Monday, August 15, 2011

I Got Boinged, and Other News

The reaction to my post "The Carbohydrate Hypothesis of Obesity: a Critical Examination" has been overwhelmingly positive, particularly among the scientists I've heard from. 

On Saturday, the inimitable maker and writer Mark Frauenfelder posted a link to my post on the variety blog BoingBoing.  BoingBoing has been on my sidebar for three years, and it's the place I go when I need a break.  It's a fun assortment of science, news, technology and entertainment.  BoingBoing was originally a zine started by Frauenfelder and his wife in 1988, and it has been on the web since 1995.  Today, it has multiple contributing authors and it draws several hundred thousand hits per day.  I'm thrilled that Frauenfelder posted my article there.  Apparently he likes my blog.  Thanks!

I added a new section (IIB) to my original post.  It discusses what human genetics can teach us about the mechanisms of common obesity.  It is consistent with the rest of the evidence suggesting that body fatness is primarily regulated by the brain, not by fat tissue, and that leptin signaling plays a dominant role in this process. 

23 comments:

Frauenfelder said...

Thanks for the kind words, Stephan! I really like your blog. Please email me because I would like to talk to you about writing for Boing Boing: mark@boingboing.net

Ross said...

That post is also in the slow-motion process of being reddit'ed...

Aravind said...

Hello Stephan,

Related to the genetics addition to your last post (which I loved)...I posted a comment at Peter's blog (at Hyperlipid) regarding your Carb post and here was a snippet of his response -

"...there is a difference between a broken and an unbroken human being. My grandmother was a type two diabetic. My X chromosome and many of my mitochondria may well have come from her. I personally appear to benefit from carbohydrate restriction.

What you can eat as a 20 year old athlete and what you can eat as a 55 year old clinician may not be the same if your grandmother was a type 2 diabetic.

I would like to follow Stephan's references to see if they can convince me that hyperinsulinaemia is irrelevant to weight gain/loss"....

You have CLEARLY differentiated cause of derangement vs remediation post derangement, so I am not at all questioning that.

Unless I am misreading Peter's response, seems like he is advocating a "pre-emptive strike" based on genetics/epigenetics prior to derangement. I am not asking you to interpret what Peter wrote but rather what related thoughts you might have on this?

Thanks,
Aravind

Ashley said...

Stephan,
Wonderful work! Congratulations! It was great meeting you at AHS. I'll email soon with some ideas on food reward. Talked about it with a few fellow psychologists - they are very interested, and have some intervention ideas.
Best,
Ashley

Dave Tate said...

Congrats on getting Boinged!

Ruth Almon said...

Couldn't happen to a nicer guy.

Peter said...

I onced asked Taubes why vegetarians tend to be skinny despite high carb diets, and he speculated that it was because they tend to avoid processed foods. In other words, processed foods are what make us fat, overlapping with your view.

I've also heard him say that starches might be fine if you haven't previously damaged your metabolism with sugar.

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antispirit said...

This post was totally not what I thought it would be.

Stephen said...

First, let me say I'm not a scientist, just a regular person who finds all of this interesting.

I've read that Leptin, Insulin and Ghrelin work together to keep our weight in balance.

We're hungry. Ghrelin is released to tell our brain we're hungry. We eat. Insulin is released to suppress ghrelin and deal with fats. Leptin is also released to say to the brain I"m full. It's supposed to work in balance to keep our weight stable.

But: Chronic overeating makes more insulin to drive more fat into tissue. Over time we get insulin resistant. Also, as fat increases more leptin is released to say I'm full. However chronic overeating also interferes with leptin signaling causing leptin resistance as well (we don't know we're full). A cascade starts that is hard to stop.

So, to this non-scientist it seems that obesity is a result of an imbalance of the ghrelin, insulin, leptin cycle.

Interesting stuff.

Taylor said...

Stephen, don't forget amylin, adiponectin, SOC3, PPAR, CCK, dopamine... Its dizzying really.

Unknown said...

"But: Chronic overeating makes more insulin to drive more fat into tissue. Over time we get insulin resistant. Also, as fat increases more leptin is released to say I'm full. However chronic overeating also interferes with leptin signaling causing leptin resistance as well (we don't know we're full). A cascade starts that is hard to stop."

How about chronic overeating of "good food". I think overeating would only apply to processed junk food, gluton , soy, sugar fructose , and foods that contain high levels of lectins in them ect. Eat till your full or till you stuffed with "good food" and you won't have insulin or leptin resistance ever and you can probably reverse both.

Roberto said...

Stephan

My question is rather off-topic, but I'd appreciate any insight you might have.

What happens to energy balance when a person (or animal) eats a diet that provides ample calories,
but is deficient is key nutrients? Say white flour and butter exclusively. Would one eat excessively in search of those nutrients and take in excess calories as a result, leading to fat gain? Do you know of any studies that have investigated that?

Denise Minger revealed the clear association between obesity and white flour consumption from
the China Study Data. I noticed from her graphs that those people were eating an absurd percentage
of their total calories from white flour. Perhaps the obvious nutrient deficiencies that would result from such a diet led to their weight gain.

