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Hey everyone,

Rob here. Recently came across an article What If Obesity Is Nobody’s Fault?

I thought it was interesting and sent it over to Matt and Ari Whitten to get their take, and it ended up being pretty insightful, and right up the alley of 180D readers. Below is the lightly edited transcript of our exchanges.

Archangel-280x300ROB:

Hey Ari,

Came across this article- ‘ What If Obesity Is Nobody’s Fault?’

Basically, in some mice a gene can result in obesity despite seemingly identical calorie input and out, tracking intake, metabolic rate and excreted mouse poop.

Don’t know much more about the research, but thought you might be curious.

Matty- thought you might be too.

ARI:

It’s an interesting article, for sure. Thanks for sharing, Rob.

This article is jumping the gun on many things.

I would say that if they promote this conceptualization of obesity, they would just have to form some way of accounting for numerous bodies of research which are in direct conflict with it (for example, thousands of studies showing that the first law of thermodyamics does hold in human beings, the thousands of studies showing that food reward/palatability influence body fat gain, etc.) Ari

Not to mention, if we say that it’s genetic factors that influence obesity, the fact that obesity is a modern phenomenon that is increasing rapidly just in the last few generations would also have to be accounted for. (Naturally, if genetics are staying relatively constant in a population over a few generations, but obesity rates are skyrocketing, that sort of puts a big hole in theory that it’s a genetic issue).

It’s an interesting article, but I suspect that they will eventually find that this theory isn’t really that valid and doesn’t have much explanatory power.

Just my 2 cents. Thanks for sharing! Interesting stuff :)

 

MATT:

Yeah, that’s a common line of thinking in obesity research. They know that simply eating less or exercising more than one naturally desires in order to lose weight or prevent obesity isn’t an acceptable modern solution to the problem. Attempts to intervene with calorie manipulation have no long-term effectiveness for the vast majority who attempt it. So there’s really no choice but to look at the metabolic/hormonal, and hereditary differences between those that effortlessly maintain weight homeostasis and those that do not. And try to make progress there in finding solutions.

The tricky part is that most obese people are in energy homeostasis 95% of the time, no different from lean people. They just have a tendency to gain weight under stress, over the holidays, etc. The rest of the time they often are indistinguishably different, metabolically and otherwise, from the effortlessly lean. And when there are differences, it’s often impossible to discern the chicken from the egg so-to-speak.

 

ROB:

Well what’s interesting to me is that the homeostasis/metabolism argument usually, in its nuanced iteration, recognizes that bigger bodies tend to require more energy to stay in energy balance than smaller bodies.  So yes, a 200lb person and 100lb person may both be weight stable eating ad libitum, but the 200lb person is probably weight stable eating more calories.

Sometimes, in the case of metabolic adaptation, that’s not the case, and the 100lb person is weight stable eating the same number of calories as the 200lb person.  But in those cases, I always presumed they were pooping more out, or their body temps were higher and thus they were using more energy, or they were fidgety throughout the day, or their muscles were less thrifty and the same amount of movement resulted in greater calorie use.

What this is suggesting is that even if you control those variables, some animals get fat on the same number of calories.  So where do the calories that comprise the fat stores come from if it’s getting burned at the same rate and pooped out at the same rate? Assuming they’re actually controlling for all the variables and not missing something obvious, is there another element here that explains the apparent contradiction of thermodynamics? Because even the metabolism-aware of us, as far as I know, don’t discount that calories matter.

As Ari mentioned, there are thousands of studies showing that thermodynamics apply, and also that genetics can’t fully account for the rapid rise in recent times of obesity.

But it is interesting to me, and it does make me wonder whether it’s 1) tightly controlled, 2) reproducible and 3) going to lead to some more dramatic insight into thermodynamics.

 

MATT:

MattRight. Bigger people require more calories, which is often met with the foolish comment that “fat people have a higher metabolic rate than lean people.” On any meaningful basis (energy consumption per unit of lean tissue), they do not. It’s typically lower, although, like I said, lean and fat people alike are usually weight stable at any given time.

