member Gili Zilberman-Shapira and graduate students Tal Korem and David Zeevi in Prof. Segal's lab to discover that artificial sweeteners, even though they do not contain sugar, nonetheless have a direct effect on the body's ability to utilize glucose. Glucose intolerance -- generally thought to occur when the body cannot cope with large amounts of sugar in the diet -- is the first step on the path to metabolic syndrome and adult-onset diabetes.

The scientists gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the U.S. Food and Drug Administration (FDA). These mice developed glucose intolerance, as compared to mice that drank water, or even sugar water. Repeating the experiment with different types of mice and different doses of the artificial sweeteners produced the same results -- these substances were somehow inducing glucose intolerance.

Next, the researchers investigated a hypothesis that the gut microbiota are involved in this phenomenon. They thought the bacteria might do this by reacting to new substances like artificial sweeteners, which the body itself may not recognize as "food." Indeed, artificial sweeteners are not absorbed in the gastrointestinal tract, but in passing through they encounter trillions of the bacteria in the gut microbiota.

The researchers treated mice with antibiotics to eradicate many of their gut bacteria; this resulted in a full reversal of the artificial sweeteners' effects on glucose metabolism. Next, they transferred the microbiota from mice that consumed artificial sweeteners to "germ-free," or sterile, mice -- resulting in a complete transmission of the glucose intolerance into the recipient mice. This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host's metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance in the sterile mice. A detailed characterization of the microbiota in these mice revealed profound changes to their bacterial populations, including new microbial functions that are known to infer a propensity to obesity, diabetes, and complications of these problems in both mice and humans.

Does the human microbiome function in the same way? Dr. Elinav and Prof. Segal had a means to test this as well. As a first step, they looked at data collected from their Personalized Nutrition Project (PersonalNutrition.org), the largest human trial to date to look at the connection between nutrition and microbiota. Here, they uncovered a significant association between self-reported consumption of artificial sweeteners, personal configurations of gut bacteria, and the propensity for glucose intolerance. They next conducted a controlled experiment, asking a group of volunteers who did not generally eat or drink artificially sweetened foods to consume them for a week, and then undergo tests of their glucose levels and gut microbiota compositions.

The findings showed that many -- but not all -- of the volunteers had begun to develop glucose intolerance after just one week of artificial sweetener consumption. The composition of their gut microbiota explained the difference: the researchers discovered two different populations of human gut bacteria -- one that induced glucose intolerance when exposed to the sweeteners, and one that had no effect either way. Dr. Elinav believes that certain bacteria in the guts of those who developed glucose intolerance reacted to the chemical sweeteners by secreting substances that then provoked an inflammatory response similar to sugar overdose, promoting changes in the body's ability to utilize sugar.

Prof. Segal states, "The results of our experiments highlight the importance of personalized medicine and nutrition to our overall health. We believe that an integrated analysis of individualized 'big data' from our genome, microbiome, and dietary habits could transform our ability to understand how foods and nutritional supplements affect a person's health and risk of disease."

According to Dr. Elinav, "Our relationship with our own individual mix of gut bacteria is a huge factor in determining how the food we eat affects us. Especially intriguing is the link between use of artificial sweeteners -- through the bacteria in our guts -- to a tendency to develop the very disorders they were designed to prevent; this calls for reassessment of today's massive, unsupervised consumption of these substances."

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Many people think weight loss is simply about cutting calories. They believe that to lose weight, you must reduce calories (either eat less or burn more), to gain weight you must add calories, and to maintain weight you keep calories constant. To these folks, calories in, calories out is the only thing that matters. They usually oppose the Primal Blueprint because they assume that we “deny” the importance of calories in weight loss.

Well, they’re wrong. I don’t deny the importance of calories. Calories absolutely count. And if someone has lost weight, they have necessarily expended more calories than they consumed. That said, there are some major misconceptions about calories, body weight, fat loss, and health. These calorie myths are often rooted in truth but presented in black-or-white terms that are useless at best, harmful at worst, and do little to help the average person lose body fat.


Let’s dig right in.

Calories in, calories out is all you need to know.

Simple is nice. Simple is good. But overly simple is dangerously inaccurate, so let’s break this statement down.

What does “calories in” refer to?

