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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.
(fulltext)

“…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.
(fulltext)

“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.
(fulltext)

“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.

Conclusions

  • 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.

JS


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

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What Is Hunger, and Why Are We Hungry?
J. Stanton’s AHS 2012 Presentation, Including Slides

The response to the written version of my 2013 AHS presentation has been overwhelmingly positive. Based on page views, the number of people willing to read my work greatly exceeds the number of people willing to watch it in video form!

Therefore, I present to you the full text of my presentation to the 2012 Ancestral Health Symposium—including slides. (The original video can be found here.)

This is some of my finest work. It provides a theoretical and practical framework for understanding hunger—an understanding sadly obscured by oversimplification and moralizing, from both scientists and policymakers. This is doubly unfortunate because the science of hunger is well-established, uncomplicated, and consonant with real-world experience.

I’ll leave you with the “Learning Objectives” from the program:

Upon completion of the session, participants will be able to:

  • Enumerate and understand the mental and physical processes which interact to produce hunger.
  • Describe how evolutionarily discordant diet and behavior can cause inappropriate hunger signals.
  • Address some of their own hunger issues, and/or further investigate the subject in their own research.

Note: You may wish to bring up the bibliography in another browser window in order to follow along with the references.


Introduction

Hello. I’m J. Stanton, gnolls.org.

People aren’t obese because they enjoy being obese, and diets don’t fail because people dislike being slim and healthy! Diets fail because hunger overrides our other motivations.

There is an inflection point somewhere around 1980. What happened? The standard explanation is that fat people are just gluttonous and lazy, so:

Well…maybe not.

It’s also popular to blame junk food…

So much for that idea.

Lately it’s become popular to blame fast food…

But the data doesn’t support that either. (The blue line is food eaten away from home, the red line is fast food…and we can see that the increase in fast food actually slowed down in the mid-1970s, just before obesity began skyrocketing.)

Note from JS: I have been specifically accused of misrepresenting this data. This is a very serious charge—so let me demonstrate that my interpretation is correct. Let’s compare the time periods from 1962 (the first year for which we have obesity data) to 1979, and from 1980 to 2008 (the last year for which we have obesity data).

1962-1979

  • 0.51% per year increase in fast food, as % of total food dollars
  • 0.09% per year increase in adult obesity
  • 0.03% per year increase in extreme obesity
  • 0.08% per year increase in child obesity
        (Child data begins in 1966, and is adjusted for the shorter timespan.)

1980-2008

  • 0.23% per year increase in fast food as % of total food dollars—less than half the rate during 1962-1979
  • 0.67% per year increase in adult obesity—7.4x the rate during 1962-1979
  • 0.16% per year increase in extreme obesity—5.3x the rate during 1962-1979
  • 0.39% per year increase in child obesity—4.9x the rate during 1962-1979

My interpretation of the data stands.

Why We Can’t Just Blame “Palatability” or “Reward”

Now before I explain the science of hunger, there is a very simple and seductive model which is wrong—and if we fall into it, we’ve made a logical error from which we can never, ever recover. That error is: food has a property called “palatability”, or “reward”, which causes us to eat it. So if a food has too much palatability—it’s “hyperpalatable”—we overeat it and get fat.

First, as we’ve already discussed, this hypothesis doesn’t fit the data.

The second problem is that palatability is like pornography. We all know it when we see it—but we just can’t seem to give it a rigorous definition.

For instance, why do different people like different foods? Hundreds of millions of people around the world find these foods delicious. Why can I get twelve different sauces for my chicken wings? 31 flavors of ice cream? And that is because, just like pornography, palatability is subjective. It is a property we assign to food.

The second problem is: why do we ever stop eating? All Oreos taste exactly the same…yet at some point, we don’t want any more. The Oreo didn’t change: we did.

The third problem is that the foods we overeat often aren’t the foods that taste the best—the classic conundrum being “I like prime rib much more than I like Pringles…but I can’t stop eating the Pringles. Why not?” Low-carbers get this all the time: “Your food isn’t really rewarding…it just tastes like it.”

So: what happens now is that the naive model does a little shuffle step. It redefines palatability as “that which we can’t stop eating”. (Or, it substitutes the generic term “rewarding”.)

In other words, “We overeat that which we overeat…because it’s overeatable.”

Of course, if we’re writing a grant proposal, we’ll use the term “obesogenic”. And with that little shuffle step, we’ve just bypassed the entire science of hunger.

