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6:4 type-2 diabetes diet versus drugs

6-4-Diet for diabetes versus medications     3/3/20

Chapter 4:  Diabetes, diet versus meds:  1. Introduction   2. The tidal wave of t2d   3.  Early history of diabetes   4. Modern health care before the drugs for t2d    5. Dietary low-carb management of t2d, Merck 1950-61    6. Low carb diet for diabetes mellitus   7.  Fructose damaging MTD is the starting point.  8. NAFLD to IR and fatty pancreas leads to t2d    9. Bariatric surgery and t2d    10. Curing t2d with ketogenic diet or fasting   11. Supplements and exercise   12.  Confusion from the past, on ketoacidosis and hypoglycemia   13. Homeostasis and don’t upset the apple cart   14. Treating the sign, glucotoxicity, instead of the cause IR    15. Drugs for treating t2d    16. The wonder drug, metformin?     17. The ADA 2019 guidelines     18. Short list of what is weight loss, managing t2d and lowering risk for CAWD    19. What causes t1d   20. What caused the children with t1d to waste?      


Abbreviation:   ADA  American Diabetic Association    ATP adenosine triphosphate   B4 fructose, mitochondrial dysfunction, reduced production of ATP, reduced autophagy    CC contributing cause   CVD cardiovascular disease   CAWD conditions associated with the western diet   DKA diabetic ketone acidosis   IR insulin resistance   KOL key opinion leader (pharma’s stooge)    LADA latent autoimmune diabetes in adults    MTD mitochondria   MTDD mitochondrial dysfunction   RAPT reduced production of ATP   t1d type-1 diabetes   t2d type-2 diabetes    Wiki Wikipedia    WRS weight regulatory system


Table 1. US Diabetes Forecasts, 2015 to 2030






Total United States











Diagnosed diabetes





Undiagnosed diabetes





Total with diabetes






The total of prediabetic and diabetic is 140,576,000 for 2020, that is one half of the adult population.  With pharma wanting to treat the prediabetics with drugs, this entails an even greater profit for pharma than with statins for which over 30% of the adult population are taking them and over 60% of the men between the age of 60 & 70.  As explained the lipid hypothesis is crapolla, so too is drugs for prediabetics (#s 16 & 17).  

  1. Introduction:  Diabetes type 2 is of epidemic proportions, with the new guidelines there will be over 30% of adults will qualify by the guidelines for blood sugar lowering drugs.  The claim is that these drugs will significantly reduce their chance of becoming diabetic.  As you should by now expect it is based on tobacco science.  There is good reason to believe based on the science on IR, that there will be an increased risk of progressing to t2d because most of these drugs promote insulin resistance and the recommendation to consume less fat and more easily digested carbs to prevent hypoglycemia. 

    Oh, and the numbers for diabetics, the claimed 10% is like that for obesity.  For obesity, the morbidly obese, the official 7% based on a phone survey, are not counted as obese.  So too with the diabetics, those undiagnosed diabetics are not counted with the diagnosed.  Put the two together and we have 17.1% of the population as of 2020 with t2d.  In 2019 there were 253.8 adults; divide that into 43.3 and you have 17.1% adult t2d.  Shameful government figure of 10%.  Children are normally not counted for adult onset diabetes!  

    T2d is a condition that is virtual unknown among LSPs.[2]  It is the extreme form of IR for which elevated insulin increase fat storage including in the pancreas.  Excessively large lipid droplets cause pancreatic which with increase in size hinders the beta cell production of insulin.   Less insulin thus causes elevated serum glucose level.  T2d increases the risks for all of the CAWD because the foundation of MTDD reduces ATP and autophagy, and increases IR.  .  Given those numbers of diabetics, it causal association with CAWD, the effect upon quality of life, and financial burden, I feel obligated to develop the topic and pour into the reader’s ear that t2d can be managed by a low carb diet.   Yes with 70 million Americans with t2d (diagnosed and undiagnosed) by 2030, we have unprecedented health disaster.    

    3.       Among CAWD is t2d, for which the road to diabetes mellitus starts with fructation within the MTD of the hepatocytes and their subsequent IR which eventual progress to IR first in the liver and then in other metabolically active tissues, most significantly the myocytes and adiposities.  IR lays the foundation that distinguished LSPs from HSPs—measurements of the difference in insulin are approximately 100%.  MTDD which causes IR are the major CC for CAWD.  The diabetics have compared to the general population an elevated risk for all of the CAWD; their MTDD and IR is greater as too endothelia dysfunction, RATP, RRA, and other issues discussed in Section 3.    

