The folly of the American Diabetes Association’s dietary recommendations

            An eminent diabetologist, Dr Ralph DeFronzo, described the deterioration into diabetes in the Lilley Lecture of 1987, the pre-eminent forum of accumulated medical wisdom and insight:


               … there are two primary defects responsible for the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM).  In some NIDDM patients the primary defect starts at the level of the β-cell and manifests itself as an impairment in insulin secretion; these individuals are represented by the lean diabetic patient.  In other NIDDM patients the primary defect starts as an impairment in tissue (muscle and liver) sensitivity to insulin; these individuals are represented by the obese diabetic.  However, whichever defect – diminished insulin secretion or insulin resistance – initiates the development of NIDDM, it will subsequently lead to the emergence of the second abnormality (DeFronzo 1987).


            Dr DeFronzo’s first category includes insulin-dependent diabetics who have no β-cells, and are generally lean and sensitive to insulin, at least initially.  But what he describes is startling: whether there is diminished insulin secretion or insulin resistance, the second abnormality will emerge.  The insulin-deficient become insulin-resistant and the insulin-resistant become insulin-deficient!  Then, in both cases, high blood sugar becomes an agent of further destruction and it’s startling to learn that high blood sugar is almost universal in the diabetic population receiving medical care:


               … there appears to be abundant evidence from both animal and human studies that sustained chronic hyper-glycemia can lead to the development of defects in both insulin secretion and insulin action.  Furthermore, it appears that these deleterious effects of hyperglycemia are mediated by downregulation of the glucose transport system. Recognition of the important pathogenetic role of hyperglycemia per se in the evolution of NIDDM has important therapeutic implications.


               Over the last decade, we have performed oral glucose (100-g) tolerance tests (OGTT) in many normal-weight NIDDM subjects.  All subjects had fasting hyperglycemia (mean ± SE 148 ± 8).  After glucose ingestion, the plasma glucose concentrations were >200 mg/dl at all time points …



            Yet, inexplicably, only completely out-of-control diabetics are treated so as to achieve normal blood sugars:



               Thus, in the poorly controlled diabetic with fasting plasma glucose levels >200 mg/dl it seems reasonable to institute a short course of intensive insulin therapy (4-6 wk) or severe caloric restriction (10-14 days under close supervision by a physician) to restore normoglycemia and reverse the deleterious effects of hyperglycemia on cell function (DeFronzo 1987).



            The treatment suggested to all diabetics is the low-fat American Diabetes Association diet, yet this diet causes the hyperglycemia which eventually makes all diabetics both insulin-dependent and insulin resistant!  There is no doubt that this is still the case today, in spite of treatment with insulin-stimulating sulfonylurea drugs and the insulin-sensitizing drug metformin.  The findings of the UK Prospective Diabetes Study included that:


               The study showed an initial increase in β-cell function (from 46 to 78%) at 1 year in subjects on a sulfonylurea, followed by a steady decline in function to 52% at 6 years.  Subjects on diet only (n = 486) exhibited a gradual decline in β-cell function of ~ 4% per year.  Insulin sensitivity only changed in subjects on metformin (n ~ 159), increasing from 51 to 62% at 1 year and remaining at 62% at 6 years (Wallace 2004).



            In other words, the American Diabetes Association diet alone destroys β-cells at the rate of about 4% per year, and the diet plus a sulfonylurea drug improves β-cell performance initially but then destroys them at a rate near 5% per year.  At these rates, diet alone will destroy all β-cells in 11 years, while diet plus a sulfonylurea drug will destroy them in 16 years. 


            Furthermore, physicians are slow to treat high HbA1c levels in the way that Dr DeFronzo suggested way back in 1987.  At the 2006 Scientific Sessions of the American Diabetes Association, we learned that:


            The majority of patients with Type 2 diabetes have very high HbA1c levels, and it takes physicians months before they intensify oral antidiabetic therapy … a study of 9,416 patients … [showed that] Mean HbA1c was 8.4% at baseline when therapy was initiated.  Only 33% had levels at or below the ADA goal of 7%, and 67% had A1c levels approaching 10% (Kerr 2006).



            That Dr DeFronzo’s prescription of caloric restriction is effective was demonstrated in a study of obese, hyperglycemic diabetics.  “Severe” caloric restriction quickly lowered their fasting blood sugar from 326mg% (!) to 150mg%, and their β-cells showed significant recovery (Stanik 1980).  However, a similar study showed that subjects with diabetes of less than two years duration responded far better than subjects who’d had diabetes for more than five years: caloric restriction brought the less-than-two-year diabetics down to 119mg%, but the more-than-five-year group averaged 175mg% (Nagulesparan 1981), for the reason that chronic hyperglycemia had killed more β-cells in the diabetics of long standing.