Now. I’m beating this dead horse for a very good reason, which is that like phlogiston, spontaneous generation, and the luminiferous ether, this very simple and very seductive error absolutely prevents us from understanding hunger. Once again:

Palatability and reward are subjective properties we assign to food based on our past experience, and our current nutritional and metabolic state.

What Is Hunger?

So: what is hunger?

It turns out there is a large body of established science. I could easily teach a semester-long class, I asked for forty minutes, and they gave me twenty—so I’ll do my best.

Hunger is not a singular motivation. It is the interaction of four different clinically measurable, provably distinct biochemical processes:

  • Satiety: Our body’s nutritional and metabolic state. It includes both our biochemical response to the absorption of nutrients, and our access to stored nutrients.
  • Satiation: An estimate of future satiety, based on the sensory and cognitive experience of eating.
  • Hedonic impact (“likes”): The pleasure we experience from an action. “Palatability” is the hedonic impact of food.
  • Incentive salience (“wants”): Our actual motivation to obtain something we “like”. It is largely, but not exclusively, a product of the other three motivations.

Two more factors interact with hunger to modulate our food intake:

  • Availability: How difficult it is to get something we want.
  • Willpower: The conscious overriding action of the forebrain, known as “executive function”.

Availability and Willpower

Let’s talk about availability for a moment. Even though we might want prime rib much more than leftovers, we eat the leftovers because they’re what’s available to us. If I want prime rib, that’s three hours and a trip to the store, or 40 dollars and a trip to the restaurant. In contrast, we don’t have to want processed snack foods much at all, because all we have to do is open the bag.

They’re not hyperpalatable — they’re hyperavailable.

The Reward System—Hedonic Impact (“Likes”) and Incentive Salience (“Wants”)

Time doesn’t permit me to explore the biochemistry and neuroscience of the reward system—so for the details, I’ll point you to the pioneering work of Dr. Kent Berridge, whose work I was proud to introduce to the community last July. [In this article series, starting with the very first installment. References are also linked in my bibliography. -JS] A couple quick notes:

It’s important to note that likes and wants are not limited to food. Any experience we “like” — that has hedonic impact—is capable of producing a “want” for more—incentive salience.

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—because it drops us right back into the cognitive trap of the naive model.

But if liking and wanting are subjective, what determines them? Yes, taste is one part of it, but the interesting question isn’t why we eat: it’s why we can’t stop eating.

And so we move on to satiation and satiety.

Satiation and Satiety

Two quick examples: You’ve just left the all-you-can-eat Brazilian steakhouse. What tastes good to you right now?

Almost nothing.

Now: you’ve just hiked seventeen miles over three mountain passes with a 40-pound pack, and that dehydrated lasagna is the best thing you’ve ever tasted.

Again, the food didn’t change—but somehow its hedonic impact, how much we like it — and, therefore, its incentive salience, how much we want it—did change.

Now. Satiation and satiety are synonyms in common usage: so why do we distinguish them? The answer lies in gastrointestinal transit time: it takes hours for the nutrients in food to be digested and absorbed, which means that the satiety response is not a useful signal to stop eating.

(I deleted this passage from the speech as given, because I was concerned about running out of time. However, I think the concepts are valuable, so I’ll reprint it here.)

Furthermore, we must distinguish two types of satiation: positive and negative. When we eat real food, we are rewarded twice: once by the pleasure of eating, and again by the pleasures of positive satiation and satiety.

In contrast, negative satiation is that sick feeling we get when we’ve eaten too many empty calories. It’s our body’s way of telling us “We can’t dispose of any more of that.” So we receive that quick hit of pleasure, or hedonic impact, from eating tasty but nutritionally empty non-food—but it’s over the moment that candy slides down our throat, and we never receive the hedonic impact of positive satiation and satiety that tells us “You’re done, you can stop eating now.”

And with each bite of empty calories, we not only receive less and less pleasure—we make it more and more difficult to achieve the pleasures of positive satiation and satiety.

Furthermore, because satiation is the sensory experience of eating, it can be fooled. It’s well known that:

  • People eat more in groups than when eating alone
  • People eat more when they’re able to eat more quickly
  • Hidden calorie preloads are never completely compensated for

However, the failure of dietary fiber to affect body weight or fat mass in controlled interventions (Papathanasopoulos 2010) suggests that faking satiation with indigestible bulk is not a useful long-term strategy for weight loss. You can fool satiation, but you can’t fool satiety.