My guess is that the difference in metabolic rate and TEE was simply too slight to be noted in the research, or the differences happened intermittently. Like I’ve noted before, a 50-year old with 50 pounds of body fat has only accumulated 9.58 calories more than they’ve burned per day on average over that span. In a mouse that’s probably the equivalent of .1 calories per day, which is probably completely unmeasurable.

I found it interesting in MRC Greenwood’s research that mice fed ad libitum (lean strain vs. obese-prone strain) began gaining fat before their calorie intake increased vs. the lean controls. In other words, both strains of mice ate the same amount at first. Then one strain started gaining fat FOLLOWED by an increase in food intake when eating to appetite. Basically as if calories were lost to fat tissue and had to be made up with increased dietary consumption to deliver the same number of calories to the lean tissue as the lean mice were receiving.

ROB:

Yeah, that makes sense: some fat-favoring fuel partitioning initially, followed by the need to fuel that new mass with added energy while still maintaining the lean mass.

Good points too about the intermittent and/or nigh impossible to measure scale of the extra calorie accumulation.

ARI:

I agree with pretty much all of what Matt said.

In general, I think that likely the major issue with the article is that the author was engaging in black-and-white thinking (probably on purpose) in order to generate a sensational headline that was basically meant to suggest “Obesity is no one’s fault… it may very well be all genetic factors outside of your control… the food industry may have no role…your personal choices of lifestyle habits and dietary habits may have no role…! It’s not any differences in calories in or calories out. It may just be 100% pure genetics and other factors outside of our control that make some people become fat while doing all the same things as everyone else who is lean.”

Yet, even the scientists involved in this experiment said:“The first law of thermodynamics requires that energy be balanced, and I am not willing to throw that out the window.”

Also, the thinking behind the article is a little misguided. For example, they said “How exactly obesity occurs without excess calorie intake or decreased output remains unclear.”

We have an enormous body of evidence linking obesity with increased calorie intake. (In contradiction to some people, like Taubes, who have suggested that obese people don’t eat more calories than lean people. We know that this is wrong. It is use of old flawed data based on self-reporting of calorie intakes. It has since been found that obese people systematically under-report their calorie intakes by 30-50% and that under metabolic ward conditions, they do indeed eat way more calories than lean people).
We have an enormous body of evidence showing that obesity is linked with lower energy expenditure. “Evidence suggests that low NEAT may occur in obesity but in a very specific fashion. Obese individuals appear to exhibit an innate tendency to be seated for 2.5 hours per day more than sedentary lean counterparts.” http://atvb.ahajournals.org/content/26/4/729.full
Etc.–there’s plenty more…

So it’s fundamentally incorrect thinking to assume “lean and obese people are all doing the same things–there’s no differences in calories in, calories out–so maybe it’s just genetics.”

That’s just bad thinking.

Now, acknowledging that there is extensive evidence documenting that there are differences in calories in, calories out between lean and obese people, there are still a couple more important things to consider:

We still have to acknowledge that it’s not black-and-white–that obviously some people DO have stronger or weaker genetic susceptibility to obesity than others. Given the same environment and very similar behaviors (food intake, energy expenditure etc), people with a certain genotype may very well become obese while some stay lean. (And in animals, playing with a single gene can create obese rats). So there is clearly a genetic component intertwined with behavioral differences.

Even acknowledging that there is a huge body of evidence differences in calories in, calories out between lean and obese people, we could still enter into a chicken-and-egg argument over what came first–is it the person’s innate propensity for obesity driving those behaviors like increased calorie intake or decreased NEAT, or those behaviors driving the obesity?

It’s a legitimate question. Obviously I favor the latter camp.
Mostly because I have yet to see anyone in the former camp (those saying it’s a person’s innate susceptibility to obesity driving everything) account for the simple fact that the obesity epidemic is a fundamentally new thing–that obesity rates have skyrocketed in just the last 2-4 generations, despite basically no significant change in population genetics.
Or that the obesity epidemic has occurred in conjunction with massive changes in the reward/variety/palatability of the food supply, when we know from an enormous body of evidence (roughly 3,000 studies) showing that increasing food reward/palatability of the diet can reliably make lean animals fat, and that decreasing it makes fat animals lean–while allowing them to eat however much they want.