            β-cells are not the only cell type to be damaged by high blood sugar, and the Diabetes Control and Complications Study showed that this damage causes the diabetic complications of blindness, cataracts, heart attack, stroke and the amputation of limbs.  An exacting study has described the relationship between high blood sugar and the risk of various complications (Stratton 2000):


            The graph at bottom left shows that risk of amputation or death from peripheral vascular disease doubles between an HbA1c of 5.6% (like mine) and the low end of “tight control” at 7%.  But recall that “67% [of Type 2 diabetics] had HbA1c levels approaching 10%” (Kerr 2006), and we see that the risk for these people is more than 10 times higher.  But anyone who’s prepared to avoid sugars, starches and starchy vegetables can maintain an HbA1c of 5.6% like mine. 


So why does the ADA advocate a low-fat diet?   

            It’s a mystery. 


            Ancient studies showed insulin sensitivity increases with increase of carbohydrate in the diet (Himsworth ), but other studies demonstrate that cells remodel themselves to burn the proportion of carbohydrate and fat in the diet, so insulin sensitivity will inevitably be “worse” in cells adapted to burning fat (). 


            The hoary old knee-jerk fear that fats promote heart disease must play a part.  This fear, implicit and unquestioned in the preamble of every low-fat diet study, is, in fact, irrelevant.  Diabetic complications rob the diabetic of vitality, the enjoyment of life, and eventually of life itself; it is the “macrovascular complication” of heart disease which kills most diabetics.  Hyperglycemia accelerates the development of macrovascular complications, so prescribing a diet which guarantees hyperglycemia in the interests of avoiding heart disease is a protracted oxymoron.  This deadly error causes the complications of diabetes which are, then, iatrogenic diseases, caused by the “Medical Nutrition Therapy” prescribed to treat it.  The lesson of my experience is crystal clear and unequivocal: avoid carbohydrates, avoid hyperglycemia.


            Numerous studies in the medical literature agree that treating insulin-resistant conditions with a low-fat, high-carbohydrate diet worsens features of metabolic syndrome (Gerhard 2004); and the Insulin Resistance Atherosclerosis study established that 92% of Type 2 diabetics are insulin resistant (Haffner 1999).  The prestigious American Association of Clinical Endocrinologists (AACE) goes so far as to say: “Of greatest importance is the avoidance of low fat-high carbohydrate diets unless weight loss is also occurring.  The more insulin resistant an individual is, the more insulin they must secrete in order to maintain normal glucose homeostasis, as a consequence, in the absence of weight loss, manifestations of the Insulin Resistance Syndrome will be accentuated when insulin resistant persons increase the amount of carbohydrates in their diet (50)” (AACE on IRS). 


            Even insulin-sensitive people don’t do that well on such diets.  Dr Gerald Reaven fed 10 healthy post-menopausal women either 60% or 40% carbohydrate diets.  The higher carbohydrate level worsened insulin resistance and elevated unhealthy blood fats: “Because these changes would increase risk of ischemic heart disease in postmenopausal women, it seems reasonable to question the wisdom of recommending that postmenopausal women consume low-fat, high-carbohydrate diets” (Jeppesen 1997).  And these were healthy women. 


            When Dr Reaven made a similar experiment in Type 2 diabetics, he found the same adverse changes.  He compared the 20% fat, 60% carbohydrate ADA-pattern diet which included 10% of calories as sugar, as the ADA diet allows, with a diet containing 40% fat and 40% carbohydrate, and found that:


               Although plasma fasting glucose and insulin concentrations were similar with both diets, incremental glucose and insulin responses from 8 a.m. to 4 p.m. were higher (p<0.01), and mean … 24-hour urine glucose excretion was significantly greater (55 … versus 26 … g/24 hours p<0.02) in response to the low-fat, high-carbohydrate diet. In addition, fasting and postprandial triglyceride levels were increased (p < 0.001 and p < 0.05, respectively) and high-density lipoprotein (HDL) cholesterol concentrations were reduced (p<0.02) when patients with NIDDM ate the low-fat, high-carbohydrate diet … These results document that low-fat, high-carbohydrate diets, containing moderate amounts of sucrose, similar in composition to the recommendations of the ADA, have deleterious metabolic effects when consumed by patients with NIDDM for 15 days. Until it can be shown that these untoward effects are evanescent, and that long-term ingestion of similar diets will result in beneficial metabolic changes, it seems prudent to avoid the use of low-fat, high-carbohydrate diets containing moderate amounts of sucrose in patients with NIDDM (Coulston 1987).



            In other words, they did better on the lower carbohydrate diet and got worse on the ADA-pattern diet; but both diets provoked “glycosurea”, the spilling of sugar in the urine, which means that both diets elevated blood sugars far beyond the normal range into the territory where kidney deterioration and progression of the other diabetic complications is inevitable.