Makro said...

Stephan has been writing a lot about the causes of obesity recently, so I thought that I would chip in with my five cents, going a bit beyond the comments I dropped last round.

A lot of the discussion has been focusing on the hyperinsulinemia-based hypothesis of obesity (not to be confused with the old-school-Taubesian carbohydrate hypothesis) versus other possible explanations, such as the role of food reward in overeating and obesity.

Now, I believe that there is plenty to indicate that there is room for several overlapping causes of obesity, and that there is plenty of research that indicates that there exists several modes of obesity, and that people hence respond differently to different interventions.

More specifically, it seems as if the (significant share of) obese and overweight people who have impaired insulin sensitivity do derive significant benefit (in terms of weight loss) from:

1) Reducing carbohydrate consumption (compared to other dietary interventions) (Citations: Gardner et al (2007), Ebbeling et al (2007), Cornier et al (2001), Pittas et al (2005) )

Note that these studies isolate insulin-resistant subjects from insulin-sensitive subjects and compare the efficacy of carbohydrate restriction between the groups. Insulin-resistant subjects are shown to benefit (much) more than insulin-sensitive subjects from carbohydrate restriction.

or

2)Being treated with insulin-suppressing drugs (Octreotide), with there being a smooth insulin-reduction-weight-reduction response curve. (Lustig et al, 1999 )
This also seems to indicate to me that hyperinsulenemia plays an important role in causing obesity in a significant share of cases, and especially in the most serious ones (fatter people seem to be more insulin resistance).

This is not an ironclad conclusion, but compared to the usual standards employed in obesity research for establishing causality, I´d say the hypothesis looks pretty strong, especially if the hyperinsulenemia-leptin resistance link holds up.

The flip side of this is that there is another significant portion of the overweight and obese that do not appear to have an insulin resistance problem.

Hence, an explanation for their obesity is needed, and I see no reason why (for instance) Stephan´s Reward-based theory of obesity cannot fit the bill for them (no citations as this very blog is full of ‘em).

Of course, both mechanisms might overlap in some individuals.

Well, those were my cents for today. Thanks for a great blog!

Makro (A.k.a Ekonomen)

Stephen said...

@ Taylor,

Yes, it is a dizzying alphabet soup! That's probably why there's so much controversy out there and why I feel I'm being pulled in different directions all the time.

I think I might just settle on Michael Pollan's advice to eat food, not too much, mostly plants (although I'm not sold on the mostly plants bit, I'm a carnivore at heart).

Makro said...

Whoops, I forgot the references:

Sources:

Gardner et al (2007), JAMA, “Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial.”

Ebbeling et al (2007), JAMA, “Effects of a Low–Glycemic Load vs Low-Fat Diet in Obese Young Adults”

Cornier et al (2001), Obesity research, “Insulin sensitivity determines the effectiveness of macronutrient composition of the diet on weight loss.”

Pittas et al (2005), Diabetes care, “A Low-Glycemic Load Diet Facilitates Greater Weight Loss in Overweight Adults With High Insulin Secretion but Not in Overweight Adults With Low Insulin Secretion in the CALERIE Trial.”

Lustig et al (1999), The Journal of Pediatrics, “Hypothalamic obesity caused by cranial insult in children: Altered glucose and insulin dynamics and reversal by a somatostatin agonist.”

alan said...

interesting site/thoughts. your palatability hypothesis is very interesting. however, i have seen very little about the psychological side of the equation. i find myself eating (or continuing to eat) when i a not hungry (or even full), presumably for emotional reasons. i think this is a bigger problem for most people than set points or actually being full. thoughts?

Helen said...

@ Taylor,

I've only dipped my toe in this and I agree - I started to learn about PPAR and CCK a few months ago, after a year of trying to school myself in various aspects of diabetes, and fell off the alphabet soup train at that point. Which led me back to my own version of the Michael Pollan dictum, while watching my glucose meter.

@ Unknown - The only time I've gained significant weight (outside of pregnancy), I was on a nearly Paleo, Weston A. Price-inspired diet. It was pretty darned palatable. I lost weight when I was on a low-fat diet that was extremely unrewarding. I didn't do this on purpose to lose weight - was having upper GI pain & gallbladder issues - but it did the trick better than low-carb had (initiated after WAFP/Paleo weight gain), and it lowered my blood sugars a bit, too.

Kamal said...

@Aravind: It's time for you to stop commenting on blogs! We're supposed to be deconditioning our technology reward pathways for 26 more days.

Also, interesting point. My family is full of underweight type 2 diabetics, spanning several generations. All while eating fairly healthy lacto-vegetarian diets with rice and potatoes.

Helen said...

@ Kamal,

Sometimes familial diabetes like that is a MODY form (mature-onset diabetes of the young, a term that's being phased out) - due to a monogenic mutation in glucose-sensing/insulin-producing pathways. These can be tested for genetically. They've traditionally been misdiagnosed as either Type I, if found in children, or Type II, if found in adults.

The Blood Sugar 101 web site has more on this.

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