It’s Just Calories, Right?
What I’ll call the standard model of obesity is the notion that being overweight is the result of eating too much—and probably exercising too little—and that obesity is effectively the result of gluttony. The corollary to this is that you can eat whatever you want, so long as you eat “in moderation.”
While it’s true that in order to gain weight you must eat more calories than you expend, and that in order to lose weight you must expend more calories than you consume—this is known as physics—it turns out that this is not a particularly helpful observation when you consider living creatures like humans. Following that advice doesn’t work very well. In fact, for the majority of people who try it, it doesn’t work at all.
In terms of science, fat people are a very difficult group to study. As we saw in the comments to Barhka’s post, one quickly gets into multiple issues. Accusations of gluttony, sloth, lack of diligence (leading to lack of compliance with diet plans), and problems with the diet plans themselves make the whole topic a sea of confounding variables. It’s very difficult to boil things down to a reasonably likely sequence of cause and effect, and the calories-in-calories-out model boils down to blaming the obese for their affliction, which I don’t think is either correct or productive.
So we’re not going to discuss fat people. We’re going to discuss fit, athletic people.
Let’s discuss Joe Friel. Joe eliminates many of the annoying variables that people run into when studying fat people:
- He’s not a glutton: most of us would be happy to have his weight problem.
- He’s not slothful: he’s been a competitive athlete for decades at this point, and exercises regularly to an extent most people could only hope to emulate.
- He’s not lacking in diligence, as it takes a great deal of diligence to be a successful coach, author, and athlete over the course of decades. It doesn’t just happen, you have to work at it, and work hard.
- And he’s certainly not lacking in knowledge about healthy diets, in fact, he wrote the book on it, originally published 10 years ago, and he has been following that diet for 21 years. (No, Mike H., this is not a post about that diet.)
Yet, nevertheless, he had a weight problem. He would follow the calories-in-calories out model, and lose weight during racing season. But he’d be miserable, always hungry. And then when he stopped exercising in the offseason—because you cannot keep up that level of activity year-round—he would gain weight.
He had a problem. Not any more.
“…The primary change I made was greatly reducing sugar and cutting back on fruit. I used to eat 5 to 7 servings of fruit a day. That’s roughly 600 calories of carbs from fruit, about 20 to 25% of my calories for the day….”And as a result:
…The bottom line is that last fall I lost 8 pounds in 9 weeks by eating more fat and less carbohydrate. That was 5% of my body weight (160 pounds – at the time I was well on my way to my normal winter weight). I was never hungry. In fact, it seemed like the more fat I ate, the more weight I lost.
I learned that weight loss is not just calories in vs calories out. I used to lose weight that way. It works in the short term …If a guy whose business it is to be fit can’t make the standard model of obesity work, who can? And Friel’s got company. The L.A. Lakers, Lindsey Vonn, Bode Miller, and Jenson Button are examples of top athletes who’ve lost weight using this approach while maintaining their competitive edge. Another top triathlon coach explains:
“Are we fated to be overfat? It’s a worldwide epidemic and it even affects many of those who workout regularly, including athletes….”Sadly, it’s not quite this simple, although adopting a low-carb diet does work for a lot of people. In fact, in the research, it always beats every other approach it’s tested against.
(We’re talking obesity, remember. We can get to health in another post, although there are no negative health implications I’m aware of.)
It’s Not Just Fat Humans…
Humans are the fattest primates. We’re supposed to have some fat on us, more than a racer like Joe Friel or a bodybuilder would like for their sports. (And women are supposed to have more fat than men—sorry, ladies.) Even for Joe Friel, it’s unlikely he would have become obese eating what he was eating, as people have been eating fruit since before we were human without getting obese.
The confounder to the question we’re examining is that Americans didn’t suddenly start eating more carbohydrates and then got fat. We’ve eaten just as much carbohydrate in the past without getting fat. And there are plenty of healthy cultures around the world that eat as much or more than we do, without the obesity problem.
So with apologies to Gary Taubes and his books Good Calories, Bad Calories and Why We Get Fat, it seems that carbohydrates are a necessary but not sufficient idea to explain our obesity problem.
For that, we’re going to abandon athletes altogether and move on to rats. Obesity scientists love rats, mainly because they know exactly how to make rats obese. It’s as simple as ordering D12492 from Research Diets, and feeding it to rats. Voila!
“It tastes kind of like raw cookie dough, and the rats are crazy about it.”But again, we have a confounder.
Because it’s not just rats in obesity labs fed D12492 that are getting fat. All the rats in the labs are getting fat. And the wild rats that live in our cities. (Rural rats also, but less so.) In fact, all the animals that live with and around humans, and depend on human foods are getting fatter. One scientists sums it up:
“Perhaps this problem isn’t as simple as just energy intake and energy expenditure, which has been the prevailing message over the last 10 years.”Which is the conclusion they’re coming to in humans:
“A recent international study fails to support the common belief that the number of calories burned in physical activity is a key factor in rising rates of obesity…. Diet is a more likely explanation than physical activity expenditure for why Chicago women weigh more than Nigerian women, Luke said….”So much for that standard model of obesity.
