Diabetes Treatment: New Dogma, Old Dogma or Just Carbophobic Myopia?

One of the points of contention raised in my brief exchange with Dr. Ron Rosedale over on the PaleoHacks forum is the notion that insulin is a harmful drug, and that diabetes should not be treated with insulin to "cover" dietary glucose.  This will only make the diabetic sicker and move them down the path of progression of their disease.   This reminded me of the flurry of blog hit pieces on the ADA's Hope Warshaw a while back.  One of the things these bloggers took special exception to was Warshaw's use of the term dogma and calling LC "old" dogma.  For starters:

Old Dogma: Losing weight will make blood glucose levels plummet no matter how long you have had type 2 diabetes. The message that people continually hear from their providers is "If you'd only lose weight, your blood glucose would go down." And the common reply from people with type 2 is "I'll try harder with my 'diet' over the next few months, but please don't put me on a diabetes medication."

New Reality: Research shows that the greatest impact of weight loss on blood glucose is in the first few months and years after diagnosis. (Read the Look AHEAD trial results, a study about the effect of weight loss on heart disease in type 2 diabetes.) In fact, the biggest bang for the effort per pound is likely in the prediabetes phase. (The sad fact is that most people don't know that they have prediabetes.)Large studies have shown that with loss of five to seven percent of body weight (approximately 10 to 20 pounds) and 150 minutes of physical activity (30 minutes five times a week), people can prevent or delay the progression to type 2. Once insulin production is on a dwindling course (particularly after 10 years with type 2), weight loss has less impact on glucose control.

There's absolutely nothing wrong with this part of her writings.  It is true, that the earlier the intervention, the more likely the disease can be reversed.  I do find her "reality" unduly defeatist, because one would imagine that the morbidly obese tend to have fairly long-standing diabetes, and yet gastric bypass surgery restores proper glucose metabolism in a surprisingly high percentage of patients.   Still, that bolded part (my emphasis) of her comments is a sentiment you hear all too often in low carb circles.  Why just this disease?  If one reads about low carb forums like Jimmy's, Active Low Carbers or Low Carb Friends, it doesn't take long to get the impression that a surprisingly high percentage of the participants are on some medication or other for something that may or may not be related to their weight and diet:  thyroid meds, blood pressure meds, antidepressants, etc. etc.  And yet many of these same folks will resist going on any diabetes medications even if they are unable to do what they think is the right thing -- avoid all carbs in all perpetuity -- for this condition.      No insulin or insulin secretagogues for these folks!  This is the sad legacy of the Taubesian demonization of insulin.  I'm going to address this issue in a future post.  For now, Warshaw continues:  

Old Dogma: People with type 2 diabetes should follow a low carbohydrate diet.

New Reality: Nutrition recommendations for people with type 2 diabetes from the American Diabetes Association and other health authorities echo the recently unveiled U.S. 2010 Dietary Guidelines (1/31/11) for carbohydrate: about 45 to 65 percent of calories. (Americans currently eat about 45 to 50 percent of calories as carbohydrate--not a "high carb" intake.)

Countless research studies do not show long term (greater than six months to a year) benefit of low carb diets on blood glucose, weight control, or blood fats. People with type 2 diabetes, like the general public, should lighten up on added sugars and sweets (yes, they're carbohydrate). They should eat sufficient amounts of fruits, vegetables, whole grains, and low fat dairy foods--all healthy sources of carbohydrate.

If one substitutes "safe starches" for whole grains, and perhaps drops the obligatory "low fat" from the dairy recommendation, this is not so far off what many, many who consider themselves paleo-inspired or ancestral-styled in their diets.  But calling low carb old dogma??  How dare she!!  Low carbers are  the avant garde thinkers of nutrition world!  They're too smart to fall for conventional wisdom!!    Diabetes is a disease of glucose intolerance, how stupid is Hope to suggest we give diabetics more of what they are intolerant of!  That's downright criminal ... it would be like giving gluten to a celiac, peanuts to a kid with a severe allergy.  Heck, to a diabetic all carbs are poison!   You see Hope, her minions at the ADA and all of those doctors and researchers in Big Pharma really just want to keep you sick.  That way they can sell you their books and medications.  This is different from, say Mark Sisson with his Contest Giveaways, hawking of supplements and all manner of (pricey, some might say overpriced) PB stuff, and engaging the likes of Jimmy Moore to help push PB to #1 on Amazon, exactly how?  But I digress ...

