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!)

Friday, July 20, 2012

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 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!!

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…  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. 
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. 

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}  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.


Charles Grashow said...

Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol

Normalisation of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are
reversible by reducing dietary energy intake.

This study demonstrates that the twin defects of beta cell failure and insulin resistance that underlie type 2 diabetes can be reversed by acute negative energy balance alone.

Swede said...

Dye Uh Beet US

P2ZR said...

'on MDA (where my comments go into the ether)'

Will I be parading my naivete when I say that that somewhat surprises and dismays me? I know that Matt Stone got himself banned there way back when, but err...that's Matt Stone. I *did* wonder how they always managed to have a homogeneous group of Sisson-worshipping Grok wanna-bes commenting there, but had always assumed it was because the more scientifically-minded don't actually comment there, and the 'worker bees' (love how that term furthers cult of personality!!) just had to weed out relatively useless snark. I get it now. The conventional-wisdom-sheeple-disdaining Grokka-bes need to be carefully herded by the dutiful thought-managing Sissonites. The primalsphere makes sense now.

'I don't see a meta-analysis that looked at 1100 studies, I can only presume he is referring to his book as one.'

~cringe~ Is this another one of those I-need-to-hide-underground-now misunderstandings like the 'amazingly well-controlled trial' gaffe of our favorite fiction writer?

ShottleBop said...

"The results of early insulin treatment or crash diets or gastric bypass create ECD (extreme cognitive dissonance) for the proponents of carbohydrate restriction."

Not for all of them. Dr. Bernstein, for example, has long recounted the story of Gerald Reaven's experiments with the BioStator back in the 70s. Newly diagnosed T2s were hospitalized for two weeks, and their blood sugars were clamped at 90 for the duration. After the treatment, patients retained improved pancreatic function for two years. As Dr. Bernstein described it, in a 2008 article written for "Diabetes Health" (available at

At about the time I started my practice, Gerald Reaven, author of Syndrome X, used the Biostator GCIIS, an "artificial pancreas," to normalize the blood sugar of 32 patients for two weeks. The cumbersome and expensive device constantly measured blood sugar and clamped it at 90 mg/dl. One outcome was that high A1c levels dropped dramatically. The study then followed the patients, half of them male, half female, and also found that it took two years of ordinary living [and likely inappropriate diet] for their A1c's to return to pre-study levels. To me this implied the most important finding-that beta cell burnout dysfunction could be halted or reversed by a combination of exogenous insulin and normal blood sugars. By giving overworked beta cells a rest, they could improve or regain function. A similar study by a Taiwanese group recently came to the same conclusion.

Dr. Bernstein still believes that a low-carb diet has benefits: "The problem with injected insulin is that large doses cannot be absorbed predictably. So the more insulin a patient must inject, the higher the likelihood of unpredictable blood sugars." Since the amount of insulin one needs is directly affected by the amount of carbs ingested, he recommends carb restriction. (He does not, however, recommend that diabetics work to maintain a state of ketosis.)

ShottleBop said...

As I understand McGarry's 2001 Banting Lecture, he was of the view that obesity (at least, obesity characterized by high levels of intramuscular fat) was a major stepstone on the road to diabetes, and that losing weight should help: "As discussed, the combination of the modern diet and sedentary lifestyle has resulted in an increase in obesity/type 2 diabetes. It is evident that if people would eat fewer calories and increase their activity level, then this would reverse ectopic fact accumulation and lessen insulin resistance." (

More recently, the folks at the Diabetes Education and Research Center--Philadelphia, in a blog post dated January 1, 2011 (posted at, reiterated for readers the substance of McGarry's Banting Lecture. It inspired one question:

"That is very interesting. What diet would be best to follow. High or low carbohydrate?"

The answer, by the author of the blog post:

"It's hard to make a blanket statement about which diet is best. While some people find it easier to lose weight and manage blood glucose on a low-carb diet, the diabetic kidney may have difficulty handling the extra protein.

Dr. Barnard found high-carb low-fat diets result in better blood glucose, cholesterol, and more weight loss than the standard diet from the American Diabetes Association. See:

It's best to make this decision about diet with a professional: a dietitian, physician, or certified diabetes educator, since it is so patient unique."

ProudDaddy said...