    With official US CDC figures 2015 at 26% seniors and nearly 10% of diagnosed adults with diabetes, a critical look at the diabetes wing of CAWD is merited.  Pharma is waving the hyperglycemia flag.  Those numbers, 10% & 26% for 2015, are of course low because it is in the interest of industries that profit from sugar that our official numbers are low—another example like for dietary sugar (1:3).  Moreover, over 20% of the population fit the pre-2018 blood markers for t2d (HbA1c and fasting glucose) but haven’t been diagnosed.  Add to the numbers the new ADA (2018) guidelines—as you guessed—will push those numbers skyward.  The ADA guidelines lowered the blood markers for t2d (#16).  Over one quarter of those with insulin resistance now by the wave of the KOL wand will be medicated according to guidelines.  Since only about 25% of the once prediabetic will progress to t2d, that entails, assuming that the drugs work, 75% of those treated will not benefit and they will have only the side effects.  This is again profits before people.  Twenty-five drugged given the lack of quality evidence for benefit (#15), none will benefit and all will be harmed (the bell-curve fallacy).[3]  No drug as of 2019 has been approved (patented) for treating prediabetics.  The new guidelines would be considered criminal if the deliberately causing harm was a crime, and we had a government which put people before profits.  The Ricco statue would be used to incarcerate every big-pharma executive---dream on! 

    6        As you shall see in this chapter, framing the problem as hyperglycemia, and having the fix drugs is like fishing in a pond stocked with starving trout.[4]  First, the problem isn’t glucose but that of excess insulin used to lower glucose.  Fasting Insulin levels in pmol/L:  Nondiabetic lean 50, nondiabetic obese 178, Prediabetic 253, diabetic obese 382,[5]  The Kitavans on a high carb low sugar diet, their fasting insulin is 29 is nearly half the lean nondiabetics Swedes.  As stated before, the cells being stuffed with glucose whose metabolism has been slowed by MTDD, the cells withdraw some of the glucose receptors.  The drugs given don’t affect the cause of hyperglycemia, just mask the blood sugar reading it by stuffing more glucose into the cells,[6] masking the IR by lowering contrary to evolutionary design the blood glucose.  So why is IR so deadly? 

    An excess of insulin affects many system--the current list is at 3:5 5.  The overall consequence is increased risk for the CAWD.  Some of the consequence for IR is through leptin, gain weight.  Insulin causes cells to turns off fat metabolism; this causes the free fatty acids to be converted into triglycerides for storage.  Third big one is that insulin downregulates lipolysis, the metabolism of fats.  The time window for fat metabolism is reduced with IR. Insulin downregulates gluco and glycogenesis, thereby increases the duration the amount of sugars in the blood and more significantly in the cytosol of cells.  Fourth, glycation and fructation is increased with IR.  Fifth is the decrease of autophagy and other homeostatic functions.  Sixth, the combination of these effects is causal for NAFLD and thus another major monkey wrench through into hemostatic mechanisms involving the liver.  Seventh, the NHANES study in 1999 placed the rate at 33%; a guestimate would be 50% now, and if the amount of fat was lowered to LSP level, probably over 85%.  [7]  Insulin is what I call a gate way hormone thus one whose effects are highly regulated.  IR is a major CC for CAWD.

    Now back to extreme IR, t2d.  Sadly, I must teach about profits before people, drugs to treat pre-diabetic (#13, 14, 15, 16).  True to pharma’s business model, the lowest standard trials have been used “to prove” that metformin, acarbose, and thiazolidinediones lower risk of developing t2d; and there are several other classes of diabetic drugs in the process of “proving” that they too lower risk.  But why bother giving a drug to those who won’t benefit, the 75% who won’t develop t2d:  Because people with prediabetes may develop diabetes but may also change back to normoglycaemia almost any time, doctors should be careful about treating prediabetes because we are not sure whether this will result in more benefit than harm, especially when done on a global scale affecting many people worldwide.”[8]  Metformin the most prescribed is a gateway drug that only very slightly lowers blood glucose.  How much is not known because of the low-quality industry studies (#15). 

    9        The inflammation of the pancreas that results in t2d is caused by the accumulation and growth of lipid droplets in the pancreas, a process caused by excessive fructose, MTDD, and IR.  IR, lipid droplets, and MTDD upset pancreatic homeostasis which causes the lipid droplet to gradually increase in size.  There isn’t evidence in quality studies that metformin or the other 2 drugs recommended by the ADA (#16) as to their altering this process.   In part because of nausea, patients don’t stay on just metformin for years; they are on the path to eventual insulin injections, if they live long enough.

    The physician’s belief in the gateway drugs’ effectiveness is based on marketing, lowest quality clinical trials.  The studies are not long-term, have “in general, the reporting of serious side effects was sparse.” [9]  As I have repeated commented, without seeing the raw data, what we have is marketing dressed as science.  All included trials had deficiencies in the way they were conducted or how key items were reported. For the individual comparisons the number of participants was small, resulting in a high risk of random errors (play of chance).” [10]  Should we expect otherwise when journals don’t get the raw data?