Satiety

And satiety is the key to understanding hunger, because, as we’ve seen:

  • Satiation is just an estimate of future satiety based on the sensory and cognitive experience of eating.
  • Both our likes and our wants are very strongly modulated by satiation and satiety.

If we do an experiment where we sit teenagers down at the mall food court and let them have all the food they want for an hour, we find that the lean kids eat a huge amount of food—nearly as much as the obese kids. (Ebbeling 2004) In other words, both groups want the same amount of food. The difference is that the lean kids compensate for that over the rest of the day, but the obese kids do not. And this strongly suggests that obesity is primarily a failure of satiety.

So: we are clearly converging on a primarily nutritional model of hunger, because that’s the definition of satiety. Let’s explore some of the evidence.

We can begin by asking the obvious question: “What else could hunger possibly be for?” Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would have been strongly selected against.

Moving on to the science: taste receptors are not just located on our tongues—they’re located throughout our bodies. (Steinert 2011, Iwatsuki 2012) In our intestines, they modulate the release of satiety hormones like CCK, NPY, VIP, and GLP-1. In the pancreas, they modulate the release of insulin, among other systems…and these effects are so powerful that:

“…The postabsorptive effects of glucose are sufficient for the postingestive behavioral and dopaminergic reward-related responses that result from sugar consumption.” (Oliveira-Maia 2011)

[In other words, you can inject sugar into a rat and get the "food reward" response...even though the rat never tasted the sugar. Also see de Araujo 2008, Ren 2010, Oliveira-Maia 2012. -JS]

Yes, satiety is rewarding in itself…so by eating food that doesn’t produce satiety, you’re chasing a reward that never comes. Does this sound familiar?

Our taste buds both produce and respond to satiety hormones (Shin 2010)…which directly alter the perception of taste. So it might not be your imagination that food doesn’t taste as good when you’re sated.

There are opioid receptors in the walls of your portal vein (Duraffourd 2012)…and they’re not there because your liver wants to get high. They’re a protein sensor—they bond to freshly digested protein fragments.

So, now that I’ve convinced you a nutrient-driven model of satiety and hunger is both biologically and evolutionarily plausible, let’s review some of the experimental evidence.

  • The obese tend to be deficient in many different micronutrients: iron, calcium, zinc, vitamin A, vitamin C, vitamin D, vitamin E, vitamin K, B1, B2, B12, folate. (Leão 2012, García 2009, Xanthakos 2009, Kaidar-Person 2009)

But that’s associative data, so let’s talk about some interventions:

  • Protein leverage. Animals from rats to people tend to eat until they’ve ingested a sufficient amount of complete protein to meet their daily needs.
  • Women given multivitamins lose weight and fat mass: women given placebo do not. (Li 2010)
  • If calories are held constant, weight and fat remain the same, but the placebo group experiences greater hunger than the multivitamin group. (Major 2008)
  • Calcium and vitamin D supplementation alone can decrease body weight and fat mass, but ONLY if you are calcium-deficient. (Major 2009)

And here’s the blockbuster, courtesy of nutrition pioneers Dr. Donald Davis and Dr. Roger Williams:

Feed rats a plausible human diet. Not the “cafeteria diet”, not a “high-fat” diet, a real food diet. Meat, flour, eggs, vegetables, and fruit, all ground up together so it’s uniform. Split them in two groups, supplement one group with a very comprehensive list of vitamins, minerals, and other micronutrients, and let them feed freely.

Then, after several weeks, give both groups free access to granulated sugar for an entire day.

The non-supplemented rats—eating a plausible whole-foods diet of meat, flour, eggs, vegetables, and fruit—consumed 67% more sugar than the supplemented rats. (Davis 1976)

Wow.

And this is something we absolutely cannot explain via the palatability model. The sugar didn’t change…the diet didn’t change. The only difference is micronutrient content.

So: satiety modulates reward

…and junk food is self-reinforcing. The more empty calories you eat, the more you’ll crave empty calories.

Why It’s Critically Important To Understand Hunger

The problem with popularizing for mass consumption is that it’s easy to simplify a concept until it’s no longer true. In the process of oversimplification, concepts also become politicized—and the naive model, in which palatability is a property of food that causes obesity, is being used to resurrect the diet-heart hypothesis.