Evelyn: Knowing your interest in NEFA and considering the quote above about FFA, I am curious about your take on the following study:

Bickerton et al. (incl. Frayn) "Adipose tissue fatty acid metabolism in insulin-resistance men" Diabetologia, 2008

As I interpret the study, we need to be looking at esterified fats rather than NEFA, but as you well know, I've been wrong before (publicly!).

As YOU know, but it can't hurt to remind people, the study of a VLCal diet that was helpful for T2D suggested that pancreatic and hepatic triglycerides might be causing or aggravating the condition.

Evelyn aka CarbSane said...

I blogged a bit on that lecture:
Unfortunately, I'm easily distracted and blog on what floats my boat from time to time. I don't think I ever got around to blogging on one paper I have of his that I remember being revelation-worthy.

ShottleBop said...

@Evelyn: to your knowledge, has anyone ever tried to integrate the results of research conducted with respect to the role of fat metabolism in the etiology of diabetes with the results of research conducted with respect to role of methylglyoxal produced as the result of glucose metabolism? (See, for example, "Chronic methylglyoxal infusion by minipump causes pancreatic beta-cell dysfunction and induces type 2 diabetes in Sprague-Dawley rats," available at, and referring to "high carbohydrate-induced type 2 diabetes" using syntax that would indicate the existence of more than one recognized etiology for type 2, at least one of which is involves the high consumption of carbohydrate.)

Evelyn aka CarbSane said...

The way I see it, the elevated NEFA causes the triglyceride accumulation because fatty acids can traverse cell membranes without transporters. But oil and water don't mix so the "free" fatty acid is "high energy" and "toxic". Much better for the cell's immediate zen state to esterify fatty acids that aren't being oxidized for energy, where they can all glom together in a droplet. That's not a bad thing per se, because conditioned endurance athletes have high muscle triglyceride levels, but in the obese state, it's just a ... well ... clog ;-) The cell tries to keep it's internal house clean but at some point that fat glob in the corner impacts operations. Thinking out loud: More fat than is needed for oxidation goes into the mitochondria that do not oxidize them b/c the energy is not needed and we get mitochondrial dysfunction. When mitochondria are forced to burn fat it backs up carbohydrate metabolism but the hormones tell them to burn carb and slow lipid oxidation. The drain is backing up! Mayhem.

Evelyn aka CarbSane said...

I don't have his book(s?). Does Bernstein discuss EIT for T2's in his books? Encourage newly diagnosed T2's to discuss this with their doctor?

ProudDaddy said...

My only concern is that the study I referenced, as I understood it, was that NEFA was NOT elevated (insulin-resistant vs insulin-sensitive). I suppose it could be theorized that the insulin-sensitive were all destined to be resistant, so NEFA could still be the originating cause... Or I could be misunderstanding something.

Evelyn aka CarbSane said...

Sorry, I accidentally sent you to spam :( I'm looking at Fig 2"d" -- Muscle NEFA uptake. And "It may be that a consistent elevation of NEFA concentrations in obesity occurs only in the presence of type 2 diabetes"

Something's not adding up to me, because fasting trigs according to Hellerstein's extensive works, are largely comprised of FA's from NEFA -- the extracellular (adipocyte) TAG/FA cycle. Seems the muscle is taking up NEFA and the liver is working overtime recycling NEFA in the IR men. Meanwhile, their fat and muscle is not taking up the TG. (Is that how it appears to you?

ProudDaddy said...

Yep, I see the same things in Figs. 2 & 4. What do you think of the authors possible explanation for the difference in this vs. previous studies (namely that this was really the first to compare these things in people of comparable fatness but differing insulin resistance)?

I know we can't discount bias just because the authors say they were surprised, but it helps.

Maybe it was there and I missed it, but I would be curious to know what the TG tissue levels were (hepatic & muscular). (I'm confused as to whether TG levels are inter- or intracellular.)

Re your first (9:40) comment, I hope you're not talking about Bailor's "clog"! (smiley face)

Morris said...