Due to those two things above, I favor a focus on the changes in diet and lifestyle factors being at cause

In general, I agree with Guyenet’s conclusions:

“Conclusion

Here are the main points to walk away with:
1.  In a healthy environment, genes alone do not usually cause obesity and lifestyle-related diseases, and population variability in these characteristics is low (i.e., most people are lean and free of these diseases).
2.  In an unhealthy environment, genetically susceptible people become obese and/or develop disease, while others remain lean and healthy because they are not genetically susceptible.
3. This results in an increase in population variability (e.g., more variability in body fatness between individuals).
4.  Diet and lifestyle environment have a major impact on obesity risk.  For a genetically susceptible person, maintaining a leaner state is usually possible but it requires stepping out of the typical fattening environment.  Genes are not destiny.”

http://wholehealthsource.blogspot.com/2013/07/the-genetics-of-obesity-part-iii.html

 

ROB:

Thanks Ari,

Appreciate the thorough reply.  The crux of it for me is what Matt was getting at: there probably are some obvious methodological issues at play explaining the apparent contradiction of thermodynamics.

Everything else aligns with the obesity model you, Stephen, Matt  and others have written about.

 

MATT:

My last tidbit is a quick word on “genetics,” which has always been a strong pet peeve of mine. I look at genetics and heredity as completely separate concepts.

You can inherit a slow metabolism from your mother eating lots of polyunsaturated fat. You can inherit a propensity to store fat if your mother dieted before or during pregnancy. Epigenetics shows that we can actually inherit things from actions and occurrences in our grandparents generation and maybe beyond. We can inherit hyperinflammatory responses to the environment from the high AA content of our parents’ diet. We can inherit excesses of stored heavy metals and estrogenic chemicals that affect metabolism, hormones, and fuel partitioning. This has all changed in the last few generations tremendously, it is just as hereditary as actual genetic changes and may actually be less mutable than genetic tendencies, but it is no way genetic.

There are a lot of interesting rabbit holes down the mitochondrial DNA path as well that don’t fit the commonly understood genetics beliefs.

And ultimately I think the differences between Ari’s beliefs and mine can be summarized by the following statement:

Eating clean prevents obesity and makes you lean. However, more than 90% of people that attempt to eat Clean-eating_thumbclean (or make any kind of significant dietary change on a long-term basis) fail and end up fatter than they would have been if they just kept eating a normal diet. For that reason, I still can’t condone dietary restriction. I feel like when I do I’m helping 10% of people get leaner and 90% of people embark on an unsustainable journey destined to failure. I still feel strongly that attempts to do unsustainable things with diet and exercise are the leading cause of going from overweight to obese.

 

ARI:

Matt,

I actually would not say that’s our fundamental difference. Because I agree with what you said 100%.

So I actually think the major difference is not that we disagree that restrictive/unsustainable diets are counterproductive, it’s that we seem to be defining what types of things are sustainable vs. unsustainable differently.

You said “more than 90% of people that attempt to eat clean (or make any kind of significant dietary change on a long-term basis) fail and end up fatter than they would have been if they just kept eating a normal diet.”

If it’s cool with you, can we be more specific about how we talk about this?

Is basically everyone who makes *ANY* type of change in diet destined for failure? Or is it specific types of changes in diet?

For example, is asking someone to add in an orange or banana to each meal–while continuing to eat all their meals as they normally do other than that–sustainable? Does it require such suffering that people just can’t keep it up?

Should that be lumped into “attempt at eating clean” in the same way that someone adopts a 100% raw vegan diet, or a zero-carb, 75% fat ketogenic diet?

I certainly don’t think so.

(Since I am not a fan of just addressing diet alone, perhaps it would be okay to also inject things like NEAT, exercise, or circadian rhythm habits into this?)