The story goes like this:

You have not become fat, sick, and diabetic because we’ve been telling you to eat the wrong foods for 35 years! These massive surpluses of corn, soy, and wheat we’ve created by an agricultural policy that subsidizes the destructive chemically-based monocropping of genetically modified birdseed by giant multinational corporations are completely a coincidence. And our dietary edicts, from the original Dietary Guidelines for Americans to the Food Pyramid to the Food Plate are not just excuses to turn you into passively compliant grain disposal units—which consequently require heroic doses of highly profitable, patented pharmaceuticals to keep you alive. No, no, no.

That is NOT the problem. Pay no attention to the 500 billion dollar income stream behind the curtain.

You are the problem, because YOU DID IT WRONG.

You didn’t eat those hard, dense, bitter whole grain breads we told you to. You’ve been putting salt and butter on your vegetables. You’ve been putting dressing on your salad. You’ve been eating food that tastes good, not the dry, tasteless, low-fat whole grains we told you to.

But that’s okay. It’s not really your fault. We know you’re weak and stupid and can’t be trusted to make your own decisions. The fault lies with those evil corporations who have been making food that tastes too darn good, and you just can’t resist it. So we’re going to save you.

We’re going to tax sugar! Because just like liquor taxes have stopped us from drinking, sugar taxes will stop us from drinking soda and eating candy.

That is the new narrative. And there are people here playing footsie with it.

And THAT is why we must understand the real science of hunger.

First, because we quite literally can’t afford not to. 35 more years of the obesity epidemic will bankrupt Medicare, our government, our health care system, and us.

But far more important is that the cost in human lives and human suffering will be incalculable. Millions will suffer terribly and die needlessly. Been to a cheap nursing home lately? It’s an ugly reality.

However! There is good news, which is that the real science of hunger is not complicated—and if I’ve done my job here, you now have enough of a handle on the concepts to figure out for yourself how the science of hunger applies to your own research, and your own issues around food. And I challenge each one of you—individually and collectively—to follow the path of science, not the path of politics.

So I’ll close with some takeaways.

Takeaways

  • Hunger does not exist to make us fat. It exists to keep us alive.
  • Hunger is the interaction of four biochemically and neurologically distinct motivations: likes, wants, satiation, and satiety.
  • Our resulting desire to consume is modulated by availability and willpower.
  • Cells and organs throughout our bodies are full of taste and nutrient receptors that sense their external and internal environment. In response, they issue hormonal and neural signals in order to maintain an environment which keeps them alive and functional. These homeostases define our current nutritional and metabolic state—our “satiety”.
  • “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. (Remember the rats.)
  • Our food consumption is primarily determined by its ability to produce satiation and satiety, not its hedonic impact.

Conclusions

  • Obesity is primarily a failure of satiety.
  • Your mother was right. The problem isn’t “hyperpalatability”: it’s empty calories.

I’m J. Stanton, gnolls.org. Thank you.

(My bibliography is available at this link.)


Let me be clear. This is the best theoretical and empirical framework we currently have for understanding hunger. Any concept or phenomenon we’re having difficulty with can be reduced to its effect on the four motivations (likes, wants, satiation, and satiety) and two modifying factors (availability and willpower)…and any hypotheses that conflate, bypass, or oversimplify them (e.g. treating “reward” as a property of food) will inevitably produce contradiction, confusion, and a lack of progress towards our goal of better health.

I invite my readers to analyze their own observations about hunger using this framework!

Live in freedom, live in beauty.

JS


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What Is Metabolic Flexibility, and Why Is It Important? J. Stanton’s AHS 2013 Presentation, Including Slides

As you might have heard, nearly all of the AHS 2013 videos are unwatchable due to technical and production failures. Therefore, I’m publishing my own presentation here in written form, exactly as it was given at the 2013 Ancestral Health Symposium in Atlanta—including slides.

This work is likely to be controversial, as it directly contradicts a great deal of received wisdom—both within mainstream obesity research and within the ancestral health community. The evidence places the energy requirements of the individual cell, and defects of energy production at the cellular level, at the beginning of the causal chain of both obesity and the metabolic syndrome.