            Similarly, Dr Arbhimanyu Garg performed a similar study in 42 Type 2 diabetics and found that, “In NIDDM patients, high-carbohydrate [55% carbohydrate, 30% fat] diets compared with high-monounsaturated fat [40% carbohydrate, 45% fat] diets cause persistent deterioration of glycemic control, as well as increased plasma triglyceride and very low density lipoprotein levels, which may not be desirable” (Garg 1994). 


            There are dozens of such studies, and their results are consistent: higher carbohydrate diets cause deterioration of diabetic control and elevation of heart risk factors, while lower levels of carbohydrates improve all aspects of the condition and lower risk factors for heart disease.  Yet the ADA advocates a low-fat, high-carbohydrate diet for Type 2 diabetics.


The ADA’s rationale for a high-carbohydrate diet

            The ADA advice for diabetics goes like this:


               The message today: Eat more whole grains!  Whole grains and starches are good for you because they have very little fat, saturated fat, or cholesterol.  They are packed with vitamins, minerals, and fiber.  Yes, foods with carbohydrate -- starches, vegetables, fruits, and dairy products -- will raise your blood glucose more quickly than meats and fats, but they are the healthiest foods for you.  Your doctor may need to adjust your medications when you eat more carbohydrates. You may need to increase your activity level or try spacing carbohydrates throughout the day.

               On average Americans eat around 40-45% of our calories as carbohydrate.  This is a moderate amount of carbohydrate, not high.  Currently some controversy about carbohydrates is raging due to a few new diet books. These books encourage a low carbohydrate, high protein and moderate fat intake.  These diets are not in synch with the American Diabetes Association nutrition recommendations, which are based on years of research and clinical experience.  In addition, these trendy diets are hard to follow year after year.

               A way to see how carbohydrates affect your blood glucose is to monitor your blood 1&1/2 to 2 hours after meals. Checking your blood glucose at this point tells you how high your blood glucose went from the carbohydrates you ate. For good diabetes control, keep your after-meal blood glucose levels at 180 or below (ADA Diabetes Food Pyramid FAQ).



            In other words, forget the Zone (40% carbohydrate) and South Beach (45% carbohydrate) diets, go for maximum carbohydrates!  But there are troubling questions about the effectiveness of this approach for weight loss: “overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN [very high carbohydrate] diets” (Gardner 2007).  More troubling questions arise over the effects of the high-carbohydrate diets on lipid profiles:

Table. Changes From Baseline at 12 Months*






Weight, kg





LDL, mg/dL





HDL, mg/dL










Systolic BP






*LDL, low-density lipoprotein cholesterol; HDL, high-density lipoprotein cholesterol; and BP, blood pressure.
Source: JAMA. 2007;297:969-977.

            In an interview, the researcher, Dr Christopher Gardner, remarked that "After all those [statistical] adjustments... everything that was still significant favored Atkins, more weight loss than Zone, better triglycerides than Zone, better HDL than Ornish, better blood pressure than all three … there is something really interesting, I think, about carbohydrates and the emphasis really seems to be on cutting back those simple carbs" (Lie 2007).


The science behind the recommendation …

            In the ADA’s most recent summary of the research underlying their nutritional recommendations is their Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications (Franz 2002), there is not a shred of high-quality research evidence cited in support of their opinion that “Carbohydrate and monounsaturated fat should together provide 60–70% of energy intake”, certainly no randomized controlled clinical trials which are the gold standard among research studies.  It is the consensus opinion of the ADA Expert Panel.  The only high-quality evidence cited relates to how destructive very high carbohydrate diets are!


            In their current update, Nutrition Recommendations and Interventions for Diabetics (ADA 2006), they add their opinion that “Low-carbohydrate diets (restricting total carbohydrate to <130g/day) [about 25% of calories in a 2000 calorie diet] are not recommended in the treatment of overweight/obesity  … [or] diabetes”, and cite the Institute of Medicine’s Dietary Reference Intakes: Carbohydrate, Fiber, Fat etc. (IOM DRIs), in which it is made clear that the amount of glucose necessary to power the obligate glucose-consuming tissues like the brain and blood cells is about 130 grams.  But this is a specious rationale!  By definition, RDAs are for healthy people, being “the average daily dietary nutrient intake level sufficient to meet the nutrient requirement of nearly all (97 to 98%) healthy individuals in a particular life stage and gender group” (p 22).  Diabetics are not healthy people.  My experience is that carbohydrates are a metabolic poison for me, and, moreover, a poison which steadily worsens the condition, and that 130 grams per day is far too much; my diet contains nearer 30 grams/day, or 6%.


