Diabetes Treatment & Stuffs

I think if I were someone without my background and diagnosed with diabetes, I'd probably go crazy.  Really!  I try to imagine what it would be like to get some direction from my doctor who likely hooks me up with a diabetes educator.  I'd probably go looking for additional information on the internet, and no doubt find all of the conflicting information from all sides including the low carbohydrate community -- many of whom are medical doctors.  There is so much misinformation out there -- from both sides -- but the LC advocates are more dangerous, IMO, because they are not vetted and weeded at least of the worst charlatans.  I think most people who are diagnosed with diabetes just want effective treatment.  Unfortunately, for too many, current protocols only manage the disease and postpone physiological decline, and diabetes is all rather complicated making being your own patient-advocate all the more difficult.  

Perhaps it is some sort of grand conspiracy between the medical establishment, the agriculture department and drug companies to make us all fat, sick and diabetic ... and keep us that way.  I don't believe that.  I went to school with, and know, way too many doctors to believe that the majority of them are just non-caring pill pushers to the end of padding their wallets.  There are clearly financial interests competing and corroborating, but coordinated?  Some call me paranoid.  ;-)

I think, instead, that diabetes is misunderstood by many in the medical profession and here is where I see a huge problem -- there is an enormous disconnect between what an amazing amount of scientific research reveals and what is taught to medical professionals and thus to patients.  A fundamental misunderstanding of what diabetes is and the role of insulin in the body.  To this end, I believe that when the dust finally settles, the enduring legacy of Gary Taubes will be how he furthered this disconnect and set back progress, because those he influences most are MD's, while researchers walk out of his lectures in disgust.  At some point one has to ask themselves why that might be ... even though his disdain for them is evident, most are far too professional to let that get to them.   

It is a shame that Taubes so woefully misrepresented giants in the field and their works, but he does reference a little gem I think all should read.  From the late J. Denis McGarry:  What If Minkowski Had Been Ageusic? An Alternative Angle on Diabetes.  I blogged on this in:  GCBC Reference Check ~ Part V of ? ~ Insulin Resistance: Taubes v. McGarry  (I recommend the next person who wants to accuse me of engaging solely in ad hominem attacks read the GCBC Reference Check series first.)  

A second classic paper I suggest reading, if you haven't already because I cite it often, is:  Insulin:  understanding its action in health and disease.  This paper was published -- perhaps unfortunately in a journal of anesthesia instead of a prominent diabetes and/or an obesity journal -- in 2000.  

Things have been confused, however, by a 20 yr ‘black age’ of endocrinology (between approximately 1960 and 1980), where leading scientists—through extrapolating beyond their new discoveries—confused scientific thinking and teaching. [...] The effects of this ‘black age’ are still with us because these incorrect hypotheses have, with the passage of time, been turned into dogma and become cast into ‘tablets of stone’ in undergraduate textbooks. They are also carried forward into postgraduate teaching. For example, even in well respected texts it is still common to find statements such as ‘The basic action of insulin is to facilitate glucose entry into cells, primarily skeletal muscle and hepatocytes.’

Listen to Gary Taubes lecture.  He refers to all of the "good science" from the 60's and 70's that he claims goes ignored by the idiots researching this stuff for the past few decades.    Taubes has resurrected this "black age" era of incorrect hypotheses in GCBC.  He did it by deliberately ignoring any new evidence that countered it.  

When one reads Taubes, insulin is detrimental agent in the body that should be minimized.  Others say it is life-shortening and should be minimized.  The emphatic blinkered view of insulin = bad is epitomized by one Dr. Ron Rosedale.  Rosedale, who believes we're all somewhere on the spectrum of diabetic, also believes that insulin has no place in the treatment of T2 diabetes.  At the end of this post I've C&P'd an exchange I had with him last October on PaleoHacks:  {it's rather long, but I gave up trying to cut it down and don't want to risk taking it out of context}.  The bottom line is that even when  presented with evidence that early insulin therapy -- 2 weeks! -- normalized glucose levels in T2's and fully half remained diabetes free after one year, Rosedale still declares his diet a superior treatment.  I could go down the who's who list of LC docs -- many of whom are more than condescending of their peers -- and LC is better than an LF diet made up of crappy SAD foods -- but it doesn't reverse the disease or stop it in its tracks.  