However, as my bibliography shows, both metabolic flexibility and its origin in mitochondrial energy production are well-established, easily measurable phenomena—particularly within the field of exercise physiology—and the body of research continues to accumulate, finding defects of cellular energy production within the pathology of numerous diseases, from Alzheimer’s to Type II diabetes. It’s an exciting field—and it gives us both a theoretical framework in which to understand real-world phenomena, and many useful takeways for everyday life.

Yes, these pathologies are multifactorial. And, as I said in my 2012 AHS presentation on hunger, I don’t claim to have made a revolutionary new discovery. I’m bringing an existing field of research to light, and integrating it into our understanding.

So: here it is. Put on your thinking cap and enjoy.


Introduction

Hello. I’m J. Stanton, gnolls.org.

You may wish to open the bibliography in another browser tab or window so that you can follow the references.

Life requires energy.

The human body contains somewhere between 10 and 100 trillion individual cells. Each one of these trillions of cells must continually convert fuel into energy in order to keep itself alive—and, thereby, keep us alive. In fact, a substantial fraction of our body mass is dedicated to providing a constant supply of fuel to every one of our trillions of cells, and removing the waste products of their energy production. Our respiratory system; our digestive system; our circulatory and lymphatic systems; substantial parts of our endocrine and nervous systems; and, lest we forget, each of these systems is itself made up of cells with their own energy requirements.

In short, the reason that large animals, including humans, are so heinously complicated is because every one of our 50-plus trillion cells requires a massive, complex, interdependent infrastructure to ensure it receives both an uninterrupted supply of fuel and of the cofactors required to burn it—independent of wild variances in energy demand via activity level and external temperature, and wild variances in energy supply via meal timing and composition.

Therefore, when we’re asking high-level questions such as “What causes obesity and the metabolic syndrome? And why did that process accelerate so dramatically after 1979?” it behooves us to examine our internal infrastructure—our energy supply chain—for bottlenecks and disruptions.

(Please note: While I’m happy to throw around terms like homeostasis and oxidative phosphorylation, I will use layman’s terms when possible in order to make this talk more accessible.)

What Is Metabolic Flexibility?

Unlike an automobile engine, which usually requires one very specific type and composition of fuel, most of the cells in our body can burn several very different fuels. However, we produce the overwhelming majority of our energy from two of them: glucose, the sugar from which starch is also formed, and fat. Metabolic flexibility is the ability to switch back and forth between the two major energy substrates—glucose and fat—based on availability and need.

How Is Metabolic Flexibility Measured?

Without a steady supply of oxygen, our cells can only produce a small amount of energy; they can only produce it from glucose; and the waste products quickly build up within the cell and prevent further energy production. This is called anaerobic respiration: it’s why we can’t sprint or hold our breath for very long, and why lack of oxygen, via blood loss, heart failure, or stroke, kills us so quickly.

In contrast, our cells require oxygen to efficiently extract all the energy from glucose. Furthermore, they require oxygen to burn fat at all! So except for a few specialized tissues, like red blood cells, and a few temporary conditions, like heavy sprinting and holding our breath, almost all of our energy comes from burning fuel with oxygen—called aerobic respiration.

Now. It turns out that a molecule of glucose contains six oxygen atoms—whereas a fat molecule contains only one, and releases a far greater amount of energy to the cell when we burn it. So while fat contains more energy by weight, it takes more oxygen to extract that energy from fat than it does from carbohydrate.

Next: Oxygen enters our body as oxygen gas (O2), but once it’s been used to burn fuel, it leaves as CO2—carbon dioxide. So we can hook a person up to a respirator, and compare how much oxygen and carbon dioxide they inhale with how much they exhale. This process is called “indirect calorimetry”, and it produces two things. First, we get an approximation of how much energy a person is consuming. Second, it produces what is called the Respiratory Exchange Ratio, also called the Respiratory Quotient— an approximation of how much glucose vs. how much fat your body is burning for energy. The RER, or RQ, varies between 0.7, representing 100% fat oxidation, and 1.0, representing 100% glucose oxidation…so lower values mean we’re burning more fat, and higher values mean we’re burning more glucose.

It’s important to note that the RER, or RQ, is a somewhat blunt instrument: it doesn’t account for protein oxidation, gluconeogenesis, or anaerobic respiration, and rapid changes can throw it off. However, it’s a good approximation that is relatively easy and non-invasive to measure.

Why Is Metabolic Flexibility Important?