            A second difficulty with this citation is that the Institute of Medicine is at pains to point out that the absolute requirement for carbohydrates in human nutrition is actually zero, “provided that adequate amounts of protein and fat are consumed”, but they wish to err on the side of caution because although various populations thrive on very low carbohydrate diets, “a comparison with populations ingesting the majority of food energy as carbohydrate has never been done” (p 275).  This isn’t scientific evidence, it’s an opinion.  We think that you should eat lots of carbohydrates, and the scientific evidence is, er, other people think the same thing.  It’s a different world, in which there is resort to Aristotelian logic as though Francis Bacon had never formulated the scientific method.  We reason what should be, and then assert it.  And where, as Bacon put it: “For what a man had rather were true, he more readily believes.”  Without a doubt, we have followed Alice down the rabbit hole!


            A close reading of the material intended for medical professionals gives implicit approval to a 25% carbohydrate diet, but the material intended for the public says: go all-out for carbohydrates.  The material intended for medical professionals acknowledges the destructive potential of high carbohydrate diets, but the material intended for the public says no such thing.  Is this because the ADA feels the public can’t be trusted to make their own decision if given the facts?  Or is it because it would piss off major contributors such as General Mills and Cadbury-Schweppes?


            The ADA go on to justify the presence of carbohydrates in the diabetic’s diet: “An important reason for not recommending low-carbohydrate diets is that they eliminate many foods that are important sources of energy, fiber, vitamins, and minerals and are important in dietary palatability.”  About 80% of diabetics are overweight or obese at diagnosis, so the ADA’s concern about energy intake is puzzling.  As to palatability, de gustibus non est disputandum – matters of taste cannot be debated.  To evaluate the importance of starchy foods as sources of fiber, vitamins and minerals, I used the USDA National Nutrient Database to discover the amounts of nutrients in a representative group of starchy foods – potatoes, peas and carrots, oatmeal and un-enriched whole-grain bread (less 10% for the sugar in the ADA diet) – and an equal number of calories from low-starch group foods I’ve replace them with in my diet: almonds, eggplant, asparagus and bell peppers.  There was 35% more fiber in the low-starch group.  Minerals were between 3.94 (calcium) and 1.33 (copper) times higher, while sodium (0.07), iron (0.68) and selenium (0.2) were lower; but lower is better where sodium is concerned, and copious amounts of iron and selenium are supplied by red meat and salmon, respectively.  Vitamins were between 34 (vitamin E) and 1.4 (B1) times higher in the low-starch group, but B6 (0.7) and vitamin A (0.5) were lower; again, salmon is a rich source of vitamin B6, and eggs supply abundant vitamin A.  The claim that we may suffer deficiencies without high-carbohydrate foods is absurd because high-carbohydrate foods actually have lower ratios of nutrients to calories than do low-starch foods.


            That this prescription makes high blood sugars inevitable is implicit in the advice from the ADA FAQ: “For good diabetes control, keep your after-meal blood glucose levels at 180 or below.”  A glucose level of 180mg% is not only egregiously high, it’s the renal threshold where glucose begins to appear in the urine.  But even this admonition is honored mainly in the breach.  A typical study gave the mean HbA1c of 17 diabetics in the experimental groups at 9.9%, and that of the control group at 10% (Georgopoulos 1995); an HbA1c of 10% corresponds to a blood sugar of 247mg%, which guarantees chronic glycosurea.   In Dr Gerald Reaven’s diet comparison excerpted above, “24-hour urine glucose excretion was significantly greater (55 versus 26g/24 hours p<0.02) in response to the low-fat, high-carbohydrate [ADA] diet” (Coulston 1987).  The researchers are sanguine to the point of complacency about the condition of their experimental subjects, since any sugar in the urine means a diabetic is dangerously out of control. 


            This is where the mystery deepens: the clear and present danger is diabetic complications caused by elevated blood sugars (as graphically illustrated above), yet the ADA dietary recommendations cause such high blood sugars that sugar appears in the urine, even when monounsaturated fats replace some carbohydrate.  As well as making complications inevitable, Dr DeFronzo has pointed out that hyperglycemia causes both increased insulin resistance and the progressive loss of β-cell function which eventually renders insulin necessary.  In other words, the hyperglycemia attendant upon the ADA dietary prescription causes the progression of diabetes.  The ADA is silent on this consequence of their recommendations, and the researchers in the field are seemingly oblivious of the danger.


            Yet the low-carbohydrate diet I eat which renders my blood sugar normal is “not in synch” with the ADA recommendations: “Currently some controversy about carbohydrates is raging due to a few new diet books.  These books encourage a low carbohydrate, high protein and moderate fat intake.  These diets are not in synch with the American Diabetes Association nutrition recommendations, which are based on years of research and clinical experience.  In addition, these trendy diets are hard to follow year after year.”  But I’ve followed a far more stringent diet for nine years with considerable pleasure, my blood sugar is usually below 120mg% after meals, I do not experience glycosurea, and my HbA1c is in the normal range at 5.6%.  My blood fats improved with carbohydrate restriction, to the point where I’m at very low risk by the usual yardsticks.