Evelyn said “The way I see it, the elevated NEFA causes the triglyceride accumulation because fatty acids can traverse cell membranes without transporters. But oil and water don't mix so the "free" fatty acid is "high energy" and "toxic"…..When mitochondria are forced to burn fat it backs up carbohydrate metabolism but the hormones tell them to burn carb and slow lipid oxidation. The drain is backing up! Mayhem.
I take the above to possibly suggest that NEFA = “bad”. Please elaborate. Do you mean that NEFA metabolism is less desirable than glucose only in those with disregulated metabolism or in general? If the latter it seems strange that evolution would not favor a more efficient energy process (lower energy to transect the cell and mitochondrial membranes as you say and bypass liver processing altogether). If you mean the latter, can you provide sources?

Evelyn aka CarbSane said...

Yeah, I was joking about the clog :D

As you'll see, I decided to blog on this study.

Re: "I'm confused as to whether TG levels are inter- or intracellular"

You know, I've always wondered this myself. My thoughts are that it has to be intracellular, because "lipid droplets" are organelles in the cells -- the major organelle in a fat cell taking up most of what would be the cytoplasm in other cells.

So in muscle/organs you have lipid droplets growing very large so they appear to be fat cells? Or do adipocytes infiltrate the organ/muscle or differentiate (with lipid transferred to these cells) or does the organ/muscle cell dedifferentiate when its fat load gets too high? It doesn't seem plausible that these lipid droplets exist as something like butter between the cells.

Evelyn aka CarbSane said...

The methylglyoxal comes up here from time to time. I've not come across much independently. So no idea really. To me, there are just too many 80% carb cultures with almost no diabetes to make carb consumption causative.

Evelyn aka CarbSane said...

If we're talking lipid oxidation vs. glucose oxidation being a preferable fuel I have some thoughts on that for a blog post -- hopefully in the near future.

I wouldn't say NEFA are "bad", just that the cells can "refuse delivery" of glucose, but they cannot refuse the NEFA. Similarly their concentration in the cytosol cannot be very high so they must be stored in droplets. When those droplets get large it is reasonable to expect that like the fat cells, there is excessive "release" into the cytosol and then the fatty acids can get into the mitochondria whether they are needed or not, and for lack of a better word "gum up" the works.

Glucose and metabolites OTOH can be regulated more tightly through transporters and membrane surface enzyme complexes.

rodeo said...

From what I remember from Sonksen's paper on insulin and muscle tissue that you sometimes link to the transporters were not the issue but there were always enough transporters even at basal insulin levels to fascilitate glucose uptake and uptake was mostly driven by concentration gradients. I think the same would be true for NEFA, sure the cell can't refuse them but the fatty acids wander back thru the cell membrane as easily as it got there.

Or am I missing something?

Evelyn aka CarbSane said...

Glucose still requires a transporter though. My recent readings indicate that the number of adipocyte transporters declines first (odd that, eh??!!) I'm not sure if it's glucose per se or insulin (perhaps both), but glucose influx into cells stimulates glycolysis, whereas fatty acid delivery does not stimulate fatty acid oxidation TTBOMK.

Fatty acids do traverse passively via a "flip-flop" mechanism, so yes, they should wander back and forth at equilibrium. It is my understanding, however, that esterification "sucks them in". For example in adipocytes, ASP stimulates the rate limiting enzyme in esterification which would be removing NEFA from the cell side so that NEFA liberated outside the cell by LPL would flow in (down gradient) as continuous removal by esterification maintains a high gradient.

So perhaps the high insulin favors esterification of NEFA in the muscle cells so rather than drifting in and out at physiologically acceptable levels, the NEFA are being "removed" by esterification on entry so there's a greater gradient in?

ProudDaddy said...

The simple-minded part of me thinks marbled steak, but I'm guessing the experts are measuring something else when they say IMTG. You're probaby right, but, like with organ TGs, would lipid droplets show up via imaging techniques? Then, there is the question of how they get into the cells. Are they converted to NEFAs in muscle tissue? Etc., etc.

Thanks for blogging on the study. I even understood some of the science!

Evelyn aka CarbSane said...

The lipid droplets are definitely inside the cells. NEFA diffuse in, that which isn't oxidized for energy are esterified for "local storage". That term lipid droplet is misleading. Perhaps an SAT analogy is apt: LD are to cells as adipose tissue is to the body. The LD is not an inert blog as the name would imply. I intended to blog about that over a year ago, but I do get easily distracted by what interests or impacts me from day to day, and that really fell by the wayside.

