• 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.


Intermittent Fasting Matters (Sometimes): There Is No Such Thing As A “Calorie” To Your Body, Part VIII

Caution: contains SCIENCE!

In previous installments, we’ve proven the following:

  • A calorie is not a calorie when you eat it at a different time of day.
  • A calorie is not a calorie when you eat it in a differently processed form.
  • A calorie is not a calorie when you eat it as a wholly different food.
  • A calorie is not a calorie when you eat it as protein, instead of carbohydrate or fat.
  • A calorie is not a calorie when you change the type of fat, or when you substitute it for sugar.
  • A calorie is not a calorie at the low end of the carbohydrate curve (< 10%).
  • Controlled weight-loss studies do not produce results consistent with “calorie math”.
  • Even if all calories were equal (and we’ve proven they’re not), the errors in estimating our true “calorie” intake exceed the changes calculated by the 3500-calorie rule (“calorie math”) by approximately two orders of magnitude.

(This is a multi-part series. Return to Part I, Part II, Part III, Part IV, Part V, Part VI, or Part VII.)

What’s More Important: Losing Weight, or Not Gaining It?

It’s instructive to keep in mind that these two questions are not the same—and as such, they may have different answers:

  • What diet will help me lose weight most easily and efficiently?
  • What diet will stop me from gaining weight most easily and efficiently?

As we saw in Part II, the entire obesity crisis in America resulted from the average American gaining roughly one pound per year. So instead of asking “How can we lose weight?” it’s perhaps more important to ask “How can we avoid gaining weight in the first place?”

The first question is answered by underfeeding studies: the second question is answered by overfeeding studies. I’ll return to this important distinction later in this series.

Intermittent Fasting, Time-Restricted Feeding, and “High-Fat Diets”

Cell Metab. 2012 Jun 6;15(6):848-60. doi: 10.1016/j.cmet.2012.04.019. Epub 2012 May 17.
Time-restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high-fat diet.
Hatori M, Vollmers C, Zarrinpar A, DiTacchio L, Bushong EA, Gill S, Leblanc M, Chaix A, Joens M, Fitzpatrick JA, Ellisman MH, Panda S.
(Fulltext here)

Mice under tRF consume equivalent calories from HFD as those with ad lib access, yet are protected against obesity, hyperinsulinemia, hepatic steatosis, inflammation, and have improved motor coordination.”

Experimental setup: Half the mice were fed standard chow, half were fed the standard “high-fat diet”. Each half was subdivided into ad libitum-fed mice, who had 24/7 access to food, and time-restricted mice, who only had access to food for eight hours out of 24.

I use scare quotes around “high-fat diet” for several reasons, many alluded to in the previous installment.

First, the “high-fat diet” contains 20% purified sugars.

Second, unlike the standard chow diet, which contains actual food similar to the natural diet of seed-eating, primarily herbivorous mice (the primary ingredients are “ground corn, dehulled soybean meal, dried beet pulp, fish meal, ground oats”), the “high-fat diet” consists entirely of purified laboratory ingredients (the primary ingredients are “lard, casein, maltodextrin, sucrose, powdered cellulose, soybean oil”), none of which occur in or resemble the natural diet of mice. (PDF of ingredients for chow diet, high-fat diet.)

Result: instead of speaking of a “chow diet” and a “high-fat diet”, it’s more appropriate to speak of a species-appropriate diet, or “natural diet”, and a species-inappropriate diet, or “industrial diet”.

Returning to the study, we have four groups of mice: natural/ad-lib (“NA”), natural/time-restricted (“NT”), industrial/ad-lib (“FA”), industrial/time-restricted (“FT”).

First, we find that despite the radically different diets and restricted feeding windows, all four groups consumed almost exactly the same number of “calories”:

Calories consumed, by group

Interestingly, both time-restricted groups (NT and FT) were more active than the ad-lib groups (NA and FA):

Energy expenditure by group

However, only one of the groups got fat: the group which ate the industrial diet ad libitum.

Body weight, by group

The extra weight was almost entirely fat mass:

Body composition by group

Just to make the point clear, the researchers even included pictures of a representative FA and FT mouse:

FA = ad-lib industrial diet. FT = time-restricted industrial diet

Remember, both mice not only ate the same diet—they consumed the same number of “calories” each day.

How about that?

There is much more fascinating data in this paper: at the risk of overquoting, here are some passages of interest. (Emphasis mine.)