            The ADA protests that low-carbohydrate diet studies are short-term and that their safety has not been proven.  But this is disingenuous, as the area has actually been quite thoroughly researched.  For example “The ketogenic diet is a low-carbohydrate, adequate-protein, high-fat diet that biochemically mimics the fasting state and has been used to successfully treat seizures for 85 years” (Huffman 2006).  A long-term follow-up study from Johns Hopkins University showed that “Three to 6 years after initiation, the ketogenic diet had proven to be effective in the control of difficult-to-control seizures in children.  The diet often allows decrease or discontinuation of medication.  It is more effective than many of the newer anticonvulsants and is well-tolerated when it is effective” (Hemingway 2001).  A year-long Korean study concluded that “The KD [Ketogenic Diet] is a safe and effective alternative therapy for intractable childhood epilepsy” (Kang 2005).  Several studies a year or more in length establish that less extreme low-carbohydrate diets, used for glycemic control in diabetics or for weight loss in both diabetics and healthy people, are well-tolerated and without side-effects.  For example, Dr Jørgen Nielsen found a 20% carbohydrate diet lowered the average HbA1c of 16 obese diabetics from 8% to 6.6% in six months, and it was still low at 6.9% after 22 months (Nielsen 2006).  A definitive study followed 66 obese people, some with high cholesterol, on a diet containing less than 20 grams of carbohydrate for 56 weeks to determine the truth of the conventional wisdom that such a diet would cause deterioration of the lipid profile.  Everybody lost weight and found their cholesterol, LDL-cholesterol and triglycerides fell, while HDL-cholesterol increased, and the study concluded that low-carbohydrate diets are safe to use “for a longer period of time” (Dashti 2006).  So there is, in fact, a great deal of long-term research into very low-carbohydrate diets which find them safe and effective.


            A claim that low-carbohydrate diets are ineffective for glycemic control would be mendacious, but the ADA has sidestepped this necessity with impressive cunning by claiming that low-carbohydrate diets cannot be recommended.  However, numerous studies demonstrate that lower-carbohydrate diets are very effective at lowering HbA1c:


                                                  Effect of Carbohydrate Intake on HbA1c in Seven Low-Carbohydrate Diet Studies                                                                                          




Duration wks

BMI pre

BMI post


Carbs pre

Carbs post

HbA1c pre

HbA1c post

HbA1c final


Boden 2005













Gannon 2004













Gumbiner 1998













Gutierrez 1998


2, no OHAs*











Gutierrez 1998


2, OHAs*











O'Neill 2003


20x2, 10x1











Nielsen 2006













Yancy 2005













                                                                                    *OHAs: prior treatment with Oral Hypoglycemic Agents                                                                                                                                                        


               Left: Interestingly, these seven low-carbohydrate (<25% of calories) studies show that there is a strong correlation between the percentage of calories as carbohydrate and HbA1c at the end of the study; “R2 = 0.8374” means that, statistically speaking, the differences in the percentage of carbohydrate calories accounts for about 84% of the change in the values of HbA1c.  The rest of the variation likely comes from duration of diabetes and the degree of obesity.  Right: Weight loss no doubt contributes to the lowering of HbA1c for weight loss occurred in all 7 studies, but the absolute intake of carbohydrate was far more important.  A review of very low-calorie diet therapy for obese diabetics points out that “Metabolic benefits occur quickly with only modest weight reduction, suggesting that calorie restriction plays a more critical role [than the absolute amount of weight lost]” (Henry 1991).  It seems that, in low-carbohydrate diets, caloric restriction is a necessary but not sufficient condition for improvement of the diabetic state, and that it is the degree of restriction of carbohydrate which predicts the degree of benefit which will accrue: only the diets with less than 8% of carbohydrate achieved an HbA1c of less than 6%.


            This is in good agreement with my experience.  My diet contains about 6% carbohydrate, like Dr Richard Bernstein’s diet upon which it is based, and my HbA1c is 5.6%.  Before Dr Bernstein published his book in 1998, I ate about 25% of calories as carbohydrate and my HbA1c wandered between 7 and 8%:

A graph of my HbA1c scores before and after I adopted a low-carbohydrate diet


            Conversely, high-carbohydrate diets improve HbA1c only if they are calorie-restricted, and this effect is barely strong enough to be clinically useful for Type 2 diabetics.  For example, when Dr Leonie Heilbronn restricted calories by 30% in two diets containing 60% carbohydrate which were made up of either of low or high Glycemic Index foods and fed them to two groups of diabetics for 8 weeks, she found that “Urinary glucose excretion was not significantly changed … in either group” (Heilbronn 1999).  There is a trivial improvement in the low Glycemic Index group, but any urinary glucose excretion means microalbinurea (the loss of protein through the kidneys) is not far behind, which will be followed by macroalbinurea and eventually by kidney failure.  The literature is rife with such studies (Gumbiner 1998, Parker 2002,), performed by researchers who are cavalier to the point of indifference.  Where are the Ethics Committees?  How can a literature search be so bungled that low-carbohydrate, blood sugar-normalizing diet studies are overlooked? 