Calories in — what we eat. We can’t metabolize sunlight or oxygen. We can’t feast on the souls of the damned. The food we eat determines “calories in” entirely. Simple.

“Calories out” is where it gets confusing. There are several components to “calories out”:

Resting energy expenditure — the energy used to handle basic, day-to-day physiological functions and maintenance
Thermic effect of food — the energy used to digest food and process nutrients
Active energy expenditure — the energy used during movement (both deliberate activity like lifting weights, jogging, and walking, plus spontaneous activity like shivering and fidgeting)
Not so simple, is it? There are a lot more variables to consider.

Oh, and about those variables…

Calories in and calories out are independent variables.

That would be nice. You could drop energy intake and maintain your resting metabolic rate while burning the same amount of energy digesting food (even though you’re eating less of it) and working out. The fat would melt off at a predictable, constant rate. Anyone with basic arithmetic skills (or a calculator) could become a successful weight loss coach and very few people would be overweight.

In reality, the amount and type of calories we eat affect the amount of energy we expend:

During calorie restriction, the body “defends” its body weight by lowering resting metabolic rate and reducing spontaneous physical activity. To keep weight loss going, you often have to lower food intake even more (to counteract the reduced metabolic rate) and remind yourself to fidget, tap your feet, twiddle your thumbs, and shiver (to recreate the missing spontaneous movement). And you have to do it again when the body readjusts.

Whole foods take more energy to process and digest than processed foods. In one example, subjects either ate a “whole food” sandwich (multigrain bread with cheddar cheese) or a “processed food” sandwich (white bread with cheese product). Both meals were isocaloric (same number of calories) and featured roughly identical macronutrient (protein, fat, carb) ratios. Those eating the multigrain sandwiches expended 137 calories postprandially (after their meal). The white bread group expended only 73 calories, a 50% reduction in the thermic effect of food.

Protein takes more energy to process and digest than other macronutrients. Compared to a low-fat, high-carb diet, a high-protein diet increased postprandial energy expenditure by 100% in healthy young women. And in both obese and lean adults, eating a high-protein meal was far more energetically costly (by almost 3-fold) than eating a high-fat meal.
Calories in affects calories out. The two variables are anything but independent of each other.

Weight gain is caused by eating more calories than you expend.

Calorie fetishists love pointing out that weight gain requires overeating. That is, everyone who gains weight necessarily ate more calories than they expended. Okay. We’ve established that everyone agrees on this. But it’s just restating the issue. It doesn’t tell us anything new or useful. It’s merely descriptive, not explanatory.

To show you what I mean, let’s do the same thing with other phenomena.

Why was Martin Luther King Jr. assassinated? Because someone pointed a sniper rifle at him and fired it.

Why did Usain Bolt win the 100 m final in the Beijing Olympics? Because he crossed the finish line first.

Why is the restaurant so crowded? Because more people entered than left.

These are technically true, but they ignore the ultimate causes. In King’s case, they fail to discuss racism, the civil rights movement, or the motivation of the shooter. They don’t mention Bolt’s training, genetics, or his childhood. They don’t discuss why the restaurant has attracted so many customers — new menu, Valentine’s Day, graduation? They simply restate the original statement using different words. They just describe what happened.

I’m interested in what truly causes us to eat more than we expend and/or expend less than we eat. I don’t care to merely describe weight gain because that doesn’t help anyone.

A calorie is a calorie.

Look. I loved Carl Sagan. Like everyone else, I got chills when he’d wax poetic about our place in the universe and our shared origins as “star-stuff.” But just because steak comes from the same star-stuff as a baked potato, isocaloric amounts of each do not have identical metabolic fates in our bodies when consumed.

We even have a study that examined this. For two weeks, participants either supplemented their diets with isocaloric amounts of candy (mostly sugar) or roasted peanuts (mostly fat and protein). This was added to their regular diet. After two weeks, researchers found that body weight, waist circumference, LDL, and ApoB (a rough measure of LDL particle number) were highest in the candy group, indicating increased fat mass and worsening metabolic health. In the peanut group, basal metabolic rate shot up and neither body weight nor waist size saw any significant increases.

Does this invalidate the relevance of energy balance? Of course not. Since the peanut group’s metabolic rate increased, they expended more calories in response to added calories, thus remaining in balance. But it does elegantly and definitively invalidate the simplistic notion that all calories, especially added calories, are treated equally by the body.

