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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:
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:
Link to cover story (requires TIME online subscription)
Yes, the cover reads:
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.
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
“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.
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.
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:
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).
- 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.)
- 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?
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.
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)
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.
- 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.
- 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!
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