            And sometimes, we just don’t see the forest for the trees.  Dr Cecilia Low compared calorie-restricted diets with 10% and 70% carbohydrate content and found clear advantages for the low-carbohydrate diet over the 6-week study period in obese Type 2 diabetics, yet she dismissed the entire approach with: “it is impractical to consume weight-maintaining diets composed of 70% fat” (Low 1996).  Never mind that the low-carbohydrate group had just completed four weeks of “re-feeding” doing precisely that, albeit on a liquid-formula diet!  Never mind that there is a whole population of free-living diabetics who approach this level routinely, and  consequently have normal blood sugars.


            On the ADA high-carbohydrate way of eating, tight blood sugar control lowers complications but markedly increases hypoglycemic episodes in insulin-dependent diabetics (Donelly 2000):


            The graphs show that the rate of progression of retinopathy is lowest at an HbA1c of 5.5%, but the rate of severe hypoglycemia is highest, about one episode per year.  Severe hypoglycemia is very risky because you may make catastrophic errors of judgment, lose control of your car, have a seizure or worse.  However, diabetic complications consequent on high blood sugars cause blindness, limb amputation, kidney failure and accelerated heart disease.  Insulin-dependent diabetics constitute only 10% of the diabetic population, yet the argument that tight control is too risky because of the attendant hypoglycemic episodes is somehow generalized to all diabetics, implicit in the ADA’s target HbA1c of 7% for good control.  Yet I take insulin, maintain an HbA1c of 5.6%, and do not have severe hypoglycemic episodes.  Nor do the patients of Dr Richard Bernstein, who wrote:


               In the 20 plus years that I have been in practice, only five of my patients have had severe hypoglycemia causing loss of consciousness. Two of these people were eating excessive amounts of carbohydrate and three made major mistakes such as taking the wrong type of insulin.  I’m sure this is a far cry from the incidence of severe hypoglycemia among patients of high carbohydrate practitioners (Bernstein Interview).



            Severe hypoglycemia is vanishingly rare on low-carbohydrate diets.  So what’s the secret?  For one thing, there’s ketosis, in which two- to four-carbon fragments of fats are formed in the liver when the diet is low in carbohydrates – these ketones can directly nourish many of the tissues, including some brain structures which would otherwise burn only glucose, so that when the blood sugar drops too low, the brain runs mostly on ketones (Johnson 1978).  So a low-carbohydrate diet protects against hypoglycemia.  The widespread prejudice against ketones and ketosis stems from the widespread misunderstanding that ketones and ketosis only occur in diabetic ketoacidosis, which is a deadly consequence of too little insulin in insulin-dependent diabetes.


            Interestingly, it is the ADA’s own much-vaunted research, used so much to justify their low-fat diet, which has demonstrated that a low-carbohydrate diet lowered HbA1c to normal in 8 overweight Type 2 diabetics.  The study was funded by the ADA with help from the beef industry and published in the ADA journal Diabetes in 2004.  A diet containing 20% carbohydrate, 30% protein, and 50% fat was compared with American Heart Association 55%-carbohydrate, 15% protein and 30% fat diet for 5 weeks, and demonstrated such improved control that the conclusion of the study was that the diet “could be a patient-empowering way to ameliorate hyperglycemia without pharmacological intervention.”  Blood sugars plummeted to almost-normal levels, serum insulin fell dramatically, triglycerides dropped to a normal 150 from syndrome X-territory near 250, and HbA1c fell two full percentage points in just five weeks; had the diet continued for three months, the researchers projected that HbA1c would have fallen to 5.6% (Gannon 2004):


               Left: Mean plasma glucose concentration before () and after () 5 weeks on the LoBAG [low-biologically-available-glucose] diet.  Right: Mean % tGHb [HbA1c] response during the 5 weeks of the control (○) or LoBAG diet ().  *The tGHb on the test diet was significantly lower at weeks 3, 4, and 5 vs. the control diet (P < 0.05).



