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Sunday, July 10, 2011

Diabetes ~ A Disease by any other Name?

A HUGE bit of prefacing here ... If you're anxious to skip that and get to the subject matter, use your browser's search function to find **** to blow right on by.  

In the coming days (perhaps weeks, hopefully not months but who knows ... life's busy these days),  I'll have more to say regarding Diabetes 101's Jenny Ruhl's interview with Jimmy Moore.  Cliff Notes version is that I'm glad I listened to the whole thing because although I found myself shaking my head at times in the  beginning, later in the interview I found myself nodding more in agreement.  A huge hats off to Jenny for her amazing composure and articulation.  Wow, you would think she did this sort of thing every day!

I gotta say, anyone who thinks Jimmy Moore is some sort of "aw shucks" kinda gracious happy-go-lucky fellow really needs to read between the lines in terms of the circumstances of the occurrence and airing of Jenny's interview however.  Given the (huge) diabetic following amongst the LLVLC crowd, to portray Jenny EVER as some sort of backup interviewee to anyone on his podcast is downright insulting and inexcusable.  But a backup to Durian Rider of all people?  I mean nothing against the guy, but what's so important about having a podcast interview with someone whose claim to fame is eating 30 bananas a day?  Jimmy normally tapes his podcasts months in advance of airing.  In my case we taped on Nov 9 and it aired Jan 17 if memory serves.   Jimmy discusses issues with taping the DR interview and efforting getting it almost as if he was doing live interviews or something.   It makes you wonder just why he would expend that much energy over a raw vegan in the first place, and not just drop him from the schedule when the issues arose.  Why not just say  there were problems in the taping and "stay tuned" for maybe later in the year.  I doubt many of Jimmy's fans even know who this guy is, let alone were chomping at the bit for that podcast.  Whassup wid dat??

When called on this by someone named Haggus in the comments, Haggus:  You really rolled out the red carpet with that “backup interview” billing.  Jimmy responded with a short:  Jenny did an outstanding job!  Haggus followed up:  I couldn’t agree more! What I thought was odd is that you described it in that particular way. Either way, it was good to finally hear her voice after reading a lot of her sage like work.  To which a still clueless Jimmy replied:  It was supposed to be Harley Johnstone and Jenny was the backup plan in place if that one couldn’t run. There was no hidden meaning to it. ;)

Now, maybe I'm making a mountain out of a molehill here, but at the beginning of the interview Jimmy tells Jenny how many of his readers have been asking for like forever when he's going to interview Jenny from Diabetes 101.  And he says basically there are so many people asking to be on, his schedule is just so packed full, etc. etc. blah blah ... I guess there just hadn't been room in his schedule up until now for a popular diabetic low carber with a pretty serious following amongst his LLVLC fans.  But because of all the issues with the Mr. 30 bananas interview that ended up falling through, now there was room for Jenny Ruhl as a backup plan.  Really?  Perhaps rather than asking some anonymous bunny eared "Taubes taunter" to come on his podcast he could have had Jenny on months ago.   Nahhh... then he wouldn't have had an excuse to squeeze yet another podcast, two in fact, of Gary repeating the same old same old I suppose.  Yes folks, drama drives hits drives the LLVLC bidnuss.   

OK vent over ...


One thing Jenny said sort of caught my ear.  Essentially that there's really no such thing as Type II Diabetes.  If I understand her correctly, what she's saying is not that there's no T2, but perhaps there are many more forms of diabetes.  This gets me thinking that what we really need is to re-name these diseases and work for diagnostic tests to adequately diagnose the different versions.  I was disappointed that Jenny did not make more clear what exactly her genetic form is.  Jenny is a MODY.  She describes this on her website as a rare form of "Type 1.5" diabetes.  MODY stands for Maturity Onset Diabetes of the Young.  She doesn't have elevated FBG but is glucose intolerant leading to skyrocketing postprandial blood sugar levels.  This particular variant  of diabetes is seen in only perhaps 2% of all diagnosed diabetics and thus an even smaller percentage of the population as a whole.  She does focus on the fact that she was thin and this probably led to her not being diagnosed sooner and misdiagnosed later.  I can certainly understand Jenny's distrust of the medical establishment, etc., that would grow from this sort of frustrating misdiagnosis.  But I do take issue with her somewhat renegade attitude that many legit type 2's take to heart in managing their diabetes.  That her rare form doesn't fit in the construct of T2, and the medical strategies for treating that form, does not negate the credibility, for lack of a better word, of those treatments and the medical professionals who counsel their use.  It's like saying that because there are lots of "subclinical hypothyroids" out there who have thyroid issues despite "normal" test results, all of those that are diagnosed hypos and treated successfully with, say, synthroid, are somehow being mishandled by the medical establishment.  

