• 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.


We Win! TIME Magazine Officially Recants (“Eat Butter…Don’t Blame Fat”), And Quotes Me

It’s been 30 years and three months since TIME Magazine’s infamous “Cholesterol…And Now The Bad News” cover featured the bacon-and-eggs frowny face—the arresting image which firmly institutionalized fat and cholesterol-phobia in America:

Cholesterol: And Now The Bad News...

The face that launched a million failed diets.

Meanwhile, my parents recently visited something even rarer than a paleo-friendly doctor—they visited a doctor whose office features current magazines in the waiting room. In it, they spotted the June 23, 2014 issue of TIME magazine, featuring the following cover story:

Click to read the cover story (requires TIME online subscription)

Link to cover story (requires TIME online subscription)

Yes, the cover reads:

Eat Butter.
Scientists labeled fat the enemy. Why they were wrong

and the first page of the article is titled
Don’t Blame Fat

The contents of the article won’t be a surprise to anyone in the Paleo community, the low-carb community, the WAPF, or anyone who has taken the time to evaluate the science and statistics on their own: thirty years of low-fat dogma has produced a nation fatter and sicker than ever, and the “science” supporting the dogma wasn’t science at all. What I find interesting are the implications and consequences of the article, so please permit me to discuss a few of them.

This Is The Tipping Point

The message on the cover could not be more stark: “Eat Butter.”

Given that opening salvo, we can expect to see Drs. Westman, Lustig, Phinney and Volek make an appearance…but the article also quotes Drs. David Ludwig, Rajiv Chowdhury, and Dariush Mozaffarian, all lead authors of recent, high-impact research papers questioning different aspects of low-fat dogma. (Several of which I’ve read and previously cited.)

And, despite the predictable grousing from vegans like Dean Ornish (who, predictably, moves the goalposts away from health issues and blames meat-eaters for environmental destruction), it’s clear that the current crop of public policy heavyweights can see that the anti-fat ship has long since crashed into a massive iceberg of scientific evidence, and are scrambling for the lifeboats

—the most comical example of such being Walter Willett, who claims “he was sitting on a piece of contrary evidence that none of the leading American science journals would publish.” Dude, you’ve been the chairman of the Department of Nutrition at the Harvard School of Public Health since 1991, at which time you already had your name on over 140 published papers. If you were sitting on data that exonerated saturated fat, it’s because you prioritized advancing your own career over public health.

Again, nothing in this article will be news to any of my readers! What I find interesting is that the mainstream academic establishment, and with it, the mainstream mass media, is finally abandoning low-fat dogma. This is a clear tipping point in the dietary debate.

Don’t Expect Public Policy To Change

Unfortunately, we can expect the US government to be the last to change, for two reasons: governments have zero accountability, and massive agricultural subsidies produce a massive surplus of grains that need to be disposed of somehow. This means several problems will continue to bedevil us:

  • Obesity research, which is mostly NIH-funded, will therefore continue to be mostly useless.
  • The government-issued low-fat dietary recommendations will continue shambling well into the 21st century, like a glassy-eyed horde of zombies. (“GRAAAAAAAAAAAINS!”)
  • Consequently, school lunches will continue to be crypto-vegetarian, protein-deficient piles of birdseed (also known as “hearthealthywholegrains”) and limp steamed vegetables. As I said years ago, long before the new school lunch regulations, “Expect school lunches to become even more disgusting and empty of nutrition. If you want your child to grow up healthy, expect to help them pack a lunch every day. Expect to be grilled by suspicious administrators who think you’re damaging your child by feeding them real food.”
  • Unhealthy packaged foods, made from heavily subsidized corn, soy, and wheat, will remain artifically cheap—while real food like fruit, vegetables, and grass-finished beef (which remains unsubsidized) will remain expensive by comparison. As a result, the health of Americans will continue to suffer.

Who Gets The Blame For Killing Millions Of People Over Three Decades?

Given the millions of dead and the incalculable suffering caused by what Philip Handler correctly called “a vast nutritional experiment”:

“What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?”

-Dr. Philip Handler, then-President of the National Academy of Sciences, in Senate testimony to the U.S. Senate Select Committee on Nutrition and Human Needs in 1977. (Yes, the one that came up with the original low-fat, low-cholesterol Dietary Goals for the United States. Quote via Gary Taubes.)