One of the more amusing ironies in all of this is the oft-heard canard:  "Before the discovery of insulin, they treated diabetics with a low carb diet".   If that's not OLD, I don't know what is.  And ummm ... How many analogies can we make here for replacement of "treatments of necessity" -- from when we didn't know the cause or have full knowledge of the mechanisms -- with modern life-saving treatments?  Before the discovery of insulin, diabetics didn't live very long either, but ...  Point being, as McGarry discusses in his (GCBC cited) masterpiece What if Minkowski Had Been Ageusic -- An Alternative Angle on Diabetes, diabetes is really not a disease of glycemic disorder, glycemic disorder is the manifestation of an underlying dysregulation in fat metabolism.  In that article, as I've discussed previously,  McGarry "wonders" over what different paths diabetes research and treatment might have taken were glucosuria, the spilling of glucose into urine that accompanies severe hyperglycemia, not the discovery of Minkowski.  Ageusics lack a sense of taste, so as legend had it, Minkowski tasted the urine of his pancreatized dogs and diabetes became synonymous with hyperglycemia.

I have presented abundant evidence on this blog, backed by the research of Edwin Bierman, J. Denis McGarry, Keith Frayn, and Guenther Boden, that "diabetes" as we know it, begins with a defect in the fat tissue metabolism ... the hyperglycemia we associate with diabetes is a symptom, not the cause.  I've blogged previously, Diabetes ~ A Disease by any other Name?, that perhaps we need to shelve the term "diabetes" and come up with more specific diagnoses/names for the various causes of hyperglycemia.   Early detection screenings might then target metabolic markers of dysfunction present far earlier in the progression of the disease.

One simply cannot read the research of that quartet of giants in the field and come away with the conclusion that carbohydrate consumption causes diabetes.  There is simply no evidence to support the notion that diabetics have exhausted their genetically susceptible pancreata.  Using insulin does not cause dysfunctional insulin secretion.  Using insulin does not cause resistance to it.   Now as I discussed in Glucose and NEFA: From Dysfunctional Metabolism to Toxicity, in agreement with the aforementioned researchers, it is the inability of fat tissue to contain free fatty acids that appears to be the initiating factor in the cascade.  Indeed there's some evidence now emerging that the defect is first evident on the uptake side of the equation, even before the fat cells lose their ability to constrain the fatty acids appropriately in their stores.  

In this regard, rather than promote insulin resistance, carbohydrate consumption should promote sensitivity.  Indeed it does ... and most of TWICHOO even supports this ... all except the part where anything that increases insulin causes insulin resistance. Think about it, it's rather ironic, but insulin serves to trap your fat in fat cells. This is what the diabetic wants!!  Here is where someone will jump on me and ask if I wish to suggest that a diabetic should eat even more carbs.  Here's the problem with that strawman ... define "more" ... more specifically, define the context.  For sure eating a ton of carbs in the context of a surplus energy SAD is detrimental, and adding more carbs on top of that without reducing something else (e.g. fat) is not prudent and will most certainly turn a bad situation worse.  But we could just as easily say the same for adding more butter or even coconut oil to a SAD.  

But there's quite a bit of evidence that dramatically increasing carbs, commensurate with decreasing fat, actually improves the situation for diabetics and sometimes even reduces their need for medications.  Yes, I did just write that. How can that be?  More carbs would require more insulin for a diabetic to "cover".  This is going to drive their blood sugars through the roof CarbSane!   Some responders to Jimmy Moore's query about safe starches were willing to concede that starch may be safe for us metabolically normal to consume, but remain steadfast that starch is unsafe for those with deranged metabolisms.   

Improved Glucose Tolerance with High Carbohydrate Feeding in Mild Diabetes

To evaluate the effect of increased dietary carbohydrate in diabetes mellitus, glucose and immunoreactive insulin levels were measured in normal persons and subjects with mild diabetes maintained on basal (45 per cent carbohydrate) and high carbohydrate (85 per cent carbohydrate) diets. Fasting plasma glucose levels fell in all subjects and oral glucose tolerance (0 to 120-minute area) significantly improved after 10 days of high carbohydrate feeding. Fasting insulin levels also were lower on the high carbohydrate diet; however, insulin responses to oral glucose did not significantly change. These data suggest that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin.