Jenny made a great point in her interview -- paraphrasing -- that diabetes is no more a disease than to say "cough" is a disease.  Yes!  But I would like to see everyone replace "diabetes" with "hyperglycemia".  Because this is the proper analogy.  Hyperglycemia -- fasting or postprandial -- is the symptom of the underlying pathology, just as cough is a symptom of a bacterial infection, lung cancer or other underlying cause.  As my regular readers are no doubt aware, "diabetes" is about more than blood sugar.  

I don't know about many of you, but until a couple of years ago, I'd heard about T2, formerly called adult onset diabetes, but I didn't know much about it.  When someone said "I'm a diabetic" that equated with the T1 situation of a pancreas that made no insulin and was never going to do so.  Clearly the advice and treatment are totally different for T1's than for any other type of hyperglycemia.  I have two papers I'll be blogging on soon.  One discusses how diverse hyperglycemia is where folks can have impaired fasting glucose (e.g. would get diagnosed prediabetic) but normal glucose tolerance while others have -- as in Jenny's case -- normal fasting glucose, but impaired glucose tolerance.  The other paper deals with hyperinsulinemia and insulin resistance, and how there are subsets of the population that have one or the other without having both.  And yet time and again, I'll hear folks assuming they have certain cases but it's never been properly assessed.  

Jenny makes one claim that, if I heard it correctly, is outright false.  It's a bit ambiguous whether she's saying  that by the time folks are diagnosed T2 they've lost 80% of their beta cells, or that by the time folks are diagnosed T2 80% have lost most of their beta cells.  Either way that's simply not true.  If it were, then you wouldn't have the basal hyperinsulinemia that clearly a good portion of T2's exhibit, and you wouldn't have the high rate of reversal of diabetes achieved with gastric bypass surgery.

The underlying pathology in what we call "diabetes" is pancreatic ß-cell dysfunction or insufficiency.  On the extreme, you have either almost total dysfunction which is likely severely reduced ß-cell mass -- the complete or near-complete inability to produce insulin at all.  This is the T1's, autoimmune forms and end-stage of what is now Type 2.  Here we see the outright destruction of the cells themselves.  But less extreme are various levels of glucose intolerance where postprandial glucose levels spike much higher than normal and/or remain elevated for extended periods.  Here the pancreatic dysfunction is impaired glucose stimulated insulin secretion (GSIS):  This is actually what Type 2 as we know it is.  It is often if not always accompanied by basal hyperinsulinemia.  I maintain that this sort of diabetes, caught early enough, is fully reversible in an encouragingly high percentage of people.  

If there's a problem with how the medical establishment treats diabetes it lies with the glucocentric means by which it is diagnosed.  Hyperglycemia, fasting or postprandial, can be due to a dyfunctional pancreas or a destroyed pancreas.  If your basal insulin levels are high, you have the former, if they are non-existent, you have the latter.  The treatment/prognosis is very different between these two cases.  But, just to throw another wrench in the works, there are non direct ß-cell functional causes for hyperglycemia!  Tissue specific insulin resistance.  If you have peripheral IR (e.g. muscles), you'll fail an OGTT or have your postprandial glucose levels come down more slowly than you'd like.  Your pancreas is doing its job but the muscle cells aren't hearing the message.  If you're diagnosed "prediabetic" by an elevated fasting blood glucose level, you likely have hepatic (liver) IR.  Again, the pancreas is still doing its "thang", the liver just isn't listening to the signals.  Perhaps you have both.  Likely if you have hepatic or chronic peripheral IR, your fat cells have been IR for quite some time.  No this is not an established fact, but this is where mountains of research points to as the initiating factor linking obesity to diabetes.  If your pancreas is still functioning at least sufficiently, the focus of any intervention should be to restore insulin sensitivity.  Yep ... you guessed it, lose weight and exercise more.  The goal should be improving insulin sensitivity.

There are several different classes of drugs for T2 diabetes.  Some that directly act on the ß-cells, others that do not.  Metformin, for example does not act on the pancreas.  It will help those with hepatic IR and may ameliorate peripheral IR, but if your ß-cells are dysfunctional or insufficient to mount an appropriate insulin response, this drug will do nothing for you.  I'm not going to go through all of the various drugs, rather I'm just pointing out how the fact that one or another doesn't work for a large percentage of hyperglycemics does not mean they are not effective and useful for a different large (or even small) percentage of hyperglycemics.  Jenny ... recall she's of a small subgroup of diabetics ... discusses taking Prandin to manage her hyperglycemia.  Here's how that drug works.   And so it appears she is able to control her hyperglycemia by improving her  ß-cell function and controlling her glycemic load.  I note she doesn't discuss gaining weight despite her medication stimulating insulin secretion....  My point?   I guess that is ultimately to find why you have hyperglycemia and not be afraid of pharmaceutical intervention specific to your condition just because there are self-righteous folks out there who keep their glucose levels low by eating no carbs.