Is asking someone to buy an under desk cycle and set a timer to go off once an hour where they use their cycle for 30 seconds unsustainable? Perhaps for some it might be, but I think most people find this a perfectly sustainable and easy habit.

Is asking someone who to do a 30-second set of bodyweight squats once per day unsustainable? Perhaps for some, but I think most people are able to sustain it perfectly well.

Is asking someone to start a meditation routine where they meditate for 5 minutes each morning inherently unsustainable?

Certainly a significant portion of people will fall out of the habit within a couple months, but I think it’s a perfectly reasonable habit to ask someone to cultivate that requires very little effort.

Is installing f.lux on one’s computer so restrictive and does it require such monumental effort that it’s unsustainable? Does the act of wearing blue blocking sunglasses to watch TV at night induce so much suffering that we just cant expect someone to actually do it?

I think (I hope) we can agree that these are incredibly simple things that basically require zero effort and are perfectly sustainable for well over 99% of people. F.lux doesn’t even require anyone to do anything–the computer does it automatically.

Now, on the opposite pole, I would put the HCG diet–a 500 calorie a day diet, that also asks people to exercise each day. Maybe slightly above that would be a zero carb, calorie-restricted ketogenic diet while running 5 miles each day.

Both of these will have absolutely terrible chances of a person being able to sustain it and are pretty much destined for failure.

The point is that I think there is clearly a spectrum here:

–  On one end is totally extreme diet/lifestyle habits which may provide short-term results, but end up being unsustainable and counterproductive.
–  On the other end, continuing to do whatever one already does–eat the Standard American Diet, be sedentary, etc.

But I think there is a pretty massive territory in between these–of habits which are unquestionably beneficial for health and body composition–and which many people find perfectly easy and sustainable, and others may find terribly difficult.

I think people need to start with wherever they’re at and do baby steps towards more health-promoting gray-areahabits–just very small tweaks to their routine that require (subjectively) very little effort. Cultivate the habit for 30-90 days (or however long it takes to develop automaticity) and then take another baby step.

But I certainly agree that trying to jump into any diet or lifestyle routine that requires tons of willpower and suffering, while initiating compensatory biological adaptations (decreased RMR, decreased NEAT, loss of muscle mass, hunger pangs, fatigue, etc) is a bad idea.

So I guess my question is: Can we be more specific about what changes exactly are unsustainable and counterproductive? Is asking anyone to do anything differently from whatever they already do inherently unsustainable, and are all types of changes in diet or lifestyle habits equally as unsustainable as every other kind of change? (I.e. it doesn’t matter whether someone adopts the HCG diet, or just uses a little less cream and sugar in their two cups of coffee…it doesn’t matter whether someone adopts a ketogenic diet or just adds an orange and a handful of blueberries into their diet–both are attempts at “eating clean” and therefore destined to fail and be counterproductive.)

MATT:

What I like about what you just wrote is that those are all examples of things that can be done that WON’T cause compensatory weight regain and feelings of defeat and desperation if you stop doing them once you’ve started. It’s exactly why huge efforts should be made to redirect people’s attention away from their diets and onto other things that can be just as effective as a dietary change with a much smaller risk of actually getting fatter from trying hard to do it right.

The type of changes you talked about making specifically also fall right in line with Stephen Guise’s concept of “mini habits,” which I imagine to be much more effective than the big, sweeping changes people often try to make to their habits–especially this time of year. A mini habit might be, for example, to read one page every day. The idea is that sitting down to read a page every single day often leads to reading a lot more than one page, and, over time, leads to reading a lot more even though the one page target is ridiculously small.

Too bad you weren’t a contributing author to Derek Doepker’s new book Ari. Many of the things you just said would have been a perfect fit.

ARI:

“It’s exactly why huge efforts should be made to redirect people’s attention away from their diets and onto other things that can be just as effective as a dietary change with a much smaller risk of actually getting fatter from trying hard to do it right.”

MOST DEFINITELY!

And yeah, I am a huge proponent of mini-habits, and I actually wrote a section about this in my upcoming  book addressing this sustainability component.