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Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Wednesday, March 16, 2011

GCBC Reference Check ~ Part V of ? ~ Insulin Resistance: Taubes v. McGarry

"Over the years, prominent diabetologists and endocrinologists -- from Yalow and Berson in the 1960's through Dennis McGarry in the 1990's -- have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity.  Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat.    
~Gary Taubes (p. 409 Sony ebook version of GCBC)



Now, before you click below and go on to read what I interpret this excerpt from GCBC to mean, and  some works of McGarry, write down what that statement means to you.

   
OK, here's what I think when I read this:  McGarry's thesis on the etiology of insulin resistance is what Taubes puts forth in GCBC.  Mainly:


carbohydrates raise insulin → insulin resistance → hyperinsulinemia  

How did I do?  Do you agree?  

Now, I'll quote some more from GCBC.  These excerpts begin on p. 396 of my ebook version:

In 1992, the University of Texas diabetologist Denis McGarry published an article in Science with the memorably idiosyncratic title "What if Minkowski Had Been Ageusic?  An Alternative Angle on  Diabetes."  The German physiologist Oskar Minkowski was the first to identify the role of the pancreas in diabetes.  The word "ageusic" refers to a condition in which the sense of taste is absent.  "Legend has it," McGarry wrote, "that on a momentous day in 1889 Oskar Minkowski noticed that urine collected from his pancreatectomized dogs attracted an inordinate number of flies.  He is said (by some) to have tasted the urine and to have been struck by its sweetness.  From this simple but astute observation he established for the first time that the pancreas produced some entity essential for control of the blood sugar concentration, which, when absent, resulted in diabetes mellitus."  Some thirty years later, when Frederick Banting and Charles Best in Toronto identified insulin as the relevant pancreatic secretion, McGarry wrote, they naturally did so in the context of Minkowski's observations about blood sugar, and thus "diabetes mellitus has been viewed ever since as a disorder primarily associated with abnormal glucose metabolism."  But if Minkowski had been ageusic and so missed the sweet taste of the urine, McGarry speculated, he might have noticed instead the smell of acetone, which is produced in the liver from the conversion of fat into ketone bodies.  "He would surely have concluded that removal of the pancreas causes fatty acid metabolism to go awry," McGarry wrote.  "Extending this hypothetical scenario, the major conclusion of Banting's work might have been that the preeminent role of insulin is in the control of fat metabolism."
OK, so now I would like you to please go read McGarry's work in full before continuing on.  Many thanks to MM for tracking this one down for me.  I'm sharing it with you through Google Docs through the link below.  As always, if there's a problem please let me know.  This might be a tough read for some, but so, frankly, was the laborious GCBC.  If you have to go through it in small doses to at least get the gist of what McGarry believed (in 1992) on this topic, please do before reading on.


I will screenshot "quote" some excerpts below.

The end of the Banting paragraph cited by Taubes above:



So the rest of Taubes on McGarry:
McGarry's parable focused on diabetes, but the point he made extends to virtually everything having to [do] with insulin.  Just as diabetes has traditionally been perceived as a disorder of carbohydrate metabolism -- even though fat metabolism is also dysfunctional -- insulin has always been perceived as a hormone that primarily functions to regulate blood sugar, though, as we've discussed, it regulates the storage and use of fat and protein in the body as well.  Becaue blood sugar could be measured easily through the first half of the twentieth century, but not yet the fats in the blood, the focus of research rested firmly on blood sugar.
Have you made it through the McGarry paper yet?  If not, please do make an effort to do so, or at least take the time to read the excerpts below:  {please click to enlarge}



FWIW, I have some more recent McGarry works (all predating GCBC by at least 5 years since McGarry passed away in 2002) that further refined and altered this progression.