Mice fed normal chow or high fat diet under a tRF regimen (NT and FT) improved diurnal rhythms in their RER compared to their ad lib fed counterparts, with higher RER during feeding and reduced RER during fasting, indicative of increased glycolysis and fat oxidation respectively (Figure 1C).
Despite equivalent energy intake from the same nutrient source, FT mice were protected against excessive body weight gain that afflicted FA mice (Figures 1J, 1K and S1), suggesting that the temporal feeding pattern reprograms the molecular mechanisms of energy metabolism and body weight regulation.
mTOR induces the expression of glucose-6-phosphate dehydrogenase (G6pdx) (Duvel et al., 2010), whose protein product is the rate limiting enzyme of the PPC and is activated by accumulation of its substrate G6-P. In turn, the PPC is a major source of NADPH which reduces glutathione. In the livers of mice under tRF, induced expression of G6pdx along with elevated G6-Pled to increased activity of the PPC as measured by higher levels of PPC intermediates and of reduced glutathione (Figures 3D, 3E and S3).
FT mice were also protected from the hepatomegaly and elevated serum alanine aminotransferase (ALT) levels that are associated with obesity-induced hepatic steatosis (Figures 4J and 4K). […] Livers from the FT mice did not have the profound increase in intracellular fat deposits, reduced mitochondrial density and reduced endoplasmic reticulum that were characteristic of the liver samples from the FA mice (Figures 5C, 5D and Table S2).
The tRF regimen temporally reprograms glucose metabolism away from gluconeogenesis towards glycolysis, reduced glutathione and anabolic pathways. Accordingly, FT mice did not display the hallmarks associated with glucose intolerance found in diet-induced obesity, instead showing glucose tolerance and insulin levels comparable to the control NA mice (Figures 3I and 3J). The overall improvement in metabolic state also paralleled improved motor coordination in the mice under tRF paradigms (Figure 3K).
Elevated β-oxidation and reduced fatty acid synthesis in the liver coupled with increased BAT energy expenditure observed in the FT mice prevented the adipocyte hypertrophy common to BAT and white adipose tissue (WAT) derived from the FA mice (Figures 6F and 6G). Furthermore, inflammation marked by extensive infiltration of macrophages and expression of proinflammatory genes, including TNFα, IL6 and CXCL2 that are generally found in the WAT of the FA mice, were attenuated in the FT mice (Figure 6H). Even in mice fed normal diet, tRF reduced the expression of inflammatory cytokines in the WAT. In summary, the tRF paradigm affected multiple tissues and improved whole body energy homeostasis, and reduced inflammation.

A Bonus Observation

Tucked into the corner of Figure 4, we see a curious graph: the FT mice (industrial “high-fat” diet, time-restricted) performed best of all the groups on the accelerating Rotarod test.


“What’s a Rotarod?” you ask.

(Perhaps the fact that ketones are the preferred fuel of the brain and heart isn’t just a biochemical curiosity.)

Takeaways: Intermittent Fasting

First, it’s clear that a calorie is not a calorie when you’re intermittent fasting.

However, the most interesting part, to me, is the difference between the natural and industrial diet groups. 16/8 intermittent fasting was only mildly beneficial to the mice eating a natural diet. However, the mice fed an industrial diet ad libitum (“FA”) were not only obese—they were in terrible metabolic shape, with fatty liver and impaired glucose metabolism. In contrast, the time-restricted industrial diet mice (“FT”) were, for the most part, just as healthy as the mice fed a natural diet.

Tentative takeaway: The less species-appropriate your diet is, the more difference intermittent fasting makes to your health and bodyweight.

This doesn’t mean you can eat all the junk food you want so long as you fast afterward! For instance, nothing about IF will stop gluten grains from causing intestinal permeability (see Fasano 2011). However, it seems that IF may be able to increase your tolerance for dietary patterns that would otherwise be unhealthy for you, cause weight gain, or both.

Also, I can’t resist the observation that most agrarian religions prescribe a significant amount of fasting. John Durant has speculated that this is a disease-fighting measure, but it may well be a general health measure that helps compensate for the inferior agrarian diet.

This series will continue! Meanwhile, you can go back to Part I, Part II, Part III, Part IV, Part V, Part VI, or Part VII.)

Live in freedom, live in beauty.


Note that the retail price of The Gnoll Credo will be dramatically increasing soon, for reasons detailed here. Meanwhile, it continues to receive reviews like “A cry of joy and terrifying beauty, an extraordinary commentary on the human condition, something that can change the way you see the world and your place in it,” and my current favorite, “Thought provoking and it inspired me to buy a crossbow.” Beat the price hike by buying your copy today.

Will You Go On A Diet, or Will You Change Your Life?

It’s New Year’s Day again—which means it’s time to resolve to lose a bunch of weight and get in shape.


Before you commit to the latest diet, cleanse, detox, or “one weird trick”, though, ask yourself a simple question:

Is this something I can do for the rest of my life?

