There’s a recently published paper that’s going around the tubes that you may have heard about. It’s controversial (more about that later), but it suggests that obesity may be the body’s attempt to protect itself from the excesses in our diet.
Diabetes researchers Roger Unger and Philipp Scherer (both from the University of Texas Southwestern Medical Center) looked at recent studies involving fat in both mice and humans and concluded:
that obesity protects the body from the effects of overeating by providing somewhere safe to deposit the dietary deluge of fat and sugar, which in excess is toxic to many body tissues.
In addition, the news report points out that by:
shifting the blame from fat to food, Unger and Scherer’s hypothesis also helps to explain why not all overweight people develop metabolic syndrome and some lean people do.
Now, the jury is still out on whether you can be overweight but healthy (see this for example, but also see a caveat), but there’s something that’s great about a hypothesis that puts at least some blame on the diet and not just on obesity.
About that controversy
You’d think that a paper purporting to show obesity as protective rather than a cause per se would be controversy enough. But no. Check out the abstract from the actual paper:
Once considered divine retribution for sins, comorbidities of obesity (metabolic syndrome) are today attributed to obesity-induced metabolic defects. Here, we propose that obesity and hyperleptinemia protect lipid-intolerant nonadipose organs against lipotoxic lipid spillover during sustained caloric surplus. Metabolic syndrome is ascribed to lipotoxicity caused by age-related resistance to antilipotoxic protection by leptin.
“The wrath of God came upon them, and slew the fattest of them…” 78th Psalm, Verse 31.
What?! Divine retribution for sins?! Biblical verses in an abstract?! Pardon my french, but WTF??
I’m not the only one wondering what the eff’s up. Over at Hyperlipid, Peter had a lot to say about this report, like:
I got as far as this diagram before having to stop. Head banging is fine for rock concerts, not so good on a hard desk.
That’s some peer review! Divine retribution, biblical verses, and the appearance of two of the seven deadly sins. The authors are even making up words: gluttonicidal. Yowsa.
Peter goes on at length (please read) and explains that he wrote his post because “we have, on page 3 under ‘Protective role of obesity,’ this AMAZING quote:”
Thus, we propose that adipogenesis delays, rather than causes, the metabolic syndrome induced by chronic caloric surplus.
So essentially, it sounds like the authors may be a bit like the blind squirrel who finds a nut. But the controversy isn’t why I wanted to write my post. It’s the diagrams Peter drew to “correct” Unger and Scherer’s. They struck me as the clearest representation I have ever seen to explain a reasonable multi-factorial approach to obesity.
Diet, the liver, and hyperinsulinemia
Last month, I wrote a post talking about the link between metabolic syndrome and the liver. Peter’s diagrams show this explicitly. (Note: his original diagrams, here and here, were specific to the Unger and Scherer hypothesis. I’ve tweaked them to be more general and less offensive — no more reference to any deadly sins!)
In this theory, the original “fault” is not overeating nor lack of activity; it’s harmful elements of the standard American (or Western) diet, including refined sugars (including alcohol and fructose), vegetable oils with their high omega 6 levels, and refined grains with their anti-nutrients.
So in part one (slide at right; click for larger version), the relatively recent excess of these elements in our diet (and I suspect especially the perfect storm of all three) can be harmful to our livers which either metabolize some of the components (e.g., fructose) or are affected by the resulting inflammation.
The impaired liver is less able to deal with the high amount of blood glucose from all the added sugar and refined starch. This leads to hyperinsulinemia.
Cause vs symptoms
It is this combination of high blood glucose, impaired liver, and excess insulin that leads to obesity and what are essentially symptoms: storage of fat rather than utilizing it, increased appetite due to preference for carbs for fuel, and sedentary behavior due to lack of energy for physical activity (see Tom Naughton for his take on why the overweight are better at storing fat than burning it).
And of course, once this is set in motion, there’s a bit of a feedback loop effect as well. Excess fat is not inert; it adds its own hormonal baggage to the equation that can sometimes act in opposition to attempts at reduction.
Excess appetite more often than not leads to eating the very foods that created the problem in the first place and thus make it worse. And lack of energy means that people tend to avoid the kind of exercise that could help restore insulin sensitivity.
What’s to like?
I may have missed it, but it seems to me that this concept of diet -> liver injury -> obesity & metabolic syndrome is not being widely discussed in the mainstream. It seems like most are too preoccupied with questions of macro-nutrient ratio and personal responsibility. I certainly hope that will change, because from my vantage point, there’s a lot to like about this hypothesis.
First, it fills in some of the gaps from theories like Taubes’ or Lustig’s that focus on one specific factor. If you’re like me and wonder why some (like Asians) do well on a traditional high-carb diet when Taubes makes such a good case against carbs, then a possible explanation is that their diets (at least until recently) included far less of the excess sugar and industrial oils found in our diet (they also don’t eat as much wheat).
Second, it is FAR more satisfying an explanation than “calories in vs calories out” and a whacked-out interpretation of the laws of thermodynamics.
Finally, it seems to me that this hypothesis might explain why diets that are very different seem to have good results when studied. For example, an Atkins or Eades low-carb diet versus an Ornish low-fat diet. Neither removes all three of the big three from above explicitly, but in practice, they certainly remove one or more: Atkins’ low-carb diet removes sugar and grains; Ornish’s low-fat diet removes most fat and also a lot of refined sugar and starch.
In other words, this hypothesis suggests that most people are likely to be successful on any diet that removes sugar, veggie oils, and refined grains. And they are also likely to put the weight back on when they add those foods back into their diets. Sounds like the story of my life!
If you don’t have metabolic syndrome and aren’t obese, you’re in luck. You’re either genetically more adapted to our modern diet or you just haven’t pushed it too far … yet. You can either wait a few more years for science to figure all this out or you could probably stay in good shape just by eating less industrial food.
For the rest of us, waiting is not really an option. I’m not a doctor, nor do I play one on TV (dating myself), but I’m inclined to go along with Kurt Harris and Stephen Guyenet. A good start is to remove the things that caused the problem to begin with. That’s my approach for now!
Update, 2/6/11: See Obesity: cause or symptom? Part 2