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!

Now what?

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!

Check out the whole post; it’s interesting. But one specific item stuck out for me. Dr. McGruff has put out a DVD, and in his post, Dr. Harris shared that at:

one point in the lecture, [Doug McGruff] hints that he does not believe in doing a lot of testing. He says, “if the number is bad, eat healthy, and if the number is good, eat healthy”. What do you need the number for?

Dr. Harris then added this sidebar:

This is profound, actually and I have been meaning to blog on this for a while. I think he is using a heuristic that could, when coupled with having the consumers of health care actually be the ones paying for it, slash our health care costs nationally by more than half, even if everyone kept eating the SAD.

For me, this is less about the policy issue (although the implications are pretty staggering), but it strikes a chord on the wellness/healing front.

No matter the number, eat healthy? Works for me.

I found Dr. Heber’s original study, but also found a plain language version via CBS News. According to the article, Dr. Heber says that:

counting servings may not be adequate if you are missing out on one or more major color categories. Not all members of the fruit and vegetable group are alike.

They have unique properties that provide combinations of substances with unique effects on human biology. Therefore, simply eating five servings a day of fruits and vegetables will not guarantee that you are eating enough of the different substances needed to stimulate the metabolic pathways of genes in the different organs where fruits and vegetables have their beneficial effects.

So, the idea behind Dr. Heber’s What Color is Your Diet? is to make sure you eat from each group every day. Like Dr. Parker, I suspect this may be a challenge for many, and others (like the zero-carbers) may not agree with this approach philosophically.

Note too that fruits & veggies aren’t the only source of these nutrients. For example, eggs are a great source of lutein. Also, keep in mind that you may benefit from (or require) fat in the diet to increase your ability to use some of these (like lycopene). Finally, there are other issues that can affect whether or not we can use these nutrients; e.g., some people require preformed vitamin A because they can’t make it from carotenes.

Me, I think it makes sense to eat veggies year-round and fruits in season. I like the idea of the color groups, so I whipped up a graphic to keep on hand for reference. Click on the image or this link for a larger version. Hope you like it!

The PCRM article goes on to say (emphasis mine):

The Farm Bill, a massive piece of federal legislation making its way through Congress, governs what children are fed in schools and what food assistance programs can distribute to recipients. The bill provides billions of dollars in subsidies, much of which goes to huge agribusinesses producing feed crops, such as corn and soy, which are then fed to animals. By funding these crops, the government supports the production of meat and dairy products—the same products that contribute to our growing rates of obesity and chronic disease. Fruit and vegetable farmers, on the other hand, receive less than 1 percent of government subsidies.

Ah, King Corn. Our friends across the pond have gone so far as to call it liquid Satan, and suggest that:

America is doomed to lead the world’s obesity rankings as long as the process by which it elects its presidents starts in Iowa — a state known for its cornfields and corn subsidies.

I love me a good infographic, but while the one above has a clever theme, it’s misleading. It’s not the meat and dairy subsidies per se that are the problem. Even if you are okay with grains being part of your diet (and not everyone agrees), they are wreaking havoc as food for feedlot animals. And that is causing lots of problems for us.

In the study, researchers started with a group of 132 obese people who weighed an average of 289 pounds before starting either a low-fat diet, a calorie-restricted diet with less than 30% of daily calories from fat, or a low-carb diet with fewer than 30 grams of fat [this probably was 30g carbs, not fat] per day for 12 months.

At 6 months, the low-carb dieters had lost more weight, but by 12 months, there was no difference between the two.

But here’s the kicker:

Three years after the study began and two years after the diets ended, researchers followed up with 40 people in the low-carb diet group and 48 in the low-fat diet group.

They found people in the low-carb diet group weighed an average of 4.9 pounds less than before they started dieting while those in the low-fat diet group weighed an average of 9.5 pounds less than they did at the start of the study.

While this sounds like a big win for the low-fat diet (or at least the way the media and low-fat fans are pushing this), look at the numbers. These folks averaged nearly 300 pounds. Yet three years after the study began, neither group had lost or maintained even 5% of their weight.