These people are firmly entrenched in the dogma that carbohydrates cause diabetes by pooping out the pancreas.  Not even the LIRKO mouse -- screaming with insulin and glucose yet not obese until their livers give out so they're just screaming with insulin and still not obese -- cannot convince them of the faultiness of this theory.  They ignore billions of non-insulin resistant, non-obese, non-diabetic cultures eating far more carbs than your average American, including Taubes' favorite traditional Pima who ate upwards of 80% carbohydrate.  No, they insist that LC is the only scientifically sound way to treat diabetes.  

So what brought on this rant?  Well, I guess Jonathan Bailor and his book where he rehashes the worst parts of GCBC.  It is very disturbing to me to see his book described as:

The single largest scientific analysis of health and fitness ever conducted proves that, contrary to what the food, fitness, and pharmaceutical industries tell us, eating less and exercising more harms our health and leads to fat gain 95.4 percent of the time. Endorsed by the world-wide scientific community including top doctors at the Harvard Medical School, John Hopkins, and UCLA, and approved as curriculum for registered dieticians (RDs) by the Academy of Nutrition and Dietetics, Jonathan Bailor’s new book The Smarter Science of Slim simplifies this analysis of more than 1,100 scientific studies into a proven lifestyle for long-term wellness by focusing on the quality of food and exercise and then eating more and exercising less – but smarter

In comments on his guest post on MDA (where my comments go into the ether) , an Erica challenged this description.  Since I don't see a meta-analysis that looked at 1100 studies, I can only presume he is referring to his book as one.  That is simply a joke.  His book is not a meta-analysis of any sort.   From the few studies I've looked at that he distilled down, his presentation is misleading at best and I'd say stronger words are warranted in many cases.  That this is what gets approved for curriculum for RD's, frankly, disgusts me.   Although I realize he's not discussing diabetes, it's a rehash of the same flawed presentation of insulin resistance that gets us NOWHERE to repeat.  And that statement that this is endorsed by the world-wide scientific community is highly exaggerated, especially when that includes mostly doctors and not scientists.   I'm sure Bailor would include Jeff Volek there, and he cites a few studies bearing his name.  And yet his dietary prescriptions are almost polar opposites to those of Dr. Nutritional Ketosis.  

It is very disillusioning, because as my new mentor justprayin reminds me, I won't make it anywhere with my message unless I tone down the criticism of these folks and play along so I can get books published.   Well, if I have to sell out to get published, what's the point anyway?   

This much I know:  Replacing the nutritional establishment that may be populated by folks indoctrinated in the flawed dogma of saturated fat phobia with a new gang indoctrinated in this flawed glucophobic dogma is not a step in the right direction.  It's one step forward, two steps back.  We need to hold these people's virtual feet  to the same fire of scientific scrutiny or we're doomed to repeat the mistakes of the past.  

Most advocates for low carb diets will ultimately acquiesce that for most, it manages the disease but does not reverse it.   Even the much ballyhooed Westman study that reduced medications by 95% is grossly exaggerated on further inspection.  The LC diet reduced the required insulin doses and nothing more in most cases.  The results of early insulin treatment or crash diets or gastric bypass create ECD (extreme cognitive dissonance) for the proponents of carbohydrate restriction.  And then there's Dr. Joel Fuhrman -- who also goes against the grain, but in a different direction.  Fuhrman advocates a plant dominated diet to reverse diabetes.  On his website it says:

Don't live with your diabetes, don't simply control your diabetes -- get rid of it!

Yeah, he's got his membership fees, and books, and such and whatnot.  Which makes him different from any number of LC advocates I could rattle off?   In some ways Bailor's program is closer to Fuhrman's than the LCHF crowd's -- because high protein improves insulin sensitivity and could thus cure diabetes.   The one difference I see between Fuhrman's approach and the LCHF approach is that with his, you consume carbohydrates, thus when you've reversed diabetes you'll actually know it because your body is properly handling carbs.  With LCHF, you'll never know it, because your blood glucose levels skyrocket eating normal amounts of carbs after prolonged low carbing, and most will not wait out the adaptive phase long enough to find out.  Here's where Bailor's program could potentially be better as it seems to allow quite a bit more carbohydrate as well as a lot of insulin sensitizing protein.  I imagine folks following this plan could slowly push the envelop and realize they process carbs just fine.  The problem, however, is that if they buy into the LC pseudoscience, they probably never will.