Weight loss and fat loss are the same thing.

People don’t want to lose weight. “Losing weight” is common parlance, but we really want to lose body fat and retain, or gain, muscle. And studies indicate that the macronutrient composition can differentially affect whether the weight lost is fat. It’s not just about total calories.

Take the 2004 study from Volek that placed overweight men and women on one of two diets: a very low-carb ketogenic diet or a low-fat diet. The low-carb group ate more calories but lost more weight and more body fat, especially dangerous abdominal fat.

Or the study from 1989 that placed healthy adult men on high-carb or high-fat diets. Even though the high-carb group lost slightly more body weight, the high-fat group lost slightly more body fat and retained more lean mass.

Just “weight” doesn’t tell us much. What kind of weight? Are we losing/gaining fat or muscle, bone, sinew, organ? Are we increasing the robustness of our colons and the number of bacterial residents (who, though small, carry weight and occupy space) from added prebiotic fiber intake? These factors matter for health. I’d argue that they’re the only factors that actually matter when losing or gaining weight because they offer insight into our health and body composition.

Exercise helps you lose weight only by burning calories.

Most people think of exercise as a way to mechanically combust calories. And that’s true, to a point. Exercise does “burn” calories, and this is a factor in weight loss. But it does lots of other cool things to our physiology that can assist with improving body composition, too.

Compared to something high intensity like burpees or something aerobic like running a 10k, lifting free weights doesn’t burn many calories when you’re lifting them. But it does improve insulin sensitivity, which reduces the amount of insulin we secrete for a given amount of carbohydrate and increases our ability to burn body fat. It increases muscle mass, which uses calories (protein). It strengthens connective tissue, which also uses calories. It even preserves metabolic rate during weight loss and boosts it for up to 72 hours post-workout. All these changes affect the fate of the calories we ingest.

If calories burnt were the most important factor, then the best way to lose weight would be to hammer it out with as much endurance exercise as you can withstand because that’s the most calorie intensive. But studies show that combination training — aerobic and resistance training — leads to greater reductions in body fat than either modality alone.

Even aerobic exercise isn’t just about mechanically burning calories. It also preferentially targets the reward regions of our brains, reducing the allure and spontaneously lowering our intake of junk food.

Counting calories allows us to accurately monitor food intake.

You’d think that, wouldn’t you? Most foods at the grocery store have labels. Even restaurants are beginning to emblazon menus with calorie counts for each item. As humans, we implicitly trust the printed word. It looks so official and authoritative, and it spells out with great specificity exactly how many calories we’re about to eat.

Except studies show that’s not the case. Whether it’s the nutritional information provided by restaurants, the calorie counts on supposedly “low-calorie” foods, or the nutritional labels on packaged foods, calorie counts are rarely accurate. Food manufacturers can even underreport calories by 20% and pass inspection by the FDA.

Maybe that’s why people have so much trouble sticking to their allotted number of calories. If only reality would bend to the will of the label!

You may roll your eyes at some of these ideas because they’re so preposterous, but consider where you’re coming from, where you’re reading this. This is how the general public – and, often, the experts and physicians advising their patients and writing policy — approaches the question of fat loss. Sure, not everyone immersed in conventional wisdom holds every one of these myths to be true. And when they’re actually faced with the statement, few will claim that a calorie of steak is metabolically identical to a calorie of white sugar or that weight loss is the same as fat loss. But when calories in, calories out is the first line of attack against excess body fat, these are the kind of myths that become entrenched.

It’s important to take them head-on.

No one wants to be fat. The obese know they’re obese. They’ve had “calories in, calories out” drummed into their heads for years. If it were really as simple as eating less and moving more, they wouldn’t be obese. And yet here we are. That might be the biggest danger of the continued propagation of these myths — they convince people that they’ve failed at something simple, basic, and central to being a healthy, moral human being.

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Yesterday’s post introduced the major myths surrounding calories, weight loss, and human regulation of body weight, but there are some other serious misconceptions surrounding the topic that need clearing up. People can really get down on themselves when they listen to all the “experts”. They’ll weigh, measure, and count themselves into oblivion only to experience middling weight loss. Or maybe they lose weight but their energy tanks, their performance in the gym suffers, and their belt size doesn’t get any better, suggesting muscle loss. They’re basing their decisions and actions on myths, and myths just don’t work. These myths do real harm, so it’s important to destroy them.