I guess the researchers must have just loved the statistical difference between 4.9 lbs and 9.5 lbs, but unless you’re a size 2 trying to get into a size 0, this study isn’t a ringing endorsement for either diet — or diets in general!

Me, I think obesity may be the cause of things like arthritis from the excess weight on joints, but if you’ve read the sidebar here, you know that I actually think that obesity is also a symptom, and what causes it is what causes diabetes and heart disease (among others): the Western diet. And our diet’s influence on inflammation probably contributes to things like arthritis as well!

But I’ve also been noodling something in my head for a while now. What to make of people whose excess weight winds up being hundreds of pounds or more?

And why aren’t many of these morbidly obese folks diabetic?

This is over-simplistic, but if diabetes is essentially excess blood glucose, then a real difference between the overweight type 2 diabetic and the morbidly obese person is that the former’s fat cells are apparently incapable of taking up excess glucose, whereas the morbidly obese person’s fat cells are able to take and take. Curiously, both are likely insulin resistant and have other metabolic syndrome markers.

Why does this matter? Because a very important question is the role of sugar intake regarding high blood sugar and heart disease. Of course, there are other potential culprits, like fructose, excessive omega 6s, etc. But it seems pretty clear that caring about blood sugar levels is important, whether or not you’re diabetic.

Usefulness of checking blood glucose levels

One of my regular go-to blogs is Dr. Davis’ Heart Scan Blog, and this is a regular topic for him. He recently convinced me of the usefulness of testing my blood sugar after a meal even though I’m not diabetic:

Blood sugar after eating (“postprandial”) is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

My fasting blood sugar level? Around 90. My blood sugar one hour after chicken salad with an olive oil vinaigrette? About 90. My blood sugar one hour after a Big Mac, fries, and Diet Coke? About 150. Yikes!! Yeah, that diet soda is a big win, eh?

[You'd have thought that seeing that would have gotten me off the processed carbs right away, but alas, it actually took me nearly a month (those carb cravings really do a number on me).]

I’m actually pretty psyched about continuing to test *my* response to carbs in my diet (mostly non-sugar, non-wheat carbs). Part of this is probably my inner sugar addict, but part of it is reading folks like Stephan Guyenet and considering that many populations have done fine on some starches, so going ultra low-carb may not be necessary (or at least as a permanent solution).

Obesity as a defense against high blood glucose

Anyways, all this is a preamble to a interesting comment from Stan I read over on Dr. Davis’ blog on blood sugar, diabetes, and morbid obesity.

Dr. Davis had written:

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.

Stan’s response (emphasis mine):

It is interesting that you confirm that thin slender people which you identify as “Lp(a)” types are so much less tolerant against high refined carbohydrates!

In my subjective observation some of the most robust people on the standard (high carb medium fat) diet are of heavy set build ( Kapha/Phlegmatic).

They are able to easily increase their adipose tissue which probably is their main defense against high blood glucose.

This protection comes at the price of putting up weight, sometimes a lot of weight. In some rare cases their body weight can grow above 500lb before this protection mechanism stops, their adipose tissue stops expanding, and then – and only then – they get diabetes! Not before, not while their fatty tissue is still growing!

In my personal opinion the only difference between the heavy set type people and us (“ascetic” body types) is that our adipose tissue is for some reason (genetic?) incapable of growing beyond a minimum (in my case I was only able to put up ~10lb extra at most) therefore our fatty tissue is not able to scoop up as much excessive glucose out of our bloodstream as their therefore we get diabetes, on a very high refined carb diet, earlier and more severe than them.

Perhaps it’s just me, but I’m surprised that so few seem to consider this possibility. Maybe it’s “well, duh, of course,” like of course this happens. But I’m not so sure.

Implications for the obese

It’d seem to me that if people really made more of this connection, then a focus on maintaining reasonable blood sugar levels would be a critical tactic for weight loss and prevention of disease. And if that were so, then industrial food products full of sugar would be even more problematic — especially if they are diet foods!

If the overweight non-diabetic paid attention to their blood sugar levels, then perhaps weight loss shakes full of sugar (have you looked at the labels for Optifast?), weight loss cookies (blech), rice cakes, 100-calorie snack packs of Oreos and so on wouldn’t be part of anyone’s weight loss plan — even one that was based on the concept of glycemic index/load.