So, to sum, if we’re looking for a dietary explanation for obesity, we’re looking for something that has the following attributes:
- It’s new, not found in the wild.
- It wasn’t a major part of the diet of the US in the 1920s.
- Consumption has been increasing over the years as obesity’s been increasing.
- It’s present in Research Diets’ D12492.
- And, ideally, we have a mechanism to explain how this novel food causes obesity.
Have We All Got The Munchies?
Given that this is a conservative, family-oriented site, I’ll assume none of you know what the munchies are, and let the scientists introduce it:
“It’s one of the most well-known effects of marijuana: the powerful surge in appetite many users feel after smoking or ingesting the drug, colloquially known as “the munchies.”…And, as that article explains, we now know exactly how this happens:
“[Marijuana] appears to give us the munchies by convincing our brains that we’re starving.”Chemically, by directly triggering appetite.
Now if the SoCons [Social Conservatives] would please resume their seats—no, it is not pot that is making us fat. Rats don’t smoke pot, for starters. But this system in our brains is named after marijuana, A.K.A. Cannabis.
(I’ve been trying to avoid geeking out, but bear with me for a moment.)
It turns out that the trigger in marijuana that activates the cannabinoid system, THC, mimics a chemical found in our brain, anandamide. Anandamide derives its name from the Hindu word ananda, which means “joy, bliss, delight“—perhaps you can see where this is going.
“Anandamide plays a role in the regulation of feeding behavior, and the neural generation of motivation and pleasure. In addition, anandamide injected directly into the forebrain reward-related brain structure nucleus accumbens enhances the pleasurable responses of rats to a rewarding sucrose taste, and enhances food intake as well.”And sure enough:
“Independent studies in rodents and humans have shown a direct association between plasma [blood] anandamide levels and obesity.”That’s “direct,” as in, if you inject a rat with THC or anandamide, they start eating [PDF], even if they’re full.
So all we need is some evidence that a food item that matches our 5-point list above increases anandamide levels, right?
To make it clear, the linoleic acid you eat is converted into anandamide in the body.
What Is Linoleic Acid?
LA, to its friends, is what’s known as an Omega-6 fat. It is primarily ingested in oils derived from seeds like soy, corn, or rapeseed (canola); but it bioaccumulates, like DDT, so you can ingest it via animals fed lots of seeds. That’s all industrially-raised pork, chicken, and turkey in the US.
Because this is far longer than I’d intended at this point, I’m going to wrap this up by going through my five-point test:
- It’s new, not found in the wild.High levels of LA only entered the diet after the discovery of a means to detoxify cottonseed oil, which was an industrial waste at the time. This hit the big time with the introduction of Crisco in 1911. The low levels of LA found in a natural diet do not appear to be harmful.
- It wasn’t a major part of the diet of the US in the 1920s.I’ll let Unilever, a major producer of foods based on seed oils explain:
“1920-1929: Unilever is formed. But during the decade the margarine market suffers declining demand as butter becomes more affordable.”
It really took off during the Depression, as it’s cheaper.
- Consumption has been increasing over the years as obesity’s been increasing.Check.
“We are eating a lot more vegetable oil than we were in 1970. It comes chiefly from the industrial, omega-6 rich oils such as soybean, corn and canola.”
- It’s present in Research Diets’ D12492.Indeed.
“It turns out that the diet obtains 32% of its fat from PUFA instead of the previously reported 17%. The ratio of omega-6 linoleic acid to omega-3 linolenic acid had been previously reported as 7.8 but is actually 14….”
The study I’ll link to again in point 5 seems to have been designed specifically to show that if you remove the LA from a diet like D12492, it no longer induces obesity.
- And, ideally, we have a mechanism to explain how this novel food causes obesity.
“Dietary Linoleic Acid Elevates … Anandamide and Induces Obesity“
So What Does This Mean For ME?
This is from an email I wrote in 2010 to the researcher who produced the chart above.
“ … Once of the first things I noticed after dropping [LA] from my diet was that I was no longer craving starch and sugar. I haven’t hit the candy bowl in 3+ weeks. Didn’t feel a need to .
“It makes me wonder if there might be a mechanism linking the two … ”I’ve been avoiding carbs and LA ever since.
To eat LA “in moderation” in America means diligently avoiding many common foods, like salad dressing, as the “moderate” amount of LA is 2/3rds to 1/8th what most of us eat. But I’ve been weight-stable ever since, regardless of exercise level, and after years of regularly putting on weight each year. And I never worry about calories.
The scientists like to say, “more study is required.” And this is true in order to prove this link. But carbohydrates and seed oils are the primary ingredients in junk food. You don’t need a PhD to figure that one out.
The biggest problem in the Modern American Diet is that much of what we eat, much of what we’re told to eat, is what our parents and grandparents understood to be junk food.
And we wonder why we’re fat.
[This post was originally published on Ricochet.com.]