Both the availability of energy, and our usage of it, change dramatically over time. We can be sleeping or sprinting; cold or hot; eating or fasting; consuming meat, fish, vegetables, potatoes, popcorn, or a Big Gulp. Our ability to adapt to these conditions depends greatly on the ability of our individual cells to be metabolically flexible—particularly our muscle cells, which use the majority of energy from our bodies. For instance:

  • When we ingest carbohydrate, metabolic flexibility helps us control blood glucose, by burning glucose instead of fat. Our RER should be high.
  • When we ingest fat without carbohydrate, met flex helps us burn the fat instead of storing it. Our RER should be low.
  • When we fast (and everyone “fasts” while they sleep), met flex helps us burn the fat stored on our butt, instead of becoming hungry for sugar or going catabolic. Our RER should be low.
  • When we exercise, met flex lets us burn more stored fat and produce more energy at all levels of effort. We can run faster, jump higher, move more weight, and go longer on less food before we “hit the wall.”

What Happens When Metabolic Flexibility Is Impaired?

When met flex is impaired, our cells can’t easily switch fuel sources: the RER, or RQ, is stuck in the middle. This leaves us unable to respond well to changing conditions. For instance:

  • When we ingest carbohydrate, we cannot dispose of blood glucose as quickly as we should. This causes poor glycemic control—wide blood sugar swings.

  • Our ability to burn fat in response to high-fat meals is reduced.
  • Consequently, we have a decreased ability to increase energy output after meals (called “post-prandial thermogenesis”.)

  • When we fast, our ability to burn our own fat is diminished.
  • Since our ability to burn fat is diminished, we have a continual demand for glucose, even at rest. Therefore, fasting makes us hungry more quickly—and becomes catabolic more quickly.
  • Therefore, a metabolically inflexible person attempting to fast or restrict food intake is very likely to also reduce their metabolic rate.
  • When we exercise, our ability to burn our own fat is diminished, and our demand for glucose increases.

What Are The Real-World Consequences Of Impaired Metabolic Flexibility?

Now that we know what’s happening internally, let’s examine what that means. In particular, I ask those with experience losing weight, and in attempting to maintain a weight-reduced state, to listen closely and critically.

  • If we have poor glycemic control, that means we have higher and more rapid blood sugar spikes and crashes. We all know this is unhealthy—but it also makes us more dependent on stimulants and bready, sugary snacks to maintain our mood, our attention span, and our ability to stay awake after meals.
  • A continual demand for glucose at rest means we will become hungry much sooner after eating. Specifically, we become hungry for sugar and carbohydrate in order to “keep our energy up”
  • Then, if we manage to ignore these hunger signals through willpower, our body is likely to reduce our energy expenditure in response, making us feel tired and listless, and making weight loss even more laborious. (At extremes, this can manifest itself as poor cold tolerance, and other signs and symptoms of hypothyroidism.)
  • Consequently, intermittent fasting and heavy caloric restriction are likely to be both difficult and unsuccessful for the metabolically inflexible. And I suspect this to be a primary mechanism behind the so-called “low carb flu”.
  • Finally, a continual demand for glucose during exercise means we will be dependent on a steady supply of energy drinks, bars, gels, and other sugary treats in order to perform physical activities that usually don’t even burn the energy we’ve ingested.

Do these consequences sound familiar to anyone?

Why Is Metabolic Flexibility Impaired?

To answer this question, we must first ask “Is metabolic flexibility a byproduct of neural and endocrine signaling, or is it an intrinsic property of individual cells?”

It turns out that if we measure the metabolic flexibility of individuals, then remove a sample of their muscle tissue and measure its response to fat and glucose in vitro (i.e. outside its neural and endocrine environment), we find the following:

“The interindividual variability in metabolic phenotypes was preserved in human myotubes separated from their neuroendocrine environment, which supports the hypothesis that metabolic switching is an intrinsic property of skeletal muscle.” (Ukropcova 2005. Also see Corpeleijn 2010, Berggren 2008)

So: while elucidating the precise mechanisms involved is still what’s known as an “active research area,” we can be reasonably sure that we are not just looking at an artifact of a broken hypothalamus or a dysfunctional HPTA axis.

Metabolic inflexibility is a metabolic defect at the level of the individual cell, multiplied by the trillions of cells that make up our muscle tissue until the effects become directly and objectively measurable via the respiratory exchange ratio.

What is this defect? Actually, there are two.