One might ask “Will there be any accountability for what amounts to mass murder?

As we’ve seen above, the answer is “No”…and the current solution seems to be “We’ll blame it all on Ancel Keys, because he’s dead.” Yet with few exceptions, the academic and professional establishments fell in line rather than risk their own political standing by confronting dogma they suspected (or, in many cases, knew definitively) to be wrong.

Don’t Expect Any Credit

You’ll notice that no one gets quoted in TIME on public health matters without an MD or PhD and a long, mainstream academic or public policy career (the single exception being Nina Teicholz, whose book “The Big Fat Surprise” was just published by a major New York house.) So don’t hold your breath for people like Drs. Mary Enig, Malcolm Kendrick, Uffe Ravnskov, Michael Eades, or John Briffa (let alone John Yudkin or Wolfgang Lutz) to get any credit, even though they all have MDs and/or PhDs.

The article doesn’t even mention Gary Taubes, who single-handedly brought fat back into the public discourse with his 2001 article “What If It’s All Been A Big Fat Lie?” and his 2007 book “Good Calories, Bad Calories”…so I predict that hell will freeze over before any Paleo source gets any mainstream credit for our work. (I know NPR journalists who tried to get an article on Paleo pubished for years, and failed.) Besides, the press has spent too much time and effort mocking Paleo with “CAVEMAN DIET HURRR DURRRR” to back out now.

This tells you what you should already know: it’s nice to have the support because it makes your eating habits less socially awkward—but the mainstream press is a trailing indicator, not a leading indicator.

J. Stanton Quoted In TIME Magazine! (By Proxy)

I laughed when I saw this quote in the article, and so will many of my readers:

“A bagel is no different than a bag of Skittles to your body,” says Dr. Dariush Mozaffarian.

The analogy is straight out of one of my most popular articles (“Mechanisms of Sugar Addiction: Or, Why You’re Addicted To Bread”), published way back in 2010, and which still gets tens of thousands of page views every month:

At the risk of quoting myself, I'll quote myself.

At the risk of quoting myself, I’ll quote myself.

No, I’m not mad! I’ve cited Dr. Mozaffarian’s work before, I’m proud that he’s among my many readers—and it’s a remarkably sticky analogy that gets an important point across to TIME’s tens of millions of readers worldwide.

Most importantly, I understand the rules of the game: since I have no MD, PhD, or high-level public policy career, my research and information will only reach the mainstream media through an intermediary with such official standing.

PROTIP: Anyone can thank me by slipping me online access to journals via an academic or professional account. Your help will remain confidential.

The Mainstream Authorities Often Aren’t Very Smart

From the TIME article:

“When you replace saturated fats with polyunsaturated and monounsaturated fats, you lower LDL cholesterol,” says Dr. Robert Eckel, a past president of the AHA and a co-author of the group’s recent guidelines. “That’s all I need to know.”

Actually, if you’re tasked with recommending dietary guidelines to an entire nation, I’m sure you need to know much more than that—starting with the fact that TG/HDL is a much stronger predictor of heart disease than LDL. For example:

Circulation. 1997 Oct 21;96(8):2520-5.
Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction.
Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, Buring JE.

“…The ratio of triglycerides to HDL was a strong predictor of myocardial infarction (RR in the highest compared with the lowest quartile=16.0; 95% CI=7.7 to 33.1; P for trend <.001).
Adjustment for available coronary risk factors did not materially alter the results.
Further adjustment for LDL did not materially alter the results.

No, that isn’t a typo! The highest 25% of TG/HDL ratio carries 16 TIMES GREATER RISK of a heart attack than the lowest 25%. And LDL wasn’t significant.

Clinics (Sao Paulo). 2008 Aug;63(4):427-32.
High ratio of triglycerides to HDL-cholesterol predicts extensive coronary disease.
da Luz PL1, Favarato D, Faria-Neto JR Jr, Lemos P, Chagas AC.