However a marbled steak looks to me like adipose tissue infiltration of the muscle but I don't know that I've read about adipocyte migration or differentiation of this nature. I'm just pretty darned sure that the marbled fat isn't just fat blobs, but fat inside cells.

When they talk about IMTG it is within the cells. They measure it with a spectroscopic method, NMR if memory serves.

ProudDaddy said...

NMR=MRI=less density if LD present?

So, if serum NEFA isn't different, why would there be more IMTG? Less oxidation/mitochondrial dysfunction, or?

Could I convince you to do the blog about LD? I learn something from every one of your scientific posts.


Karen said...

He may not say to stay in ketosis but at 6carbs for breakfast and 12 each for lunch and dinner it probably is ketosis.

ShottleBop said...

He opens Chapter 16 of the newest (2011) edition of his book, [u]The Diabetes Solution[/u] with a discussion of the benefits of insulin usage:

"Although many patients initially balk at the idea of injecting insulin, you should look at this as an opportunity, no a curse, because insulin injections will increase the likelihood that you can bring about a partial recovery of your pancreatic beta cell function. . . .

If you're afraid of insulin because you imagine that once you start, you'll never be able to stop, you've fallen victim to a common myth. In reality, injected insulin is the best means we have at this writing for preventing beta cell burnout."

(Emphasis in original.) He then goes on to tell the story of Gerald Reaven's study.

He's slso mentioned it several times during his monthly phone teleconferences (free one-hour calls during which he answers questions sent in by readers), and he advocates generally keeping your BGs at 83 or so at all times, using insulin to do so, if necessary.

Evelyn aka CarbSane said...

That's awesome. Perhaps I'll try and have him on my podcast when I get around to doing one (hopefully) ... Too bad this isn't heralded in low carb circles. <- WHY NOT???!!!

His dietary plan is very low carb -- as pointed out by Karen elsewhere and I've read on summaries of his plan on his site, etc. Curious if he mentioned this in previous editions of his book (and why not if he didn't since Reavan's study was quite old).

The need to keep BG's in the 80's sounds arbitrary to me. Normal people do not have an average BG in that range, so why should someone who is semi or totally insulin dependent be even encouraged to achieve that target?

Evelyn aka CarbSane said...

NMR is not MRI but it can detect lipids apparently. I don't think anyone needs understand all of these spectrophotometric analyses -- they all use different wave interferences and/or absorption-or-emissions proflies to see stuff.

Somehow these folks are taking up more NEFA so unless they are burning it all (doubtful), it's getting stored locally.

Hopefully I'll get a chance one day to post on LD. They are rather fascinating actually.

ShottleBop said...

I'm pretty sure that I read the same advice in the 2007 edition of his book, as well (which I picked up in early 2008, a few months after being diagnosed). I don't have that edition handy any more, however, since replacing it with the 2011 edition. I have been listening to his monthly teleconferences since shortly after that, and it has been a consistent message.

Re the 83: many people (including bloggers who generally support his approach to the treatment of diabetes) think that target is too low (and he relaxes it, to 90, for patients with no remaining beta cell capacity, so as to avoid lows). He relates that, when he first set up his practice, shortly after glucose meters were becoming more generally available, visits from medical supplies salespeople were frequent, and he'd always ask the salespeople to demonstrate on themselves. These readings, from young, apparently healthy adults, at a time before the anti-fat message had really set in (or in folks who had grown up mostly before then) seemed to cluster around 83. This is an excerpt of an interview that can be read at

"Now how on earth did I get such an odd ball number like 83? I got it because we used to be located on a major thoroughfare, and we had a sign outside that said diabetes center. All of the meter salesmen would stop by and want to demonstrate their meter. And I would say, “Yeah, I have had enough finger sticks today. It’s your turn.” So we would stick their finger. And what would we get? It was amazing. People in their twenties and thirties all were around 83. And I said, “My God, that must be what a normal blood sugar must be.” That was before the days when they started hiring diabetics. Most of the pump companies nowadays hire diabetics.

Since that time, I have looked at the epidemiologic studies. It looks like the cut off point for mortality and heart disease is around 85. Those above 85 have higher relative risks of overall mortality and also cardiac risks. So it looks like what I happened on by chance is pretty close to the cut-off point that the epidemiologic studies show."

ShottleBop said...

