Science Krispies ... Spiked Pink Leptinade Anyone?

Leptin seems a very confusing hormone to pin down.  It's still relatively new, so despite there being a ton of research already, we're still in that era of lots of conflicting research and such.   As discussed previously, I think this makes leptin ripe for serving up oversized bowls of Science Krispies.  A lot of confusion also exists as regards the relationship between leptin and insulin.  Some say they work in concert, some say leptin rules insulin, and others say insulin rules leptin.  Insulin production is distinctly different in the basal and postprandial states.  How about leptin?  

Well if we believe Dr. Ron Rosedale (doing his best Joel Osteen impersonation shown at right, from over on his  Facebook page), it's leptin that rules the roost.  Rosedale posted a few advance installments of his response to the whole "safe starches" query from Jimmy Moore.  Here's one:

It appears to me that the paleo community has now been divided between a faction that backs Taubes who believes that insulin is supreme and the major cause of obesity, and a faction backed by Harris, Jaminet, Guyenet, and others who believe that insulin and glucose is less important and that leptin is more important in obesity and perhaps other diseases, and therefore eating so-called “safe starches” is OK if not even desirable. The major issue and source of confusion that I see, is that they are both half right and half wrong, but opposite halves. Taubes is right that sugars, starch, and elevated insulin are a major source of disease if not obesity that I heralded 2 decades ago, but not fully correct as to why. The Jaminet, Guyenet, Kruse, and Harris** group is right that leptin likely supersedes insulin as far as importance in obesity, diabetes, and other chronic diseases, at least in humans. However, they (not including Kruse) are quite wrong in believing that it is therefore okay to consume “safe starches” that will largely digest into glucose. Though true that leptin, more than insulin, controls fat storage and perhaps even blood glucose levels, this does not mean that raising insulin levels via glucose is unimportant. It still plays a huge role in the control of genetic expression influencing the aging and chronic disease phenotype. 

However they all, including Harris, Jaminet, Guyenet, Kruse, Taubes, and even those who have written books after me about leptin***, seem to be missing a very critical and main functional point about leptin... Leptin levels and ultimately leptin resistance, and therefore chronic diseases of aging including obesity and diabetes, are determined more from spikes and elevations in glucose following meals than anything else including the amount of one's stored fat. Though elevations in glucose raising insulin may not be the major cause of obesity and fat accumulation (though still very important), the fact that glucose spikes leptin still places sugars, including glucose from so-called "safe starches" and fructose, at the centerpiece of obesity and disease.

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** I'm not sure I've ever seen Paul or Kurt focus on leptin in this manner

*** Seems Rosedale doesn't want anyone stealing his thunder

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Yes, that pink highlighted emphasis is mine. There's that word *fact* again that, when included in sentences, implies more than just an affirmative statement, but that somehow this is settled science. It stuck out at me, and it didn't seem to square with the postprandial profiles of leptin I've seen in the tens of studies I've read over the past few years that looked at leptin in one way, shape or form. So ... a quick search turns up this:

Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake  (Romon, et.al.  1999)

In this study they fed 22 subjects (11 each men and women, healthy non-smokers, weight stable >6 months, non-obese BMI<27) either a high carb (80%) or high fat (79%) test meal, and measured various parameters over a span of 9 hours.  The test meal composition is here and included 18% protein for each and roughly 3400 kJ = ~800 cals.   After the 9 hours, the subjects were offered an ad libitum meal.  Satiety was assessed by a standard test (VAS) every hour.  

Below are the 9-hour insulin and leptin profiles for the women (A&B) and the men (C&D)

They did not provide 9-hour glucose profiles, but it's not in dispute that the glucose profile would likely mirror the insulin profile for these meals. Perhaps my cataracts are interfering with my vision again, or perhaps one needs some special Rosedale colored specs to look through to see it, but I'm not seeing any leptin spiking going on. Are you?? Yes, the carbohydrate rich meal (~165g carb) did produce a delayed (4-5 hour) slight increase in leptin levels compared to the fat meal -- outcome more pronounced in women than in men -- but one could hardly call this a spike. And whatever the underlying mechanism of the phenomenon, 9 hr leptin exposure did not correlate with 9 hr glucose exposure as shown above right.

The satiety results are worth noting, as in the short term carbs outperformed fat, but over the 9 hours there was no difference between the two.  Leptin's action on appetite is one of appetite suppression so this is interesting.  I'm sure there will be a post or two in the future on this notion that all diabetics should necessarily avoid starch and/or that starch should be presumed harmful to anyone until proven otherwise.  But for now ...

It's Friday fellow inmates!!  And I'm in the mood for a little levity.   And how apropos that Joel Osteen has a  book out recently called Every Day a Friday.  (No, I'm neither a follower nor a fan, just saw him recently discussing the book on TV.)

Separated at birth??

Won't you join me in a toast to the weekend?  

Now being served in the Sane-Asylum Lounge:

ROSEDALE'S HARD PINK LEPTINADE  or  TAUBES' CHERRY PICKIN' MARTINI  

Cheers!