Of course, this isn’t really a big surprise. There is still an argument as far as the right diet for diabetics who absolutely need to maintain good blood sugar control!

For the non-diabetics, one way of looking at it is perhaps the morbidly obese have a genetic advantage. If we were living 10,000 years ago in times of scarcity, maybe this response to high blood sugar would be a good thing. But now, these genes in this environment seem to be just bad news. As Dr. Sharma says: “the obesity epidemic is simply the natural response to our unnatural environment.”

Matt Metzgar has an interesting take on this: maybe our environment has us in a state of perpetual winter metabolism:

In modern times, people can get trapped in a permanent winter metabolism due to lack of sun exposure and lack of plant food in their diet. What is supposed to be a transient state of the metabolism for a few months becomes a permanent condition.

Perhaps it’s just me, but the more I read, the more I firmly believe that the response to obesity needs to be a lot more sophisticated than just “eat less, move more.”

More of that later in a followup post, but for now, I think a good approach would include:

1) Reducing carbs, especially sugar and refined grains. I am not convinced ketosis is necessary, but you probably want to go low enough that you aren’t carb dependent (which means you’re body is making good use of fatty acids instead of carbs, you don’t get light-headed or ravenous between meals, etc.). I’m also not convinced that you need to go full-on paleo and avoid all grains (though the Weston Price folks may be onto something).

2) Eating a whole food diet, including protein, veggies, and a good dose of healthy fat at each meal (keeping omega 6s as low as possible, which means avoiding most vegetable oils). I also like full-fat dairy from grass-fed cows.

3) Considering some supplementation. It’s better to get micronutrients from food or nature, but that’s getting harder with our industrial food system. And it looks like a number of these micronutrients are essential for a healthy metabolism. For me, the contenders are vitamin D, magnesium, omega 3, and iodine.

4) Healing the liver and gut. For the liver, this’d involve avoiding things like alcohol and fructose (probably fruit too); for the gut, it’d involve strategies for repopulating the gut with healthy bacteria.

5) Stopping the chronic cardio! Exercise is important for health, but it may need to come later after some level of weight loss depending on where one starts. I like the idea of low level aerobics and a small amount of weight and high-intensity training.

Of course, I’m not a doctor, nor do I play one on TV (sorry, dated reference); this is just my current thinking. More to come later. For a more sophisticated take, I encourage you to check out Stephan Guyenet’s thoughts here or Kurt Harris’ approach here.

[Bob and Jillian's] contempt for the obese was obvious as they spewed insults (and saliva) in the faces of the contestants. I don’t care how fat or desperate I was, if someone did this to me I would punch them in the face and storm off the set. I checked in on the show between patients. The diet and exercise shown were prescriptive for ravenous hunger and ultimate failure. As I continued to work, I kept thinking about the importance of biologic signaling, and why it does not have to be this hard.

Read the entire post for more, but here’s the point:

The key to turning around these sorts of metabolic disasters is to send the correct biologic and hormonal signals. … A brief, but intense workout that fatigues the musculature activates growth hormone, testosterone and adrenaline which all signal to empty glycogen and fat, both short and long-term. A hunter-gatherer diet creates a low insulin signal which triggers the body to defend a lower body fat set point.

Contrast that with:

Overtraining (especially in the obese) triggers cortisol and other stress hormones. A low fat, high carbohydrate diet signals insulin release. These signals defend a high level of stored fat and drive hunger…a true prescription for misery and failure.

I know which approach I’m taking!

Every once in a while though, you get a real pearl, like:

When I found this I had a strong desire to kick myself in the face to make sure I wasn’t dreaming. I got out of my chair and walked around the office with a huge smile on my face. I was in such a good state of being that I asked out this girl from the coffee shop that I like. Posts like this slap all others square in the balls.

Though it is still spam that is COMPLETELY unrelated to the post it’s attached to (and you will still delete it), you have to give the writer an A for effort :).