Today, I’m going to focus on nine more.


The calorie count of a food is the sole determinant of its metabolic fate.

The way many people envision it, the only thing food does is provide energy for storage or immediate use.

But food is more than energy.

Protein, for example, is broken down into amino acids which provide the building blocks for human cells, muscles, and tissues. And yes, in extreme cases protein can provide energy, either through direct metabolism of the amino acids or conversion into glucose, but the vast majority of the protein we eat is directed toward structural roles. We build things with protein. And even when we do “burn” protein for energy, it’s not very efficient.

Food provides energy and raw material for building important things like muscle, cellular membranes, hormones, nerves, neurotransmitters, sperm, tears, new eyelashes, beards, or toenails. Anything the body does, or makes, or metabolizes, like convert serotonin into melatonin so you can fall asleep at night, requires both energy (to power the process) and raw materials. Food is both.

And even when food is “just” energy, it’s “metabolizable energy.” You have to expend energy to extract energy from that sweet potato and steak you just ate. It’s not gross energy.

Calorie counting is the best way to lose weight.

Since we all agree that weight loss requires that a person expend more energy than they take in, counting them should be the only way to lose weight. Nearly everyone can count and do basic math, so why not just do a little addition and subtraction? Once the stark reality of the numbers lies in front of you and the true, physics-backed path to healthy weight loss reveals itself, you’d have to acquiesce and give in and stop eating so much, you glutton, because Science implores you to and no one can deny Science.

The latest low-fat/low-carb diet study contradicts this: participants in the low-carb arm were told not to restrict calories by the researchers, yet calories were restricted and weight was lost. Detractors often point to this as proof that calories indeed matter. To me, this showcases that active consideration of calories is unnecessary. They lost weight and reduced calories without counting calories. That’s the good stuff, right?

Heck, even when you compare a strict calorie-counting diet with an ad libitum (“at liberty”) low-fat, high-carb diet, the calorie counters lose out and the ad libitum dieters have better weight loss retention after 2 years. Calorie counting just doesn’t work for most people.

At the end of the day, if you consume more calories than you expend, you will gain fat.

Gotta love that phrase, “at the end of the day.” People drop this in comment sections and that’s that: the debate is over, the argument won. Go home.

Except is that really the case? “Weight” is so non-specific. You might gain bone. You might gain muscle. You might gain glycogen. You might gain organ weight. You might gain newly repaired intestinal lining. And yeah, you might gain fat, but it’s not a foregone conclusion just because you “gained weight.”

Conscious regulation of one’s energy intake and expenditure is possible.

Imagine if you had to maintain conscious control over every physiological process in your body. When you walked, you’d say to yourself “step left, step right, step left, step right” all day long or you wouldn’t get anywhere. To provide oxygen to your body, you’d have to remember to breathe in and breathe out every few seconds. An hour or so before bedtime, you’d will your pineal gland to begin secreting melatonin so you could sleep. After eating, you’d have to alternately engage and relax your peristalsis muscles to create the undulation that forces food along the digestive tract. Performing a squat would require conscious orchestration of the contraction of dozens of agonist, antagonist, stabilizer, and synergist muscles at once. Life would get pretty unwieldy, wouldn’t it?

So where do we get the idea that eating – one of the most basic and essential physiological processes – requires constant vigilance and number crunching? What did people do before the concept of a calorie was invented?

In metabolic ward studies where calories are counted for you and food is strictly weighed, measured, and provided by the researchers, calorie counting works pretty well. Subjective feelings of appetite are immaterial when you only have access to the food provided and you can’t leave to get more.

In the real world, calorie counting doesn’t work as well. If a free-living guy is ravenous from counting calories and he drives past a McDonald’s, he has the option of stopping in for a McDouble (they still make those, right?) and fries. If a subject in a metabolic ward study is ravenous from having his calories counted for him and he has a fever dream of Ronald McDonald hand-feeding him fresh french fries, it doesn’t matter because he doesn’t have the option of eating any more food.