Metabolic inflexibility towards glucose—a low “insulin-stimulated RER”, the inability to increase glucose oxidation—appears to be limited by the glucose disposal rate: cells can’t burn more glucose because they’re insulin resistant. They can’t absorb it quickly enough.

In contrast, metabolic inflexibility towards fat—the inability to increase fat oxidation in response to fasting or fat intake—appears to be caused by mitochondrial dysfunction. (Mitochondria are the tiny organelles within each of our cells that actually perform aerobic respiration, turning fuel and oxygen into energy via the citric acid cycle—also known as the Krebs cycle or the TCA cycle.)

And while I’ll save the citation bombardment for my bibliography, which is available online,
I’ll note that this is both a subject of extensive recent research and a robust experimental result. Sample quote:

“Upon a more thorough analysis of the different components of metabolic flexibility, we found that in vivo mitochondrial function was the single predictor of basal RER.” (van den Weijer 2013)

To summarize the current consensus:

  • Impaired glucose oxidation, an inappropriately low RER, is due to insulin resistance.
  • Impaired fat oxidation, an inappropriately high RER, is due to mitochondrial dysfunction.
  • Both are metabolic defects at the level of the individual cell.

How Does Metabolic Flexibility Become Impaired?

This is a fascinating subject and a continuing area of active research, and I would require another presentation to do it justice—so permit me to summarize the current state of the scientific literature.

First, an important note: obesity and metabolic inflexibility are not equivalent! Significant populations exist of both obese normoglycemics and skinny Type 2 diabetics. That being said, let’s explore some possible causal relationships.

  • Higher basal RER is associated with subsequent weight gain, independent of total energy expenditure. (Zurlo 1990)
  • Fasting, post-prandial, and exercise-stimulated fat oxidation are impaired in the prediabetic. (Corpeleijn 2010)
  • When overfed, healthy first-degree relatives of Type 2 diabetics gain substantially more weight than those without such a family history. (Jenkins 2013)
  • Quote: “…An impaired ability to increase fatty acid oxidation precedes the development of insulin resistance in genetically susceptible individuals.” (Heilbronn 2007)
  • Quote: “Metabolic inflexibility, lower adaptation to a HFD, and reduced muscle mitochondrial mass cluster together in subjects with a family history of diabetes, supporting the role of an intrinsic metabolic defect of skeletal muscle in the pathogenesis of insulin resistance.” (Ukropcova 2007)

In other words, fat oxidation seems to fail first—and though we don’t yet know how, insulin resistance appears to be among the consequences of it. And in support of the mitochondrial theory:

  • Quote: “…Mitochondrial content is lower across the continuum of insulin sensitivity and is not limited to T2DM.” (Chomentowski 2011)
  • Mitochondria from obese Type 2 diabetics oxidize fat at a lower rate, even after adjusting for mitochondrial mass.
  • Mitochondrial dysfunction is observed in relatives of Type 2 diabetics that are not yet themselves insulin-resistant.

In summary:

  • Impaired met flex begins with an inability to increase fat oxidation in response to fasting, diet, or exercise.
  • This propensity is strongly heritable, probably due to mitochondrial dysfunction.
  • Insulin resistance follows, which causes an inability to increase glucose oxidation in response to diet. We are now metabolically inflexible.
  • Impaired metabolic flexibility is not a byproduct of a broken brain, a damaged liver, or a faulty thyroid. It is a pair of metabolic defects at the level of the individual cell, multiplied by the trillions of cells that make up our muscle tissue until the effects become directly and objectively measurable via the respiratory exchange ratio.

How Can We Regain Our Metabolic Flexibility?

First, we must remember that we have multiple problems: metabolic inflexibility towards glucose, which manifests itself as poor glycemic control—and metabolic inflexibility towards fat, which manifests itself as poor response to fasting, calorie restriction, and low-carb diets.

The proven way to improve your insulin sensitivity—and, thereby, your met flex towards glucose—is to decrease your fat mass. However, weight loss alone does not improve fat oxidation! Basal RER remains just as elevated in the post-obese as it does in type 2 diabetics and the pre-obese.

So, we have successfully restated the problem as “To lose fat, first you must lose fat.”

And now it’s time to talk about exercise. We know that exercise temporarily helps dispose of blood glucose even in the insulin resistant, and that insulin sensitivity temporarily increases after exercise. However, what’s far more important is that exercise, unlike weight loss, is proven to restore fat oxidation—both basal RER and in response to a high-fat challenge meal.