Metabolic effects of high-carbohydrate, high-fiber diets for insulin- dependent diabetic individuals

The metabolic effects of high-carbohydrate (70%), high-fiber (70 g) (HCHF) and low-carbohydrate (39%), low-fiber (10 g) (LCLF) diets were examined for 10 subjects with insulin-dependent diabetes mellitus (IDDM). After a l-wk control period subjects on a metabolic ward were randomly allocated to HCHF or LCLF diets for 4 wk. After a 6-wk washout period subjects re-entered the metabolic ward for 4 wk on the alternate diet. Artificial-pancreas studies were performed on each diet for measurement of insulin requirements. Compared with the LCLF diet, the HCHF diet reduced basal insulin requirements (P < 0.025), increased carbohydrate disposed of per unit insulin (P < 0.0008), and lowered total (P < 0.0004) and high-density-lipoprotein cholesterol (P < 0.00 1 3). Glycemic control and other lipid fractions did not differ significantly. These results suggest that in IDDM patients, HCHF diets enhance peripheral glucose disposal, decrease basal insulin requirements, and lower total cholesterol without altering glycemic control or triglycerides. 

Diets rich in natural fibre improve carbohydrate tolerance in maturity-onset, non-insulin dependent diabetics

The influence of low and high fibre diets upon carbohydrate tolerance was examined in five maturity-onset, non-insulin dependent diabetics. After 14 days on a diet rich in natural fibre (30g/ day), the subjects consumed a high fibre (13 g) test meal. They then ate a low fibre diet (10 g/day) followed by a low fibre (1 g) test meal. Mean basal plasma glucose concentrations were similar after both fibre diets; however, both mean basal plasma. insulin and gastric inhibitory polypeptide (GIP) were significantly lower after the high fibre diet. Affer the high fibre test meal, significantly lower mean plasma glucose, insulin and GIP concentrations were measured. This study is the first study to demonstrate the ability of an institutionally supervised diet of natural foodstuffs rich in fibre to improve carbohydrate tolerance in maturity-onset, non-insulin dependent diabetics. This finding is relevant to the dietary management of diabetics.

 High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus

The effects of high-carbohydrate, high plant fiber (HCF) diets on glucose and lipid metabolism of 20 lean men receiving insulin therapy for diabetes mellitus were evaluated on a metabolic ward. All men received control diets for an average of 7 days followed by HCF diets for an average of 16 days. Diets were designed to be weight-maintaining and there were no significant alterations in body weight. The daily dose of insulin was lower for each patient on the HCF diet than on the control diet. The average insulin dose was reduced from 26 ± 3 units/day (mean ± SEM) on the control diets to 11 ± 3 (P < 0.001) on the HCF diets. On the HCF diets, insulin therapy could be discontinued in nine patients receiving 15 to 20 units/day and in two patients receiving 32 units/day. Fasting and 3-hr postprandial plasma glucose values were lower in most patients on the HCF diets than on the control diets despite lower insulin doses. Serum cholesterol values dropped from 206 ± 10 mg/dl on the control diets to 147 ± 5 (P < 0.001) on the HCF diet; average fasting serum triglyceride values were not significantly altered on the HCF diets. These studies suggest that HCF diets may be the dietary therapy ofchoice for certain patients with the maturity-onset type of diabetes. 

A HIGH CARBOHYDRATE LEGUMINOUS FIBRE DIET IMPROVES ALL ASPECTS OF DIABETIC CONTROL

In a randomised cross-over study 18 noninsulin-dependent (NIDDM) and 9 insulindependent (IDDM) diabetics were put on to a high carbohydrate diet containing leguminous fibre (HL) for 6 weeks, and also a standard low carbohydrate diet (LC) for 6 weeks. During two identical 24 h metabolic profiles mean preprandial and mean 2 hour postprandial blood glucoses were significantly lower on HL in both groups, as were also several overall measures of diabetic control, including the degree of glycosuria. Total cholesterol was reduced significantly on HL in both groups, and the HDL/LDL cholesterol ratio increased significantly on HL in the NIDDM group. A diet high in complex carbohydrate and leguminous fibre improves all aspects of diabetic control, and continued use of a low carbohydrate diet no longer appears justified.

