TWICHOO Soldiers are Down to Syringes

The following tweet was brought to my attention in comments on another post:

garytaubes gary taubes 

Worried about the greatly-exaggerated death of the insulin hypothesis? Take the latest NEJM image-challenge: bit.ly/db7VF2

The image that link leads us to is at right, along with a selection of conditions for one to select as the cause of the malformation.  Well, of course, the answer is "Insulin lipohypertrophy".  When one answers and goes to the responses, they get the following explanation:

These pendulous subcutaneous periumbilical masses were attributed to 31 years of insulin injection to manage type 1 diabetes. Lipohypertrophy can be associated with glycemic flux and prevented by rotating injection sites.

I tweeted about this.  Finally!  Maybe now we can look at this poor fella instead of the woman in panties with the melon sized lumps on her thighs, that we got to see in just about every book and lecture given by this man.   It seems that TWICHOOB's are going to have to resort to the primative weapons in their Insurgency, the lowly syringe.  Because, of course, we know that *every* diabetic gains weight when they start insulin therapy.  Firstly, part of this is the correction of a pathological state.  Secondly, not every diabetic, T1 or T2 gains weight.  Often, when they do, they gain in the early stages of therapy as they adjust and learn the appropriate dosages to prevent hypoglycemia which is notorious for prompting overeating.   Unfortunately no amount of demonstrating that insulin in and of itself does not increase fat mass or cause weight gain seems to be enough for the most entrenched TWICHOOB's.   Stephan just put another nail in that coffin, but General Eenfeldt is doing his best to at least hold down the Scandanavian fort in comments.  

In his publicity stunt petition, Taubes makes this argument that insulin therapy causes weight gain and metformin causes weight loss.  Well, metformin doesn't always cause weight loss.  What does metformin do?  It's an insulin sensitizer -- T2's are basal hyperinsulinemic, so if anything, metformin is somewhat like giving a T2 insulin because metformin allows the T2's body to "see" the insulin their pancreas is pumping out! ... weeeeeeeeeeeeeerrrrrrrrrrrrrooooooouuuuuump (that's the sound of the insulin resistance causes obesity version of TWICHOO flying out the window and landing in the pit Taubes keeps digging for himself).  So sometimes, metformin causes weight loss.  But there are other drugs for T2.  Yes, some do cause weight gain, and coincidentally they stimulate insulin.  This shows insulin is what makes us fat!!  Not so fast.  Other diabetes drugs, like exenatide (Byetta), stimulate insulin but lead to weight loss in a large proportion of those taking it.  

Bottom line, there is no consistent effect on weight change for diabetics (T1 or T2) when insulin or other insulin modulating medications are given.  If it were simply insulin levels that determine fat accumulation, ALL who received insulin and related therapies would gain weight, and likely predictably on a dose-response basis.  This does not happen.  Yes, insulin therapy tends to lead to weight gain, but not in the absence of a change in intake and/or remediation of rampant glucosuria (where energy is lost through glucose in urine).  

So why did this poor man develop those fat globules on his abdomen?  Well, first, nobody disputes that hormones can influence the distribution of fat, and that hormones partition energy between lean and adipose tissue differently (especially between genders).  That is a topic for another series when I'm done with my recently started how we get fatter series, a sort-of where we get fat series.  In any case, for over three decades, this man has been injecting insulin.  And, unlike the advice given to rotate injection sites, he's probably been alternating between left and right for most of his injections for those three decades.

On Twitter, Nigel asked what the concentrations seen at the injection sites are compared to normal circulating insulin levels.  I don't even think we can make a meaningful comparison.  Circulating insulin levels are reported  in picomolar (pmol/L) or microunits per ml (µIU/ml or just µU/ml -- note this is the same as mIU/L).  Normal fasting levels are less than 60 pmol/L or less than 8.6 µIU/ml.   Insulin is secreted directly into the portal vein and is taken up and distributed by the liver.  In any case, the usual postprandial insulin spike is less than 10 fold increase in circulating levels.  In this study, for example, fasting levels averaged 53 pmol/L, and topped off around 400 in one group, roughly an 8-fold increase following a standard glucose tolerance test.   From Joslin (and other sources), it seems typical insulin doses are 1IU per 10-15g carb depending.  If we use the low end dose for a standard glucose tolerance dose of 75g, we're talking 5IU injected locally.   In this study, subjects were injected with approximately 9 IU of shorter-acting insulin and achieved circulating levels of 250-300 pmol/L in 30 minutes, or 46-53 mIU/L -- This is 9000 mIU injected locally that disperses to almost 1/200th of that concentration in circulation.  Does it suprise anyone that insulin injected repeatedly over decades at the same sites -- approximately 200X physiological levels -- might cause the fat tissue to expand at those sites??  It does not surprise me!

Of course us stupid ELMMers, possibly even idiot scientists in our midst, are really trying to tell you that this poor chap's abdominal region must be eating more and exercising less than the rest of him.  This is preposterous, but desperate times call for desperate measures for the Insurgency.  We note that the rest of him looks pretty lean still, as does the lady with the similar thigh bulges.  In any case, this is not the result of this guy eating carbs, that's for sure.

I almost feel sorry for Gary Taubes.  Nobody really wants anyone to end up that bitter demented old man (his words) muttering to himself because nobody would listen to him.  But he could have saved himself from that fate were he a more objective science journalist.  Somewhere, somehow, he became convinced that all obesity researchers are idiots, and somehow, they knew all the answers in pre-war Germany.  We are to believe there's a massive conspiracy has prevented one of the most desperate populations on the earth -- obese people -- from discovering the simple cause of and cure for their condition.  Yes, 40 years after Atkins first popularized his diet, we're all just sheeples listening to our government and all their wrong advice.

Folks the death of TWICHOO is not what's being exaggerated, it's the validity and acceptance of the hypothesis in the first place that was.   Not one single obesity researcher signed the petition.  Why not?  Oh yeah, they're all idiots, and Stephan Guyenet foremost among them apparently because earning his degree has caused him to go insane.  Why We Get Fat didn't sell nearly as many copies as I'm sure Taubes and his publisher had hoped and it's been four years of relentless lecturing and interviewing and promotion of this hypothesis -- by an increasingly militant and vocal faction I might add -- since GCBC came out.  And yet 2011 was not a good year for the hypothesis, even as some degree of carbohydrate restriction is becoming more recognized by the mainstream as a means to the end of weight loss.  For those who don't "get me" this is what it boils down to.  Low carb is a legitimate and effective means to lose weight for many, and, for some, to maintain that loss.  But to employ this strategy one need not throw common sense, their knowledge of science and their intelligence out the window and buy into the fantasy that is TWICHOO.  Gary Taubes will have to be satisfied with being a footnote in history on this one.   He's only prolonging the inevitable with his NuSI initiative, and this "War on Insulin" Insurgency is preposterous.  He'd do better to open a chain of WW-styled weight loss centers employing a low carb approach.