Besides, it’s not even possible to do it accurately without direct measurement. A group of normal weight men and women were blinded to one of two treadmill exercise sessions (burning either 200 or 300 calories). After the workout, they were taken to a buffet and told to eat as many calories as they’d just burned exercising. Both groups failed miserably.

First of all, they thought they’d burned way more calories than they actually had. The 200 calorie group guessed they’d burned around 825 calories. The 300 calorie group guessed close to 900 calories.

Second, they ate fewer calories than they estimated, but more than they actually burned. Every estimate they made was inaccurate.

And that was in normal weight individuals, the people who are least likely to have broken metabolisms and dysfunctional satiety mechanisms. If they can’t accurately predict energy intake and expenditure, how is anyone supposed to? According to many researchers, self reports of calorie intake and expenditure are “so poor” that they’re more harmful than not even trying to count.

Everyone responds to calories equally.

For the most part, people all have the same basic physiological machinery. We all metabolize carbs, fat, protein, and other nutrients along the same pathways. We all use insulin to sequester glucose into cells, for example (even people who don’t produce insulin will respond to injected insulin).

That said, we all have different capacities for using these pathways.

For instance, most overweight or obese people seem to do best on lower-carb, higher-fat diets. The literature is pretty clear on that. If you’re insulin-resistant and overweight (which is most of the overweight population), going low-carb is the best, easiest way to control hunger, spontaneously reduce food intake, and lose weight and, most importantly, body fat. Hundreds of success stories from this site and others are further testament to that.

However, the relatively rare insulin-sensitive obese phenotype does better on calorie-counting low-fat diets. If you’re obese and insulin sensitive, you’ll probably be able to lose more weight eating more carbs. That’s just a fact, and it’s just more proof that macronutrient ratios, personal history, hormonal status, and genetic background are relevant to the impact of calories.

Another example: Say you’ve got two men, both weighing 200 pounds and standing 6 feet tall. The first is active, fit, and muscular, sitting at 11% body fat. The second is sedentary and overweight, sitting at 30% body fat. If they eat an equal amount of baked potato, will those carbohydrates enjoy the same fate in both men?

The first guy has significantly more muscle. That means larger glycogen stores, the only way to store carbohydrate. The second guy has significantly less muscle, meaning he has less room to store carbohydrate as glycogen. Assuming both are equally glycogen depleted, in whose body will the greater portion of carbohydrates be sequestered as body fat?

The first guy is more likely to store the carbs as glycogen because his larger muscle mass confers greater storage capacity. The second guy is more likely to convert the carbs to fat. Once his liver and muscle glycogen stores fill up, any glucose that isn’t immediately used for energy will be converted to fat. This isn’t a huge acute contribution to overall fat gain, but it does illustrate the different metabolic fates the same number of calories can have in two different people of equal weight.

And we all know that guy who can eat a 2000 calorie meal without gaining an ounce. If you sit next to him while he eats, you can literally feel the heat emanate from his body. Or maybe he’ll start fidgeting, or get up to pace the room. Kids are often like that. You feed them a big meal and they’ll be whizzing around the room, not to “burn the calories off to avoid weight gain” but because they just received a large influx of energy and it’s only natural for a kid to use it. That used to be me back in college.

Exercise affects appetite and inadvertent calorie intake differently in men and women. In men, the higher the exercise’s intensity, the lower the appetite. This is true across most studies. But there’s also evidence that in women, intense exercise — sprints, HIIT, circuit training — actually has the potential to increase appetite and energy intake.

The only thing that might affect weight loss beyond calories in, calories out are your macronutrient ratios.

This is where we start getting somewhere. Most people will admit that different ratios of macronutrients (protein, fat, carbs) in the diet can affect weight loss. This is why bodybuilding cutting diets are made up of chicken breast and broccoli, not Coke and pizza. But they’ll go no further than talking protein, fat, and carbs.

In reality, different subtypes of protein, carbs, and fat have different metabolic effects. Take protein. Whey promotes energy expenditure relative to other proteins, like tuna, egg, or turkey. Other studies have found that both whey protein and pea protein suppress the appetite to a greater degree than milk protein or a combination of whey and pea protein. Meanwhile, fish protein eaten at lunch suppresses subsequent energy intake more than a beef protein lunch.