The above is just a sampling.  Low carbers often smugly refer to comparisons of LC to LF diets and say that the researchers or those making dietary recs are stupid to suggest that the diets are simply not low enough in fat.  Perhaps this is not so stupid after all.  Because the percentage of carbs in these diets is often higher than the 65% target Warshaw advocated, and in the range of 70-85%.  We're talking traditional Pima and Kitivan  terroir here.  Yes, those Pima, despite what Taubes would have you believe, their traditional diet was ~70–80% carbohydrate, 8–12% fat, and 12–18% protein.  What we see going on, when culture after traditional culture is exposed to the "Western Diet" is an increase in fat consumption and a decrease in carbohydrate consumption (at least as a percentage of energy calories), and an increase in obesity and diabetes.  Does this mean fat is fattening and sickening?  No.  Nor, in my book does it absolve carbohydrates of all nature.    Still ... if we're looking to ancestral solutions to a modern problem, starch may well be the answer.

It seems that if the standard "diabetes diet" advocated by the ADA is failing, this may be because ultimately it does not go far enough in terms of cutting fat.  Consider that many consider a diet to be low fat with as high a threshold as 30% of energy, and a protein sufficient diet around the 75% carb level is necessarily only 10-15%  fat.   

To sum up as regards the title of this post, as it turns out LC is the old dogma.  It's an old dogma that so-called revolutionaries would have you believe is now cutting-edge science bucking the mainstream.  The cited studies are but a smattering of what one will find as regards the causes of insulin resistance and diabetes and diet.  I think that viewing diabetes merely as hyperglycemia is the true "old dogma".   Focus on hyperglycemia is myopic and leads to erroneous oversimplifications that fasting and postprandial glucose and insulin levels are solely related to the quantity of dietary glucose.  That is simply not true.

Of course glycemic control is paramount for the diabetic, but as paradoxical as it sounds, a strong case can be made for eating more carbohydrates to that end.  This is clouded by those who "try" to follow an ADA diet that is nothing more than an attempt to lose weight on SAD-lite.  One thing that is clear, the reversal of T2 seems to necessitate extreme measures.  Be it the crash diet, or VLC, or VLF or gastric bypass, verifiable dramatic turnarounds have been reported.  

It may not be that the Perfect Health Diet is best for reversing diabetes in diobesetics, but this diet should be excellent in maintenance of a transforming intervention.  Still, I can see no way that a SAD to PHD conversion would not usher in some health improvements.   That there should be any concern that it would be unsafe for someone to try is ludicrous in my opinion.

There can be no denying that VLC diets perform very well for reversing diabetes, but they don't really work in the long run.  Oh sure, for most, if they remain very low to zero carb, their hyperglycemia will remain largely controlled.  Yet many of these people (see, for example Tom Naughton's reply to Jimmy's initial query) who were never diabetic, have essentially succeeded at turning themselves so.  The common retort to that seems to be a lot of rationalizing about the "good" kind of  "physiological insulin resistance" and how if you never eat carbs who needs proper GSIS anyway?  Well, for one, insulin is instrumental in amino acid transport.  Is the "up the fat" movement in LC circles making matters even worse for those who would otherwise retain some signalling if not consciously limiting protein?  (I believe Paul and I have some differences over protein content in the diet where he seems to favor more limits.)

In any case, I don't believe there is any such thing as "good" insulin resistance.  The glucose-sparing sort in fasting and starvation is a defense mechanism.  Of course it is ultimately beneficial to the human in that context, but that doesn't make starvation a beneficial state.  If you had a choice between no food and Happy Meals for several weeks, the meal would be more beneficial, but that doesn't make Happy Meals good for you.  So in this regard, a person with impaired insulin signaling -- even if they don't "need" it -- is at least rolling the dice that it is not impacting them otherwise given the myriad roles insulin plays in our bodies.

I remain a huge fan of VLC diets for weight loss.  The more I delve into the science, however, the less convinced I become that it is even advised in maintenance, let alone optimal.