This is that sentiment that pervades the LC community as evidenced by the whole "safe starches" debate.   Over and over we heard well, maybe they're safe for those who haven't damaged their metabolisms after all those years on the carboholic SAD.  And yet all around us there are examples -- documented in peer review articles and case studies, not internet anecdotes or even success stories from Sisson to Fuhrman to Rosedale to AWLR -- of people even with relatively longstanding diabetes (I think one subject in the crash diet study was diagnosed 9 years!) that it can be reversed.  I don't know about you, but even if I could reverse it for a year at a time, that seems far preferable to following Rosedale's diet and freezing to the core, yet he so flippantly dismissed that option (see below).

Succeed on Fuhrman's diet and maybe you buy some supplements and such.  Success on Wheat Belly's?  Nobody ever noticed all the supplies and tests and such to "track your plaque"?   I mean if we're going to accuse some docs of wanting patients to remain sick for profit .....  For most low carbers it's managing their disease with fewer medications but for many it's medications all the same at some point.  Which is not to say Furhman et.al. are curing everyone either, and if someone is beta-cell impaired, well, carbohydrate controlled eating may well be the better way to go -- depending on how much one wants to or is willing to figure out the insulin (and/or other drug) doses necessary to maintain normal glucose levels.

But insulin ain't the bad guy, and until the counter-culture dietary rebels wrap their heads around that, there can be no "unified cause" ... not one I'll sign on to anyway, and I know many have issues of their own they dare not vocalize publicly.   I'm thinking this is most of the problem in the greater community ... many have reservations like mine, to differing extents, on different issues.  I guess this is why I was ultimately so disappointed in the Real Food Summit, because if any summit was to speak to me, it should have been that one.  And yet when the "keynote" Joel Salatin makes me feel bad about my current mostly real-whole-food based diet, exactly what choir are y'all (undefined) trying to preach to??   If you can't even preach to the choir, you'll never reach the masses!!

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Ron Rosedale, MD:  There is plenty of robust evidence that chronic elevations/spikes in glucose, insulin, and leptin highly contribute to insulin and leptin resistance, that are the foundation for the development of diabetes (by its current definition of high blood sugar). Additionally, diabetes (T2) is not primarily a disease of blood sugar, but a disease of hormonal miscommunication primarily of insulin and leptin, as manifested by insulin and leptin resistance and should really be diagnosed as such.

Defining the disease of diabetes strictly by elevated blood sugar allows the real disease(s) of insulin and leptin resistance with accompanying hyperinsulinemia and hyperleptinemia (that do worsen with time in a continuum) to go unnoticed , often for decades, while damage and 'disease' secondary to this accumulates until finally islet cells start burning out, fatty liver sets in, hyperleptinemia and leptin resistance results in excess hepatic gluconeogenesis, and the diagnosis of 'diabetes' is finally made...

..drug treatment is given to lower blood sugar usually by overworking and stressing the islets even more while raising insulin, ignoring leptin, ultimately wiping out the islet cells, now requiring more and more exogenous insulin to bring down glucose that people are being told is fine to eat, all the while worsening the underlying cause… and doctors wonder why diabetics die young. 

CarbSane/Me:  Dr. Rosedale, I've been researching the literature on this for a year now. I have yet to see any study demonstrating that carbohydrates and the insulin responses they elicit contribute to insulin resistance. The only foods that seem to are those that do not elicit an insulin response (fructose and fat). If there is robust evidence, it shouldn't be difficult to provide a few review papers implicating carb induced glucose and insulin spikes. Thanks in advance, I look forward to reading those studies. 