“…A defect in the ability to oxidize lipid in skeletal muscle is evident with obesity, which is corrected with exercise training but persists after weight loss.” (Berggren 2008)

So. How much exercise do we need? We don’t know the minimum amount…but 3-5 45-minute sessions of moderately intense aerobic exercise per week, or 3 30-minute moderate aerobic sessions and one session of weight training, have been tested and proven sufficient to restore basal rates of fat oxidation to the level of healthy control subjects. And if you’re willing to do that 30-45 minutes every day, you can do so in about ten days.

Let me be clear. Exercise is not important because it burns calories! Exercise without calorie restriction is a remarkably ineffective weight loss intervention, because it usually makes us hungry enough to replace the calories we burn. Exercise is important because it restores your ability to oxidize fat—both when fasting and after meals. And we can tie this in with mitochondrial dysfunction by noting that exercise is proven to increase mitochondrial volume.

Caveat: your results may vary. Here’s the response of several healthy, lean individuals to a decrease in carbohydrate content of their diet: all over the place. So just because a study says the average obese person restored their metabolic flexibility after ten days of consistent exercise doesn’t mean you will.

Other interventions: We can decrease the carbohydrate content of our diet. For someone in energy balance, over time, basal RER will tend to converge towards the ratio of carbohydrate to fat in the diet. However, contrary to dogma which says “Don’t exercise until you’re fat-adapted,” it might be better to start exercising before playing with macronutrients—so that you have the metabolic flexibility to use them.

Finally, since the metabolically inflexible will tend to go catabolic more quickly, it’s probably a good idea to ensure you’re eating plenty of good-quality protein with each meal. And, while continual snacking is counterproductive, it’s probably not a good idea to try intermittent fasting right away. In fact, tolerance for fasting is a reasonably good diagnostic for impaired fat oxidation: if you feel light-headed after a few hours without food, you may be experiencing metabolic inflexibility regardless of your weight, bodyfat percentage, or BMI.

Conclusions and Summary

  • Metabolic flexibility is the ability of our bodies to switch back and forth between their two major energy substrates: glucose and fatty acids.
  • Met flex allows us to control blood sugar after eating, burn fat while fasting, and otherwise respond appropriately to changes in energy supply and demand.
  • Met flex is typically measured via changes in the Respiratory Exchange Ratio (RER), aka the Respiratory Quotient (RQ), which approximates the ratio of fat to carbohydrate our bodies are burning during the time period measured.
  • Metabolic inflexibility begins as a cellular-level impairment of the ability to increase or diminish fat oxidation.
  • Impaired fat oxidation contributes to insulin resistance, and a consequent inability to increase or diminish glucose oxidation.
  • Current evidence suggests that impaired fat oxidation is mitochondrial in origin, genetically and epigenetically heritable, and is among the causes, rather than the consequences, of obesity and insulin resistance.
  • Moderate exercise can restore your ability to oxidize fat. Fat loss can restore your ability to absorb and oxidize glucose.

Takeaways

  • You can’t exercise your way out of a bad diet.
  • You can’t diet your way out of not exercising.
  • Exercise is not important because it burns calories: it’s important because it restores metabolic flexibility.

So:

  • Eat plenty of complete protein.
  • Play frequently.
  • Push your limits occasionally.

And whether we brand it as “Paleo,” “Primal,” “Ancestral Health,” or, as I do, “Eat Like A Predator”—it’s good to know that our recommendations are on a sound footing—evolutionarily, empirically, and biochemically.

I’m J. Stanton, gnolls.org. Thank you.

(My bibliography is available at this link.)


I am confident that this avenue of research will continue to provide both explanations for real-world phenomena, and useful takeaways for everyday living. Much more fascinating data has come to light in the months since this presentation—and though we are in the early stages of integration, I currently believe pathologies as disparate as depression, Parkinson’s, and the metabolic syndrome will be linked via defects of energy production at the level of individual cells. Further, I believe that the resulting neural and hormonal imbalances will frequently be shown as effects, not causes: attempts by the brain (and other regulatory organs) to maintain a broken homeostasis.

Yes, these pathologies are multifactorial…and we’re still trying to figure out exactly how mitochondrial energy production becomes impaired. However, I wish to be clear about which direction the evidence is currently leading me.

Live in freedom, live in beauty.

JS


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