            Interestingly, in another study of a 20% carbohydrate diet, this time in obese diabetics, “Patients spontaneously reduced their mean energy intake to approximately 2200 kcal/day [a reduction of 30%], which is approximately the caloric intake of normal-weight individuals with the same height as our patients … Mean plasma leptin levels were lower …”  (Boden 2005).  Leptin is a hormone with helps control appetite, and sensitivity to leptin parallels sensitivity to insulin.  These diabetics lost their excessive appetites in spite of lower leptin levels, so this 20% carbohydrate diet increased their sensitivity to insulin (and therefore leptin) dramatically, perhaps in part by controlling their hyperglycemia.  Spontaneous caloric restriction is unheard of among Type II diabetics, 80% of whom are overweight at diagnosis.  Most diabetics gain weight over time, whatever advice they may be given on weight-loss, and a study has found that fully 59% of them do not exercise – in fact, this study showed that the higher their HbA1c, the greater the likelihood that the diabetic would be sedentary (Morrato 2007).  Any diabetic knows that the worse the blood-sugar control, the lower one’s energy level.  But it is the complacency with which this staggering lack of compliance with a common-sense protective prescription is viewed by the medical profession that is truly surprising.


            While mainstream medicine seems unable to think outside the box, articles such as “Can Diabetics Have Normal Blood Sugars with Diet Alone?” by Regina Wilshire summarizes some of the evidence and concludes that essentially normal glycemic control is possible for diabetics.  Similarly, Men’s Health magazine published an article by Adam Campbell entitled “The Cure for Diabetes” which points out that diabetics treated by Dr Mary Vernon with the Atkins low-carbohydrate diet are “cured” in the sense that they no longer have a blood sugar problem, so long as they stick to the diet. 


            The ADA’s much-vaunted “clinical research” has scrupulously neglected to test this way of eating since it was proposed by Dr Robert Atkins in 1972 until very recently.  But could it be that, after more than 30 years, they are surreptitiously maneuvering towards a bid to make it their own?  Now begins that medical procedure requiring the utmost skill and delicacy: distancing oneself from the defective medical advice which was once the standard of care but which has been found to maim and kill!  If diabetics weren’t rendered so compliant by their condition, the “lucky” ones who were merely maimed might band together in a class-action suit and prevail upon the ADA to accelerate their glacial pace of change. 


            However, if the American Diabetes Association was to change its stance, and diabetes was rendered a non-dangerous chronic condition requiring only a low-carbohydrate high-vegetable diet, consider what would happen.  The forty-seven percent of the country that already has diabetes or pre-diabetes would be prescribed this new low-carbohydrate diet, halving the profits of the food industry overnight.  Then the new, redesigned USDA food pyramid would advise against sugar and refined food, and the markets for genetically-modified corn (high-fructose corn syrup) and soybeans (the oil in most processed foods) would dwindle, forcing painful changes in agriculture.  Similarly, the falling demand for diabetic drugs and impedimenta would cause squeals of pain from the pharmaceutical industry, which wealds so much financial clout that it actually elects Presidents sympathetic to its needs.  And if a revolution in favor of avoiding carbohydrates were to occur, the first casualty of this new world order?  The American Diabetes Association!  Since the food industry and the pharmaceutical companies would no longer have the means or desire to support them, their continued existence depends on their aligning their dietary advice with the interests of their contributors. 


            This has not gone altogether un-remarked.  Australian physician Dr Jay Wortman wrote:


               The epidemics of obesity, metabolic syndrome and type 2 diabetes have worsened over the past decades … these conditions [may be] inter-related and may be caused by a single underlying factor related to the carbohydrate content of diet … Aboriginal people suffer more acutely from the epidemics in question and their dietary history suggests that a sudden increase in carbohydrates is to blame.  Recent studies … demonstrate that carbohydrate consumption can drive appetite and over-eating while carbohydrate restriction leads to weight loss and improvement in the markers for metabolic syndrome and type 2 diabetes. The growing evidence in support of low-carbohydrate diets will encounter resistance from economic interests threatened by changes in consumption patterns (Wortman 2006).


            His prescience stems in part from solving his own brush with diabetes:


            “… diabetes is a disorder of blood sugar, your blood sugar is too high -- my immediate instinctive response was to stop eating any food that causes your blood sugar to rise.  So I basically right away eliminated carbohydrates from my diet … In four weeks, I lost 18 pounds. My blood sugars normalized, my blood pressure became normal, and I felt much better," Wortman says. "I don't know if you're ever not diabetic, but I think for me, I've been able to reverse the effects of diabetes through diet" (Wortman Interview).



            There’s a pattern here.  Any who have experience of resolving unhealthy blood sugar excursions by eliminating carbohydrates so far as is possible never look back.  Perhaps the American Diabetes Association is nobly holding the line for evidence-based medicine.  Or (my favorite theory) these are the guys Max Planck was thinking of when he wrote:


A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it

Max Planck


            Whatever the reason, the ADA behaves as a cat’s paw for its pharmaceutical and food industry contributors, and its high-carbohydrate diet remains the standard of care while “more research” is called for.  Yet they are obtuse to the point of misrepresentation in their coverage of low-carbohydrate diet studies.  For example, researchers found that a low-carbohydrate diet dramatically reduced HbA1c and other important disturbances typical of the diabetic metabolism and concluded “The lack of negative effects, improved glucose control, and a positive nitrogen balance suggest beneficial effects for subjects with type 2 diabetes mellitus …” (Nuttall 2006).  However, the ADA summary reads “The amount of fat and carbohydrates in a person's diet does not appear to have an effect on metabolism.” 