So ...

Maybe it's all just semantics, but in medicine, semantics are everything.  It's time for some new terms for the vastly differing conditions that all share a common symptom.  That being hyperglycemia ... and IMHO just the term diabetes, type this or that,  ain't cutting it at this point.


rkoffler said...

You shine when you write posts like this ("thang" and all....)

OnePointFive said...

I agree that the results from bariatric surgery seem to suggest that there is still sufficient beta cell function to control glucose levels . Perhaps this is because these people are now eating very much smaller meals and therefore there are enough beta cells left to cope with the reduced challenge.
There is evidence from post mortem studies that obese people who don't have diabetes have greater beta cell mass than lean non diabetics. Those with diabetes and even 'prediabetes' were found to have significantly less beta cell mass in comparison to people of similar weights who were not diabetic.

We definitely don't all fit into simple pigeonholes, neither with T1 or T2 ( I'd have been diagnosed as T2, 10 years ago and still would be in countries where they don't test for antibodies, ) People diagnosed with T2 can be severely insulin resistant or severely insulin deficient and a mixture of both anywhere in between.The majority are overweight on diagnosis but there are still a number wo are normal or even under weight. I think there are probably different causes and different solutions but some people want to give the same answer.(and from some people on the internet the advice is always lower carbs, higher fat whether you're overweight and not losing or thin and desparately want to put weight on!)

OnePointFive said...

I don't know whether to put this here or on the low cal/low carb post but I don't know if you've seen this
Pathogenesis of type 2 diabetes: tracing the reverse route
from cure to cause
ie the theoretical background to the vlcal diet trial.
I've only jut skimmed it but noticed that he says
"However, in established diabetes, sudden mobilisation of the liver fat allows normal physiology to be reinstated within days, provided that long-term damage to the beta cells has not yet occurred. The published data suggest that 2–3 years of type 2 diabetes does not usually produce irreversible beta cell damage."
(which is of course seems contrary to the evidence from the PM studies I've just cited.

CarbSane said...

Thanks rkoffler!

@OnePointFive: Interesting paper there. I'll have a closer look later in the week. Perhaps even if there is reduction in beta cell mass, there is still sufficient cells to mount an appropriate response. Kind of like we have two kidney but we can function perfectly well with just one or a 50% reduction.

Chris said...

I rarely listen to Jimmy's podcasts anymore, the sponsorship stuff and the over the top "Jimmmmy Mooooooore" stuff is a little too much for me. I pick and choose the guests.

This was a good one though, although she was saying stuff that I would not expect JM to like e.g. insulin doesn't make you fat....

CarbSane said...

Hi Chris ... I listen to very few and I slide that thingy on over past the promos. I tend to listen to more of the "geeks" like Stephan, Paul J, Ned Kock, Drs. Westman, Dansinger and such. I've always found it interesting that while they may seem to be LC proponents in many ways, whenever Jimmy asks about calories that almost all have stated it in no uncertain terms that they ultimately count. It was an exasperating moment in my interview because I had no intention of discussing the twinkie diet thing with him and yet he was like so why did he lose weight. Duh!

You can almost hear his teeth grinding at statements like "insulin doesn't make you fat".

KD said...

I looked at Jenny's blog. I thought what she had to say was interesting, but certainly wouldn't use her blog as the only source of information. I thought parts of the "hospital and nursing home" part of her blog were misleading.

I've probably administered thousands of insulin injections in a variety of settings. I'm calling BS on her claims of nurses using 25 gauge 1 inch needles for insulin administration. I'll read through the rest of the blog, though with skepticism.

CarbSane said...

Welcome KD, thanks for pointing that out. I have not read a lot at her site as I came to my interest in diabetes from a bit of a "back channel" research interest. One day when I came across all this stuff about elevated free fatty acids, it led me to all of that ... I'm not diabetic myself. However I've always gotten the feeling she's very anti-medical establishment -- and undercurrent in the LC community that I see as ultimately counterproductive.

I find this particular page extremely misguided:


Wow, I had read that many moons ago before I even thought much about diabetes. Reading it again now, I think I'm feeling a blog post brewing. There is a lot of toxic "advice" there :(

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