Take carbs. In one (rat) study, isocaloric amounts of honey and table sugar had different effects on bodyweight. The rats who ate honey gained less bodyweight and body fat (particularly that really hard-to-burn epididymal pad fat we all hate so much!) than the sugar-fed rats.

Take fat. In one study, isocaloric amounts of either industrial (not grass-fed ruminant) trans-fat or a blend of monounsaturated and saturated fat were given to human subjects. Those eating the trans-fat experienced greater increases in body fat and waist circumference. There was no difference in overall bodyweight, of course, so I guess the CICO fanatics “win” this one, but the two different fat sources clearly had different metabolic fates.

There are more examples of each, but even just one is enough to dismantle the claim.

The results from studies apply to every individual human.

Lost in all the blog chatter about this or that study is the fact that the faceless participants whose bodies we’re discussing are individuals. The individual experiences of these individual subjects dissolve into the mean, the average presented in the abstract. If you’re lucky, you’ll get a +/- indicating the range of responses. But every subject from every study ever conducted has had unique reactions to the experiment.

For instance, there’s the “single low-calorie subject” from this study who experienced no reduction in liver fat. Everyone but him saw improvements. Should that guy disregard his own experience because the study’s conclusion about the effect of dieting on liver fat in the “average person” said otherwise?

You are not a statistic. This goes for every study out there, but it’s especially pertinent for diet studies. I know many people who’ve had paradoxical responses to various dietary interventions, responses that the studies don’t really capture. Are they all lying?

The concept of a calorie is applicable to the complexity of human metabolism.

Sometimes, I like to dream that we’re bomb calorimeters.

Our stomachs are buckets full of water (that’s where those “the human body is 75% water” claims originate). Suspended inside those stomach buckets is a smaller sack, called a bomb. A tube runs from our mouths and feeds directly into the bomb. When we eat something, the food goes down the tube and into the bomb. As we chew, a series of tendons attached to our jaws rub together to produce a spark. The heat travels down into the bomb to ignite the food. A separate tube runs from our lungs to the bomb carrying pure filtrated oxygen. The food combusts and the heat generated is distributed throughout the body to give us energy. The beauty of digesting our food in the bomb is that it’s a closed system, shut off and free of influence from the outside universe, so we know that what we put into the bomb is exactly what we’ll get out of digesting it. Meat, potatoes, kale, Pepsi – it’s all pure unadulterated raw fuel and it all burns equally. It’s all heat energy.

Unfortunately, that’s not how the human body works.

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The scientists all agree that a calorie is a calorie.

I contend that no one truly believes “a calorie is a calorie.” Even the researchers who claim perfect parity between different caloric sources in esteemed scientific journals contradict themselves in their own papers.

We conclude that a calorie is a calorie. From a purely thermodynamic point of view, this is clear because the human body or, indeed, any living organism cannot create or destroy energy but can only convert energy from one form to another.

No argument here.

In comparing energy balance between dietary treatments, however, it must be remembered that the units of dietary energy are metabolizable energy and not gross energy. This is perhaps unfortunate because metabolizable energy is much more difficult to determine than is gross energy, because the Atwater factors used in calculating metabolizable energy are not exact. As such, our food tables are not perfect, and small errors are associated with their use.

“Small errors.” Mistakes were made, nothing to see here, move along. Don’t worry yourself over the margins. It all evens out in the end.

In addition, we concede that the substitution of one macronutrient for another has been shown in some studies to have a statistically significant effect on the expenditure half of the energy balance equation. This has been observed most often for high-protein diets. Evidence indicates, however, that the difference in energy expenditure is small and can potentially account for less than one-third of the differences in weight loss that have been reported between high-protein or low-carbohydrate diets and high-carbohydrate or low-fat diets.

It’s just “one third” of the difference in weight loss. That’s nothing at all!

As such, a calorie is a calorie.

Even though we just explained how a calorie is not a calorie, a calorie is a calorie.

Further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.

In other words, our simplistic “calories in, calories out” approach is inadequate and other mysterious “mechanisms” are responsible for the difference in weight loss between diets. But trust us, a calorie is still a calorie!

We’re all on the same page here. Some of us just can’t admit it.

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I know it seems unpleasant, but of the two ways we typically transfer them, I promise this is the one you want.

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