    This is one of the cases where looking at earlier treatments reveals a buried past.  Prof Ben Goldacre has repeatedly stated that, it is amazing how quickly a good drug becomes bad when it goes off patent.  In my search of what is best, I have repeated found that the older treatments and are better.  One example follows here.  There is much to be learnt, starting with the ancients.  Take a deep breath, while the more technical parts might only interest diabetologist, much applies to an alternate and superior to drugs. 


2.  The tidal wave of t2d:  Yes, we have a diabetes epidemic, going back a century and it is for both types of diabetes.  Starting with records from 1867 through to 1910 the admission for diabetes average under 2 a year, from then rocket to 80 in 1938--from diabetes admissions, Pennsylvania Hospital, Philadelphia (the nation’s first hospital, founded in 1751 by Benjamin Franklin and Thomas Bond).  William Osler, considered the father of modern medicine, reported in his seminal textbook, The principles and practice of medicine, 1892, of the 3,500 patients in the first 3 years of Johns Hopkins Hospital only 10 had been diagnosed with diabetes.  “In the next 10 years 156 cases were diagnosed. . .  nearly doubling between 1879 and 1890, and then more than doubling again by 1900.” [11]

A diabetes mortality statistics in 1926, they reported a 400 percent increase in some American cities since1900, almost 1,500 percent since the Civil War. . . .  In 2012, . . . one in every seven to eight adults in this country had diabetes—12 to 14 percent, depending on the criteria used to diagnose it.  Another 30 percent are predicted to get diabetes at some point during their lives [this is consistent with the 26% of seniors, before the new lower guidelines [#13] . . . . Among U.S. military veterans, one in every four patients admitted to VA hospitals suffers from diabetes. . . .  perhaps 95% have type 2 diabetes. . . . the market for diabetic drugs and devices in the United States alone is over thirty billion dollars yearly.[12]

William Osler wrote of managing t2d with low carb diet. 

Diabetes, ischemic events, cancer, and Alzheimer’s disease[13] are diseases of the 20th century along with the conditions of obesity, fatty liver, hypertension, and IR.  Dr. Richard Thomas Williams in in Diabetes mellitus treatment (1898) wrote of low carbs; as did Richard Allen and others. Mortality associated with t2d was limited to those who didn’t limit their carbs.   Today mortality associated with t2d is limited to those who manage the condition with drugs (when compared to the low carb management).

  T1d was not treated because there was no treatment; death of children was within one year, and the condition was rare, thus the literature on early-onset diabetes was thin and physicians were concerned with the treating the condition of affluence, t2d.  Diabetes mellitus meant back then type 2 diabetes unless otherwise specified.

From the fact that it is a recent phenomenon, genes can only be a minor CC. Allow me to explain, if t2d could be caused by genes, condition would occur among the LSPs.  Evolution has eliminated genes that promote t2d among the LSP.   When LSPs switched in number to the western diet, they were more devastated by the diet then the populations that had 2 centuries to reduce the reproductive success of those with the genes promoting t2d.  Secondly, in their rural village life, social bonding is closer, thus they drank more sodas and eat more sugar loaded foods on an average than the Brits and Americans.  These factors explain the sever impact of sugar upon many of the once paleo peoples introduced to the western diet.  Many of these populations become heavy drinkers, made sever by the reduction of boredom and by social conditioning. Many of them favor the low level of alcohol which entails a longer period of socialization.  Unfortunate, the high glucose content of beer entails a delayed metabolism of both fructose and ethanol in the liver.   often of the worse form beer.[14]  The effect of ethanol damages the liver and the pancreas to cause fat accumulation[15] is another major CCs for t2d.  The combination of sugar and beer explains the high rate of t2d among aboriginal peoples such as the Pima Indians.  Ethanol increases malondialehyde and decreases the protective glutathione, both a sign of stress.[16] 

I say this because when a person in our society states that t2d runs in their family, the possibility of these two other CCs, ethanol and excessive sugar, are more likely the cause than genes.  Chance also could explain familial link.  Take a large population and some will be struck by lightning twice, with a condition that occurs in 26% of seniors, the rate for 3 out of 15 close senior relatives having t2d is over 50%.[17]  There is also a high concordance with obesity, as too for certain prescription drugs.  Yes, genes are a less like explanation. 

Yes, genes are relevant, but age is more relevant with over 50% of the diabetics over the age of 55.[18]  The concordance of identical twins is 70% for t1d,  And for t2d,

“the concordance rate is 60% to 80%.  In first degree relatives with type 2 diabetes (and in non-identical twins) the risk of developing disease is 20% to 40%, versus 5% to 7% in the population at large [1999]. . . .  epidemiologic studies indicate that type 2 diabetes appears to result from a collection of multiple genetic defects. . . “ [19]

Since both t1d and t2d were virtually unknown conditions, environmental factors are essential, but for the extremely rare exception.  This is not surprising given the role of fructose and MTDD. 