A link to this article, published last September in "Diabetes in Control", showed up on one of the diabetes forums just yesterday:

"Early Use of Insulin to Improve Beta Cell Preservation."

Conclusion: "Insulin possesses the unique ability to correct majority of the reversible factors contributing to the inexorable decline of beta cell function in the natural history of type 2 diabetes. Early initiation of insulin addresses the issues of glucotoxicity, lipotoxicity, inflammation, first phase insulin response, insulin resistance and many other factors. Backed by solid pathophysiological rationale and evidenced by animal and human studies, it sounds prudent to shift the paradigm of insulin administration in type 2 diabetes from one of ‘last resort’ to ‘first assault’."

Early use of insulin does pop up in discussions on diabetes forums from time to time; many folks report, however, that their doctors refuse to prescribe insulin for people who have A1cs lower than a number that is higher than many people present with.

LeonRover said...
This comment has been removed by the author.
LeonRover said...

"Early use of insulin does pop up in discussions on diabetes forums from time to time; many folks report, however, that their doctors refuse to prescribe insulin for people who have A1cs lower than a number that is higher than many people present with."

There are very few Bernstein-following diabetologists, endocrinolists or MDs.

Early Insulin Therapy for Type 2's is just not on the cards.

UNLESS one can afford to pay for Private Consultations at high hourly rates, and for the frequent OGTTs, OGTTs combined with insulins, HbA1Cs and put up with the difficulty of actually finding that specialist.


Evelyn aka CarbSane said...

Sorry I got so backlogged on comments lately gang. First, below I am posting for oolong who had trouble commenting here and posted on the discussion boards:

oolong writes:

For some reason, I can't make comments on your blog section. Regarding Dr. Bernstein -- although like Dr. Rosedale, he advocates is a moderate protein, very low carb, high fat diet -- Bernstein differs in that as someone posted, he thinks early type 2's can be helped by insulin to preserve beta cell function. He also differs from Rosedale in that Bernstein believes truly normal A1Cs should be in the 4s. He says blood glucose should be between 80-90 at all times -- before, during and after eating. Many on Bernstein's forum boards cannot achieve an A1C in the 4s despite eating his strict 6-12-12 plan. For those, he advocates meds or insulin depending upon c-peptide, insulin, glucose and whether the person is overweight or not. Rosedale is more lenient on carbs but equally strict on protein restriction to "moderate" amounts -- 1 gram per kilogram of bodyweight -- but no counting of acceptable carbs -- non-starchy veggies plus "good" fats. Despite this strict program, Rosedale says he rarely sees people get in the A1C of 4s and doesn't agree that someone should take insulin or meds just to get to that target. His book does not use that low of a target. Bernstein states that he arrived at his range of normal based on the blood work of the salespeople selling the glucose meters. They would invariably have bloods sugars of around 80 to 85. I find this unconvincing as most of these sales people are young and slender ( I could eat total crapola in my twenties and even early 30s still have excellent blood glucose). He admits his def of normal is somewhat arbitrary but says those "non-diabetics)" with A1Cs in the 5s often have diabetic complications. If I'm very strict and cut out all fruit -- I can get my A1C to 5. No way am I convinced I need to take meds to push it further and no way am I convinced that 5 is somehow better than 5.5 or even slightly higher for the general population. Because of my family history, I prefer to keep it at or below 5.5 -- preferably around 5.1. I just listened to Dr. Bernstein's free telephone seminar this week and he stated that when he makes a mistake and his glucose rises to 100 or 110 -- he feels tired and thirsty. So you see, he has lower targets for everyone. I would venture that with his definition of normal blood sugar -- nearly the entire population over the age of 40 would be declared a diabetic. Other low carb experts/advocates say the literature claims organ damage with prolonged blood glucose of 140 or over -- operative word in my mind is prolonged -- not the spikes one would expect to see after drinking a Slurpee. So most advocate keeping fasting glucose under 90 and post-prandial under 120 for leeway. Bernstein clearly differs.

Re: insulin to preserve beta cell function. I think Jenny Ruhl has something on this at her site -- that over the long haul, this didn't seem to be the case. Nothing works for everyone -- might be worth a shot if someone was so inclined -- but I think diabetes is complicated (my mom was obese type 2; dad was thin type 2) -- so treatment must be individualized. Fat chance of that happening any time I'll stick to low carb until something better comes along.

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