Money quote IMO:

… consider how convenient it is for the airline industry to deflect a customer’s anger over ridiculously small seats—I’m thinner than approximately 80 percent of middle-aged men and I don’t fit into one very comfortably—on to “overweight” passengers, a category that includes, according to our public health authorities, nearly seven out of 10 adult Americans.

BTW, over on HuffPo, Lee Stranahan makes my other main point re Smith: Kevin Smith did not violate Southwest Airlines policy.

Back to Campos. His article is also worth the read for his criticisms of MeMe Roth of the National Action Against Obesity. But I like Tom Naughton’s approach even better!

Tom adds:

I actually find MeMe Roth more annoying than the sue-happy lawyer. This is a woman who is obviously naturally thin. She was born on the finish line and thinks she won a race. So now she feels justified in telling other people how to eat, and in criticizing pretty much every overweight person in the public eye. …

My advice: never take advice on losing weight from anyone who’s never had to work at it. They have no flippin’ clue what they’re talking about.

Word!

Well, two things. One is that Kevin Smith really wasn’t too fat to fly based on Southwest’s 25-year policy. He was able to sit in the seat, armrests down, seatbelt buckled without an extender. Based on his report — and the followup from the airline — it appears that Southwest’s policy is very subjective: you can be removed just because people appear to be leaning away from you!

So that sucks. And in predictable fashion, Southwest seems to have handled it poorly, but just as with the Whole Foods flap re health care reform, the half-life of the controversy will be relatively short (save for being included in examples of bad corporate responses as far as social media goes).

No, the real problem is the second point: it really sucks being a fatty who needs to fly. And I’m very saddened by all the haters leaving all the hateful comments in response to this story all over the interwebs. With 2/3rds of Americans overweight or obese, I gotta wonder. Don’t these people know someone — family member? friend? co-worker? — who is overweight or obese?

Where is the compassion? Apparently nowhere to be seen when it comes to being encroached on in a plane.

Not that I think it will change anything for the haters, but I was glad to read Kate Harding’s Kevin Smith: The face of flying while fat this morning:

See, those of us who are and/or love people to whom airlines’ “person of size policies” apply don’t automatically envision the discomfort of getting stuck next to a fatty; we envision the physical and emotional pain of being the fatty crammed between two potentially hostile strangers, at the mercy of flight attendants who might decide we’re fine on one flight and a “safety risk” on the next.

Harding does a great job of describing what it’s like for those of us who fear flying while fat: please do go read the whole thing.

What irritates me is how Southwest’s policy, and other airlines as well, makes this so much harder for fatties. It’s seriously no-win. Even if you can afford it, it’s ridiculously hard to actually buy and then fly with two seats — especially on an airline like Southwest, which doesn’t pre-assign seats. In fact, one of the contributing factors on Smith’s flight was that a passenger had bought two tickets and the flight attendants had to move others to accommodate that passenger, thus delaying departure from the gate and leaving the flight attendant perhaps a little stressed when it came to Smith’s situation.

As Harding notes, Southwest’s initial response didn’t help at all:

And then I read Southwest’s apology to Smith, which includes such gems as “If a Customer cannot comfortably lower the armrest and infringes on a portion of another seat, a Customer seated adjacent would be very uncomfortable and a timely exit from the aircraft in the event of an emergency might be compromised if we allow a cramped, restricted seating arrangement.” And I think, first, “If we allowed a cramped, restricted seating arrangement? Because ‘The Greyhound of the Skies’ is positively roomy when there are no fat people on board?” And second, I think, “Translation: Fat paying customers’ fully expected discomfort only becomes a problem for us if it also makes the paying customers we care about uncomfortable.”

But really, I get that people don’t want to be encroached on. Most of us don’t like encroaching either! Too bad all the focus is on us abhorrent fatties and not on the airlines for not better accommodating ALL their passengers. I might need more than one seat to avoid spilling over in the cattle car that passes for coach these days, but I don’t need two. Some airlines are providing optional seating for taller folks at a slight price increase. Why not for wider folks?

I’m afraid that they aren’t inclined to do so, mostly because at least half the population (the skinny folks and the fatties who can pass) are happy to reward the airlines for making it all about us fatties who cannot put down the Ding-Dongs.