BTW Ron: I consider hyperglycemia a symptom not the underlying pathology. Diabetes is beta cell dysfunction. Non-diabetic obese and classical T2's can have nearly identical metabolic mileus -- elevated NEFA, hyperinsulinemia, with different glycemic outcomes (even some can have elevated FBG w/o postprandial IGT and vice versa). There's something else going on in a relatively small percentage of the population where compensation fails, and beta-cell impairment and/or destruction ensues. Which doesn't make prediabetes benign ... just not necessarily "pre" anything. 

Kurt G Harris MD:  "There is NO evidence that postprandial insulin spikes and BG spikes cause diabetes." This is the bottom line and is the loch ness monster of the CIH. I've looked for over 4 years and seen no convincing evidence that this happens. PP BG increases do not cause hyperinsulinemia. Pathological insulin resistance causes hyperinsulinemia, not the other way 'round...

Rosedale:  i.e.HbA1c;there is another explanation that I feel is most likely; these are patients on diabetic medications.To achieve lower A1 C they likely received greater amounts of medications,and the vast majority of medications used to treat diabetes excessively raise insulin,causing at the very least artificial hyperinsulinemia,islet cell stress and dysfunction, islet cell death, worsening of the underlying cause of diabetes and increased mortality.Other medications such as PPARg agonists have their own manifest problems increasing mortality.In other words, the treatment itself becomes the disease. 

There IS plenty of evidence that hyperinsulinemia is a major contributor if not the main cause of type II diabetes. Admittedly, not that easy to find, as it is not something that that gets much research money and pharmaceutical companies are turning their heads, as drugs to lower insulin are nonexistent.  Even so-called insulin sensitizers are not that. Showing that hyperinsulinemia is a major precursor to islet dysfunction and the onset of T2 diabetes is not something that Medicine (or the food industry) would wish to know about. Not only would the major therapy then be dietary and not drugs it would be more than embarrassing since the vast majority of treatment for diabetes over the last half century or longer results in hyperinsulinemia. Medicine (and its lawyers) don't want to face itself in the mirror knowing it's been helping to kill its patients.

A couple of studies... Insulin: In need of some restraint? Salk Institute Proceedings of the National Academy of Sciences,March 07, 2007 "the study reveals the "dark side" of high insulin production, the kind that results from over eating and obesity. "Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available," he says. "But when the hormone is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ."

Another study, one lay and the journal article    sciencedaily.com/releases/2008/09/…jci.org/articles/view/34587  I also know from perhaps treating 1000 diabetic patients that reducing insulin and leptin via diet rapidly improves insulin and leptin resistance, and greatly improves, if not altogether reverses, T2 diabetes and other chronic diseases of aging. The reduction in leptin and insulin happens first and appears to be a requisite. Others are now doing this including Eric Westman and Mary Vernon who have published papers.... and one must also recognize the extremely high contribution that leptin resistance plays in diabetes... may even be more important than insulin. Spikes in blood sugar cause spikes in leptin, contributing to if not causing leptin resistance resulting in centrally mediated (brain) increased gluconeogenesis, elevated insulin, islet burnout... diabetes..

Me:  Weight loss improves insulin sensitivity no matter the method. Hyperinsulinemia contributes to insulin resistance only as a down stream cycle -- e.g. when it keeps glycogen stores topped off thus reducing non-oxidative glucose disposal which is the general defect responsible for impaired glucose disposal into skeletal muscle. I don't get the relevance of the CHOP paper to all of this. Except that the basal insulin requirements deplete the ability to make insulin for GSIS. 

ncbi.nlm.nih.gov/pmc/articles/PMC508661/pdf/…

Ron, your premise seems to conflate postprandial insulin response with basal insulin. Basal insulin is stimulated significantly by free fatty acids that there is robust research, to use your term, to support are the initiating factor in the etiology of diabetes. Bierman, McGarry, Frayn, Boden, DeFronzo, the list could go on. Can't find it right now but there's a study showing early insulin therapy cures diabetes and the participants were able to stop therapy after like 8 weeks or so with normal glucose homeostasis.

