The Carb-Sane Asylum

Another two-fer for the Thursday post bumps again this week.  More explanation for why this set in the next bump. Original Publish Date:  7/26/11 In the comments on  a recent post on beta cell lipotoxicity , Ned Kock (of Health Correlator blog) posted a link to a post he made a while back entitled:   Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes .  This article deals with the concept of the "tired pancreas" in the development of diabetes.  It seems that (and hopefully he corrects me if I'm wrong here) Ned and I agree that this is not a likely explanation for diabetes.   Ned summarizes the progression of obesity induced T2 diabetes from  Unger & Zhou, 2001 .  It is worth mentioning that Unger is often summarily dismissed from the "scientific discussion roundtable" by low carbers because of the unfortunately titled "Gluttony and Sloth" paper, that, even more unfortunatel...

I'm going to try to make this as short and to the point as possible.  It's just me thinking out loud a bit, drawing on the massive amount of peer review research I've read on the topic -- a mere fraction of which I've formally blogged on -- but without any references so that I can just get this out there.  No ... this is not some manifesto grand theory on diabetes and all that to be analyzed and picked apart as if I'm presenting this as fact.  It's just a plausible analogy for what I think happens when metabolic mahem turns to "diabetes".  I'm also going to simplify things and deal with only glucose and fatty acids here. Our ß-cells metabolize glucose and fatty acids the same way our other cells like muscle cells do for energy.  Essentially this metabolism is part of the mechanism by which the ß-cell senses the circulating levels of these energy substrates.  This metabolism also produces ROS -- reactive oxidative species.  While ROS are often...

Was anyone surprised by the revelation that Paula Deen has type 2 diabetes?   See here and here , for example.  Full disclosure here.  I'm a NorthEast girl and was raised pretty agnostic in terms of regional foods/cuisines.  Still, as an adult I've enjoyed learning different cooking styles, flavors and ways of preparing foods and I'm an admitted Food Network junkie.  But Paula?  She was not one I ever watched much (unless she was judging on a competition show).  Sure, I love some Southern foods -- chicken fried steak w/gravy anyone?? -- but most of those foods are reserved for traveling to where they are local fare (although Chili's does make a pretty good version of the aforementioned steak).  And I find her accent and delivery just a wee bit over the top.  But I think every time I've ever seen the woman cook, I've seen her put half sticks of butter in a pan while saying jokingly that she's adding "a little".  Butter and Paula a...

The web went ablaze this past week or so over the ADA's Hope Warshaw, who penned a piece for Diabetes Health .  Judging from the reaction some might think is was akin to Mein Kamf   or something.  I mean the hypocrisy of those in the extended LLVLC community is just too much to bear at times.  What did Hope Warshaw write that was so inflammatory?  It's a short piece, but it boils down to this: Apparently Warshaw makes the claim that low carb is "old dogma" in diabetes circles, and Warshaw advocates eating a slightly higher carb (45%-65%) diet that by virtue of macronutrient ratios will result in a lower fat intake compared to the current (45%) average carb consumption.   Advocacy of earlier pharmaceutical intervention upon diagnosis. Cognition that weight loss is most effective in the first months or years following diagnosis and basically that we should be proactive with "prediabetes" screenings and diagnoses. Oh the horror!  String her ...

I'm going to be using insulin as my example in this post.  Endogenous insulin is the insulin produced in your body by your pancreas.  Exogenous insulin would be that derived from outside the body - e.g. insulin injections.  For the most part exogenous hormones are obtained through some "pharmaceutical" route.  In the case of insulin, subcutaneous injections. Now I’m sure most of my readers are familiar with the picture below:

If you haven't read the discussion thus far, or just to recap, here are the links: Insulin Wars IV: Todd Becker of Getting Stronger blog Insulin Wars IV.1: Todd Becker of Getting Stronger blog responds More Todd Becker (Getting Stronger blog) on Insulin  (this last one links to his piece on his blog) {Todd quoted the relevant prior exchanges in his email, so most can probably follow along just with this post} I've been putting off posting this for too long, mostly because in its entirety it is very lengthy (15 pages!) and I haven't had the length of uninterrupted time to devote to a thorough point by point response to the entire email.  So I decided to break this installment (IV.2) up into parts (a,b..., however many) so we can keep this discussion alive and continuing.  I'm also likely to address some topics out of order from Todd's email response.   Eventually it will all get up here :-)  I very much appreciate all the hard work Todd put into his response...

If you've read at all on the LC web you'll see that there's an almost grudging hatred (well that might be too strong a word, but ...) towards those who take "the easy way out" getting gastric bypass surgery.  If not aimed at the person who has undergone surgery, a palpable feeling of animosity towards the WLS "industry" and the "pusher" doctors is in the air.  At some point someone will chime in to remind everyone that "you know what kind of diet they eat don't you?", because it is low carb.  The implications of which are that the weight loss is due to going LC so why not forego the surgery.   I tend to agree with this sentiment, somewhat, especially since most WLS candidates must follow a diet and lose a bit of weight before the surgery.  Which begs the question of if one can do this before the surgery, why can't they just keep it going and lose weight w/o the surgery?  It's a fair enough question, but one with no e...

Caffeine and Insulin Sensitivity   (full text PDF free till end of the month) A number of reports have observed that acute caffeine ingestion decreases glucose tolerance and insulin sensitivity, and have raised the question whether its increased consumption throughout the world in the form of coffee and cola beverages might be of public health concern in the development of type 2 diabetes. Although some epidemiologic studies have found strong associations between coffee intake and detrimental lifestyle factors that favor obesity and diabetes, it is interesting that in spite of this, they have demonstrated that increased coffee consumption is associated with a decreased risk of developing type 2 diabetes.   When lifestyle confounders are taken into account, individuals consuming 6 cups coffee per day have at least 50% less risk of developing type 2 diabetes than those consuming 2 cups per day . Although it is perhaps premature to rec...

Taubes has 10 major conclusions for GCBC, the ones relevant to this post are quoted below: 5. Obesity is a disorder of excess fat accumulation not overeating and not sedentary behavior. 6. Consuming excess calories does not cause us to grow fatter any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger. 7. Fattening and obesity are caused by an imbalance – a disequilibrium -- in the hormonal regulation of adipose tissue and fat metabolism: Fat synthesis and storage exceeds the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance. 8. Insulin is the primary regulator of fat storage. When insulin levels are elevated – either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel. 9. By stimulating insul...