            Further, the ADA is adamantly opposed to any and all vitamin or mineral supplements except fish oil capsules in the treatment of out-of-control triglycerides.  This is awfully hard to reconcile with the staggering weight of evidence in favor of, for example, chromium, biotin and magnesium for lowering blood sugar, or the published research on deficiencies actually found in diabetics.  Spectracell Inc, who market a test for the adequacy of nutrition determined by the health or otherwise of cells in nutrient solutions deficient in a single nutrient – if the cells thrive, their owner is likely adequate in the missing nutrient – summarize the research on deficiencies found in diabetics:


               [Type II diabetes is a] widespread metabolic disease [which] has been associated with several nutrient deficiencies, some of which have been linked to progression of clinical disorders that can occur secondary to chronic diabetes. Magnesium deficiency, in particular, has been associated with type 1 and type 2 diabetes as well as with gestational diabetes. Supplementation of type 2 diabetics with magnesium was found to improve both insulin secretion and insulin sensitivity. Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might actually contribute to the development of diabetes.  A recent prospective study revealed a graded inverse relationship between serum magnesium levels and the development of diabetes.  Magnesium deficiency has also been linked to progression of clinical disorders related to chronic diabetes.


               Deficiencies of several vitamins have also been identified in diabetic individuals. Vitamin B6 levels were found to be lower in diabetic animals than in normal controls, and sub-clinical vitamin B1 deficiency was prevalent in pregnant women with gestational diabetes.


               Deficiencies of antioxidant vitamins have also been associated with diabetes.  Several studies have found that diabetic patients had at least a 30% lower level of plasma ascorbic acid than non-diabetic subjects, and a strong independent association was found between low plasma vitamin E levels and an increased risk of developing diabetes.  Subjects with clinical nephropathy had lower mean plasma ascorbic acid levels and higher mean renal clearance of ascorbic acid than patients having only microalbuminuria.  Thus, SpectraCell's antioxidant panel and functional determinations of B vitamins and minerals can help to detect diabetes-related nutrient deficiencies before they contribute to the progression of the disease or to the development and progression of its complications (Spectracell).



            The ADA is against supplementation with magnesium, even though low magnesium has been linked to the progression of diabetic complications such as retinopathy and kidney failure!  All this renders the ADA’s dietary advice antithetical to the interests of any diabetic who wants to live out his or her span: their prescription costs the average diabetic 12 years of life, and the risk of death is doubled at any age for a person with diabetes.  Consequently, Dr Lois Jovanovic of the Sansum Diabetes Clinic in Santa Barbara has called their prescription “Malpractice!”, and Dr Richard Bernstein wrote with admirable restraint that “the guidelines given by the American Diabetes Association have proven unhelpful … in managing to maintain a healthy weight and normal blood sugars.”  Dr Bernstein developed insulin-dependent diabetes in 1946 when he was 12 years old; he wrote that “For many years I accepted the medical orthodoxy and it nearly killed me” (The Diabetes Diet).


            In summary, diabetes and caloric excess coexist in those at the greatest risk of complications and death.  Either avoiding carbohydrates so far as is possible, or restricting calories in a high-carbohydrate diet lessens insulin resistance and lowers this risk.  But carbohydrates do not of themselves cause weight gain and insulin resistance, for the Kitava Islanders remain lean and insulin-sensitive throughout their lives on an unrestricted, unrefined carbohydrate diet.  It is therefore refined carbohydrates which must be at fault, probably both because they do not trigger satiety signals and because they no longer contain nutrients essential for their metabolism; so we over-feed and under-nourish our metabolisms until they fail.  A key part of any remedy, then, is to avoid refined carbohydrates altogether, and to avoid nutrient-poor carbohydrates like potatoes to a degree commensurate with the extent of the damage.  This is the polar opposite of the Medical Nutrition Therapy prescription of the ADA, but, in contrast, it has been shown to be effective.


            I personally bitterly resent the ADA’s dietary position.  It cost me fifteen years of my HbA1c score elevated by two percentage points to learn how wrong they are, and I believe their advice is life-shortening.  To the extent they believe what they say, I believe they are tragically mistaken.  To the extent that they know the low-carbohydrate approach saves lives, but put their own interests above the interests of the diabetics who turn to them for guidance, I am at a loss for words.