Rosedale:  It is the other way around. Improvement in insulin and especially leptin resistance comes first, within the first few weeks prior to significant weight loss, and this will then result in fat loss if necessary and multiple other physiologic benefits including improved cardiovascular function. The rest of what you said about insulin has little to do with the truth and is regardless trivial as a major cause of diabetes. The CHOP study just shows relevance for hyperinsulinemia resulting in islet stress contributing to islet cell death.

... free fatty acids do not stimulate insulin release. I am certainly not confusing postprandial insulin response with basal insulin. Early Insulin therapy for type I DM was tried a number of years ago including by myself, and failed to stem the disease... Insulin therapy for type II diabetics (producing their own insulin prior to significant islet cell burnout) makes them worse and should not be a part of medicine. 

CarbSane/Me: free fatty acids do not stimulate insulin release. Wrong. carbsanity.blogspot.com/2011/04/… carbsanity.blogspot.com/2011/07/… ncbi.nlm.nih.gov/pmc/articles/PMC302480/pdf/…

Regarding Early Insulin Therapy: Insulin therapy for type II diabetics (producing their own insulin prior to significant islet cell burnout) makes them worse and should not be a part of medicine {Rosedale}  http://care.diabetesjournals.org/content/32/suppl_2/S266.full  A recent study comparing intensive insulin therapy (multiple daily insulin injections or continuous subcutaneous insulin infusion) with oral hypoglycemic agents (glicazide and/or metformin) in newly diagnosed patients with type 2 diabetes provided some provocative results (21).  In this trial, 92% of 382 subjects with poorly controlled diabetes achieved glycemic targets (fasting and 2-h postprandial capillary glucose levels of <110 mg/dl and <144 mg/dl, respectively) within an average of 8 days from start of therapy (Table 2). Treatment was withdrawn after 2 weeks of normoglycemia, followed by diet and exercise management. ... By the end of 1 year, remission rates were significantly higher in the groups that had received initial insulin therapy (51 and 45% in the continuous subcutaneous insulin infusion and multiple daily insulin injections groups, respectively) compared with 27% in the oral therapy group. *Whereas in the oral agent group, acute insulin response at 1 year declined significantly compared with immediate post-treatment, it was maintained in the insulin treatment groups. * I'd say there ought to be a place in medicine for EIT in T2's.

Rosedale:  CarbSane.."A recent study comparing intensive insulin therapy (multiple daily insulin injections or continuous subcutaneous insulin infusion) with oral hypoglycemic agents (glicazide and/or metformin) in newly diagnosed patients with type 2 diabetes provided some provocative results (21)". They are comparing insulin therapy with oral agents that raise insulin by stressing islets. So raising insulin without stressing islets is better than stressing islets. Either way they are raising insulin and worsening an underlying cause of the disease.  Far better to treat T2 DM by improving insulin and leptin sensitiviy, and this is done by greatly reducing those foods that provoke insulin and leptin, i.e. starches. Like being in a smelly room reduces your ability to smell, you must reduce the odor to regain it. You do not reverse T2 diabetes by giving them more insulin.. You must reduce it.

CarbSane/Me:  What part of roughly 50% remission from diabetes after VERY short term insulin treatment did the Drs. not get? They're not stressing their islets with insulin. They reduce lipo and gluco toxicity and allow the beta cells to regain proper function. 

Rosedale:  So, are you recommending periodic treatment with insulin injections (that will ultimately increase resistance) every week? month? to reduce stress and glucotoxicity secondary to sugars from starches in their diet that is sure to recur if those people continue to eat as they had previously?...or maybe those with diabetes, diagnosed as a disease of high blood glucose, and where the typical goal of therapy is to lower it, should just minimize eating it? 

CarbSane/Me:  Ron, Did you read the paper? Or at least my quotation above? Diabetes is profoundly reversed (not just put into remission where a few grams of carbs sends BG's skyrocketing) by the early insulin treatment (and with that crash diet). Half of the EIT's were still diabetes free after a year. Yet you say EIT has no place in medicine? Really?? The mechanism is that the EIT relieves the hyperglycemia that is compounding the lipotoxicity and likley lowers the elevated NEFA causing the GSIS impairment. Now the pancreas can produce insulin properly instead of hyper-basal and impaired GSIS.