OK, what scenario for the etiology of IR and diabetes did you come away with?  Now re-read Taubes:
"Over the years, prominent diabetologists and endocrinologists -- from Yalow and Berson in the 1960's through Dennis McGarry in the 1990's -- have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity.  Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat. 
I would dare say that this is not the impression I got from McGarry's paper.  He's actually been saying a lot of what I've been saying in terms of LC to treat T2/IR.  That the hyperglycemia is a downstream symptom of a metabolic dysfunction that started with fat metabolism.

McGarry never fingerpointed at carbohydrates as causing insulin resistance.   In 1992 he has a big ? as to what starts it all.  Taubes presented it as a sort of settled science that only recently has gotten mucked up by all those hapless American researchers.

More to come ...
A preview of the NEFA trail ol' bunny ears has been hopping down here.

7 comments:

John said...

"Anything that increases insulin, induces insulin resistance, [...]"

I guess Gary Taubes didn't tell this to the Kitavans. How else could they get 69% of their calories from carbs [1] and maintain a low insulin level (4.0 microIU/ml) [2]. Luckily for them the body seems to adapt to a high amount of non-toxic carbs by becoming more insulin sensitive.

As you already know, Peter Dobromylskyj has a post describing possible mechanisms for this [3].


John

References:
[1] Lindeberg S., et al. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. Am J Clin Nutr. 1997 Oct;66(4):845-52. http://pmid.us/9322559
[2] Lindeberg S., et al. Low serum insulin in traditional Pacific Islanders--the Kitava Study. Metabolism. 1999 Oct;48(10):1216-9. http://pmid.us/10535381
[3] Dobromylskyj P. Potatoes and weight loss (1). http://high-fat-nutrition.blogspot.com/2011/03/potatoes-and-weight-loss-1.html

William said...

Good post CS. Complicated, but very interesting nonetheless. Looking forward to the "More to come..."
will be reading up on McGarry in the meantime

Bill

Jay said...

I disagree totally, there is nothing in the McGarry excerpts that contradicts the summary that Taubes presents.

blogblog said...

John said:

I guess Gary Taubes didn't tell this to the Kitavans. How else could they get 69% of their calories from carbs [1] and maintain a low insulin level (4.0 microIU/ml) [2].

It is absurd to compare different populations because they don't have the same genotype of lifestyle. Kitivans are a tiny genetically isolated group that have adapted to a particular diet over thousands of years.

Aborigines, Micronesians, Mexicans and Zulus placed on a 69% carbohydrate typically develop extreme obesity, rampant diabetes and kidney disease.

Melchior Meijer said...

"Kitivans are a tiny genetically isolated group that have adapted to a particular diet over thousands of years."

Really? Then why do they develop al the 'diseases of affluence' when they change their habitat for a mainland town where they eat a western diet with a quite comparable macro nutrient ratio?

Why are traditonal living Pima's in Mexico relatively slim and healthy on a high corn diet, while their genetically similar brothers in the US get sick and obese on a comparable high carb diet?

Answer: wheat, sugar, linoleic acid.

CarbSane said...

Frankly I'm not sure it's those agents in particular that cause obesity, it's the foods we make out of them. LA in particular as regards obesity (not disease) seems marginal at best. Neither Atkins nor Taubes spoke/speaks a peep to O6's. Many low carbers were successful (myself included in round 1 & to a lesser extent in round 2) eating mayo and creamy manufactured dressings = almost all O6. Me in round 3 was less of the mayo and dressings, but I didn't stringently drain my tuna (packed in evil soybean oil) and indeed counted on some of that oil, with a little canola or olive for my dressing. I was raised on vegetable oil (cold pressed safflower or sunflower) and was a stringbean kidlet (and no, I don't think any of that predisposed me to what I did to my body).

Melchior Meijer said...

I think the combination of these items in large amounts (the treshold mentioned by Cleave?) disrupts normal energy regulation in many people. Like in the rats offered the cafetaria diet.

And if the mix doesn't make you obese, it'll make you myopic, infertile, hypertensive, osteoporotic, diabetic, etc, etc.

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