To understand why this is important, practice reading these paragraphs out loud without laughing:

  • “Before putting anything in my mouth, I will carefully research its value in “calories”, “points”, or “blocks”. Then I will check this value against the list I’ve kept of everything else I ate today, to make sure I have enough free “calories”, “points”, or “blocks” to eat it. Then I will add it to the list. I will do this for every meal and snack, every day, without fail, until I die.”

  • “Life without beef, pork, eggs, or butter will be totally fulfilling. I won’t ever miss bacon, prime rib, or a loaded baked potato. Fat-free sour cream and non-dairy cheese taste exactly like the real thing. I love lentils.

  • “I can pedal a bicycle that goes nowhere for 40 minutes a day, week after week, month after month. This is the best and most productive use of my time.”

Has it suddenly become obvious why your New Year’s resolutions never seem to survive the change of seasons?

Lose A Bit Of Belly Fat Every Day With This One Weird Trick!

Eat like a predator, not like prey.

Yes, that’s a link. Click it.

You don’t need to buy any books, join any gyms, or spend any money on anything but food. If we needed to read an entire book to learn how to eat, our ancestors would have starved to death millions of years ago.

It’s easy. When I eat like a predator, I feel stronger. Sharper. Quicker. More alive. I like that.

When I eat like prey, I slow down. I lose my edge. I become weak, irritable, and vulnerable. I don’t like that.

Here it is again. Eat like a predator. Click it.

Live in freedom, live in beauty.


Yes, this one is aimed at new readers! Please forward it to anyone searching for help: the share widget is below. They may not have the ears to hear: as the gnolls say, hazrah nachti. You’ve done what you can.

More soon.

Carbohydrates Matter, At Least At The Low End (There Is No Such Thing As A “Calorie” To Your Body, Part VII)

Caution: contains SCIENCE!

In previous installments, we’ve proven the following:

  • A calorie is not a calorie when you eat it at a different time of day.
  • A calorie is not a calorie when you eat it in a differently processed form.
  • A calorie is not a calorie when you eat it as a wholly different food.
  • A calorie is not a calorie when you eat it as protein, instead of carbohydrate or fat.
  • A calorie is not a calorie when you change the type of fat, or when you substitute it for sugar.
  • Controlled weight-loss studies do not produce results consistent with “calorie math”.
  • Even if all calories were equal (and we’ve proven they’re not), the errors in estimating our true “calorie” intake exceed the changes calculated by the 3500-calorie rule (“calorie math”) by approximately two orders of magnitude.

(This is a multi-part series. Return to Part I, Part II, Part III, Part IV, Part V, or Part VI.)

Empirical Evidence: A Calorie Is Not A Calorie When You Add Carbohydrate To A Zero-Carb Diet

There are many anecdotal reports of people finding it difficult or impossible to gain weight on a zero-carb diet, even with massive overfeeding. Yet there are controlled trials that seem to show high-fat diets having no such overfeeding advantage. Why not?

This study provides some clues:

J Nutr Biochem. 2003 Jan;14(1):32-9.
Effects of dietary carbohydrate on the development of obesity in heterozygous Zucker rats.
Morris KL, Namey TC, Zemel MB.

“…We fed 6-week old male heterozygous (fa/+) lean rats carbohydrate-free diets containing primarily saturated fat either ad libitum or pair-fed. These diets were compared to standard chow and to a high saturated fat mixed diet containing 10% energy from sucrose for 4 weeks.”

This is a good start: many “high-fat” diet trials use industrial lard containing ~20% linoleic acid (an omega-6 fat), or industrial seed oils with even greater LA content—which, as we’ve seen in the previous installment, is strongly implicated in the development of obesity. Furthermore, most “high-fat” laboratory diets contain about 20% purified sugar…which, as we’ve previously noted, seems to be obesogenic by itself.

A Short Digression: “High-Fat” Almost Always Means High Sugar

The results of Morris 2003 call into question all obesity research featuring “high-fat diets”. First, they’re usually on a strain of mice (C57BL/6, or “black six”) specifically selected for its propensity to quickly become obese when fed high-fat diets, unlike other strains of mice (let alone other animals, like humans, that aren’t natural seed-eating herbivores). More importantly, in nearly every case, they use D12492—a mix of purified ingredients containing no actual food, and specifically designed to make C57BL/6 mice obese as quickly as possible. (More here, via Dr. Chris Masterjohn)

D12492 contains 20% purified sugars.

So be skeptical whenever you see a headline claiming negative effects for “high-fat diets”.

All diets were standardized to 20% protein and 11% corn oil. (Yes, these are industrial Frankendiets.) The carbohydrate-free diet contained 69% coconut oil; the 10% sucrose diet contained 59% coconut oil and 10% sucrose (table sugar), with no other carbohydrate; and the “standard chow” diet contained 59% cornstarch and no coconut oil.