“The odds ratios for the extent of coronary disease between the fourth and first quartiles were as follows: total cholesterol, 1.08, 95%CI (0.57–2.03), p = 0.87; LDL-c, 1.62, 95%CI (0.86–3.06), p = 0.15; triglycerides, 1.7, 95%CI (0.94–3.08), p = 0.986; HDL-c, 0.25, 95%CI (0.13–0.46), p = 0.0001; and TG/HDL-c, 3.31, 95%CI (1.78–6.14), p = 0.0002 (Figure 1).
The relationship was not significant between extent of coronary disease and total cholesterol [1.25 (0.82–1.91; p = 0.33)] or LDL-c [1.47 (0.96–2.25; p = 0.0842)].”

So the actual, measured extent of coronary disease is best predicted by TG/HDL—while neither TC or LDL (universally and erroneously known as “bad cholesterol”) is significantly predictive.

Bonus Question: What dietary modification most efficiently reduces triglycerides and increases HDL?

Answer: Replacing dietary carbohydrate with saturated fat. (Extra credit for MCTs.)

The evidence is clear: the paleo community is many years ahead of the “mainstream”, and degrees don’t magically make you smart. Meanwhile, expect to see a great deal of backing-and-filling from the AHA, the ADA, and other alphabet-soup organizations in the future.

It’s also very important to remember that the political skills required to ascend to the level of policy-making don’t usually correlate with the skills required to rationally evaluate existing evidence and determine the best course of action—and even if one is capable of it, that telling the truth is rarely compatible with advancing one’s political standing.

Bonus Section: From the “I’m Right” Files

Mol Metab. 2013 Aug 19;2(4):329-36. doi: 10.1016/j.molmet.2013.08.003.
The hormonal signature of energy deficit: Increasing the value of food reward.
Lockie SH1, Andrews ZB.

“As outlined in Section 1, using the catch-all term of ‘reward’ to describe all mesolimbic processes has led to confusion in the literature.”

The attentive reader will note that I made this very point, and dissected this very subject at length, way back in 2011 (index to my article series “Why Are We Hungry?” here), and I summarized and extended my work at AHS 2012 (video, text). For example:

“It is also very important to note that what is colloquially called “reward” is a mashing together of hedonic impact and incentive salience. Both vary independently, and both are subjective properties—so the term “food reward”, which implies a singular property of the food itself, is intrinsically misleading…

““Palatability” and “reward” are not properties of food. Our likes and wants are subjective properties we assign to food based on our past experiences, and our current state of satiation and satiety.”

-J. Stanton, AHS 2012

Moving on:

“Energy deficit serves to alter motivational state by increasing the incentive salience of certain reinforcers. [...] This ultimately manifests as increased motivation to work for a reinforcer, and serves to alter the incentive salience of food in line with metabolic need. [Emphasis mine]” -Lockie 2013

Stated simply, hunger makes food more “rewarding.” I think I’ve said that before!

(Further reading: Hopkins 2014, Domingos 2013, my AHS2012 bibliography.)

Important note: I’m not accusing anyone of plagiarism or uncredited appropriation! I’m happy to see that my work is beginning to be confirmed by work done within the academic research community.

At the present rate, I predict you’ll start to see people other than myself, Petro at Hyperlipid, Mike T Nelson, and a few exercise physiologists discover the importance of metabolic flexibility somewhere around 2018. Remember: you heard it here first.


  • Paleo and its offshoots (Primal, Perfect Health Diet) are still years ahead of the academic research, and even farther ahead of mainstream dietary advice.
  • The political savvy required to become a Recognized Authority is frequently unaccompanied by the keenest analytical mind or a burning desire to seek truth…and telling the truth is often incompatible with political advancement.
  • The mainstream of academia, politics, and the press will continue to pretend they weren’t simply, devastatingly wrong for decades, causing the deaths of millions and incalculable suffering—and that it was all Ancel Keys’ fault.
  • Don’t count on receiving any credit for having been correct long before it was popular, or even acceptable. Accept that eating like a predator, and living like a predator, is its own reward.

Live in freedom, live in beauty.


Yes, I’ll be writing more articles soon! Meanwhile, there’s much more to read in the index.

Also, I’ve updated and revamped the forum and commenting software. Hopefully comments should still work as they always have: please let me know (through the Contact link above) if you experience problems.

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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.

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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.

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