Does that matter? 10% carbohydrate is still VLC, right? That’s only 50 carbs on a 2000-calorie diet…and it’s still almost 60% coconut oil, so they should be mostly in ketosis, right?

Here’s what happened after four weeks. First, the food intake figures, from Table 2:

Table 2

The zero-carb rats ate 36% more “calories” than the chow rats, and about the same (3% more) as the 10% sucrose rats…and the pair-fed zero-carb rats ate the same number of “calories” as the 70% carb (“standard chow”) rats. (That’s what “pair-fed” means: one group is fed only as much as another group eats.) So if the CICO zealots are correct (IT’S PHYSICS!!!1!!1), the standard chow and pair-fed rats ought to be lean, while the zero-carb and 10% carb rats ought to be obese.

Meanwhile, back in reality, here’s what happened:

Figure 1A

Grams of fat gained during the 4-week feeding period, by diet.

“Weight gain was negligible in the carbohydrate free groups compared to standard diet and 10% sucrose diet (p = 0.03). This was reflected in energy efficiency which was markedly reduced (90%) in the carbohydrate-free groups compared to the other groups (p = 0.04).”
“Animals consuming the standard or mixed (10 en% sucrose) diets gained 90% more weight (p = 0.03) than animals consuming the carbohydrate-free diet ad libitum (Fig. 1A).” –Ibid.

The data is presented confusingly, so I’ll put it all together in table form.

There are a couple problems with the data presentation in this paper. First, the “feed efficiency” graph doesn’t appear to agree with the primary data they present, so I’ve used the values from Table 2 and Figure 1A to recalculate it. Second, the paper doesn’t give the actual weight of the rats, just the change in weight…but given the typical developmental schedule of a heterozygous Zucker rat, it’s likely between 200g and 400g.

Dietary group                  Dietary energy consumed
(1 kJ = ~4.2 dietary calories, or kcal)
% increase
in dietary energy
from baseline
% carbohydrate
in diet
Weight gain
per rat (g)
Weight gain
per megajoule
of energy consumed (g/MJ)
Standard (10% sucrose, 70% total carb) 22400 kJ 0% 70% 20 g 0.89
Zero-carbohydrate pair-fed 22700 kJ 1% 0% -1 g -0.04
10% sucrose, 10% total carb 29500 kJ 32% 10% 20 g 0.68
Zero-carbohydrate 30500 kJ 36% 0% 2 g 0.07

Let’s put these results in English:

  • The 10% sucrose rats ate 32% more food than the standard (70% carb) rats, but gained the same amount of weight (20g).
  • The zero-carb rats ate slightly more than the 10% sucrose rats, and 36% more than the standard rats—but gained an insignificant amount of weight (2g).
  • The pair-fed zero-carb rats ate the same amount as the standard rats (that’s what “pair-fed” means), but lost a negligible amount of weight (-1g).

Clearly, in this study, weight gain (and loss) doesn’t correspond at all to “calories” consumed! It corresponds more closely to the percentage of calories from carbohydrate—regardless of “calories”.

Conclusions: Carbohydrate Intake Matters (at least at the low end)

I’m reluctant to extrapolate directly from rats to humans—but these outcomes seem to correspond reasonably well to observed reality in humans.

  • A high-fat diet increased food intake—but the rats didn’t get fat, even on over 35% more “calories”, unless sugar was added.
  • Just 10% carbohydrate, from sugar, was enough to make a non-fattening zero-carb diet strongly fattening.
  • Even at 10% carbohydrate from sugar, it still took 32% more “calories” to gain the same amount of weight that the rats gained on a 70% carbohydrate diet.
  • It appears that much of the advantage of zero-carb diets is gone at just 10% carbohydrate.
  • The studies I’ve seen that claim no advantage to varying macronutrient intakes don’t reduce carbohydrate to 10% or below. (Or they reduce energy intake to starvation levels, which is a whole another article in itself.)
  • As I’ve previously warned in this article, almost-ketosis is a bad place to live. You get the pain of trying to adapt to ketosis without ever fully adapting—and, apparently, you also lose most of the associated resistance to weight gain. Most “paleo fails” I see are from hanging around 10% carbs, usually while exercising heavily.

This series will continue! Meanwhile, you can read earlier chapters by going back to Part I, Part II, Part III, Part IV, Part V, or Part VI.

Live in freedom, live in beauty.


Did this article clarify your own thoughts and experiences? Great! Share it using the widget below, and leave a comment. Do you feel like arguing? Please save us all some time and read the other installments (linked above) before bringing up points we’ve already covered at length.