3.  Early western history of diabetes:  The diabetes (type 2) is an ancient disease with Aretaeus of Cappadocia is credited with the first description of the condition around 130 AD and the term comes from the Greek.  

Diabetes in Greek means the thing or fluid that runs through, like a water pipe.  “Diabetes [type 1] is a strange affliction, rare among men. . . The course is through the kidneys and the bladder; for the patients never stop making water. . . . The nature of the disease is chronic and takes a long period to form; but the patient is short-lived, if the constitution of the disease be completely established; for the melting is rapid, the death speedy. [20] 

Galen a Greco-Roman a generation later writes on diabetes in several works: 

I am of the opinion that the kidneys too are affected in the rear disease, which some people call chamber-pot dropsy, other again diabetes or violent thirst [type 1].  I have seen now only twice when patients suffered from inextinguishable thirst. . . (supra)

Others state that the first complete clinical description of diabetes was made by Aulus Cornelius Celsus (30 BC–50 AD), the Roman encylopedist whose De medicina volume survived; a reading confirms Aulus’s priority.  And not surprisingly, Hippocrates wrote (or was added to his writings by later Greeks)[21] probably about diabetes mellitus, in that he refers to excessive urination, but the conditions wasn’t described.  Gemmill lists 11 Greek and Latin medical authors who mention diabetes or excessive urination.[22]  Some associated diabetes with diet.  Lacking science on metabolism and nutrients, there wasn’t in the literature a recommendation for management of t2d, and the condition was common. 

There are descriptions by the ancient Chinese, Indians, and Egyptian, with the earliest description of diabetes is in the Ebers papyrus (c. 1550 BCE) of the symptom of extreme thirst and urination are for t2d.   In about 400 BC the Indian physician Susruta-smahita described the medical knowledge of his day (with later contributors) in 134 chapters.  Therein are described 1,120 illnesses, 700 medicinal plants, and an extensive description of surgical procedures.  It might have had an effect upon the Greco-Roman understanding of the condition and thus the development of European medicine; Alexander the Great had invaded India and built several cities.  He gathered information on wild life, plants, customs of people and other matters that might be of interest for his teacher Aristotle who remained in Greece.     


4. Modern health care before the drugs for t2d:  Diabetes a condition of affluence attracted medical interest along with gout.  Not surprisingly the Arab world mainly at first through the center for education, Bizantium, of the surviving Greek and Latin texts and based on them developed schools of medicine.  Diabetes became more of an issue due to the popularity of figs and dates which are easy to preserve, and were.  The Greek and Romans before the cultivated these fruit.  Cato the Elder in c. 160 BC list several strains of figs in his agricultural handbook.  Maimoniedes (1135 to 1204) claimed to have seen more than 20 cases.  Abd al-Lalif al-Baghdadi (1162-1231 produced a treatise dedicated to diabetes.    The modern western medical literature on diabetes mellitus goes back to Paracelsus.  In the 16th century, Paracelsus (1493–1541) described diabetes as a constitutional disease affecting many organs.  "Diabetes irritates the kidneys and provokes excessive urination. He reported that evaporating urine from a diabetic patient left an excessive residue, which he called salts".[23]   It has, however, been noted that he advised tasting the urine for sweetness in other contexts.[24]  in western English medicine to Thomas Willis (1621 to 1675)[25] described the urine of diabetics as “wonderfully sweet as if imbued with honey or sugar.”[26]  Mathew Dodson (1732-1784) an English physician and experimental physiologist in 1776 identified sugar as the culprit.  He collected 2 quarts of urine from a type-2 diabetic[27] and evaporated it gradually.  He wrote that the residue smells like brown sugar.  The standard test was tasting the urines and blood for sweetness. He demonstrated the sweetness was term sugar. 

Because of  the lag in sugar chemistry, basic distinctions between glucose, sucrose, and the alcohol sugars were no recognized in this early period. 

Glucose was first isolated from raisins in 1747 by the German chemist Andreas Marggraf.[8][9] Glucose was discovered in grapes by Johann Tobias Lowitz in 1792 and recognized as different from cane sugar (sucrose). Glucose is the term coined by Jean Baptiste Dumas in 1838, which has prevailed in the chemical literature. Friedrich August Kekulé proposed the term dextrose (from Latin dexter = right), because in aqueous solution of glucose, the plane of linearly polarized light is turned to the right. . . .  ince glucose is a basic necessity of many organisms, a correct understanding of its chemical makeup and structure contributed greatly to a general advancement in organic chemistry. This understanding occurred largely as a result of the investigations of Emil Fischer [1852-1919], a German chemist who received the 1902 Nobel Prize in Chemistry for his findings.. . .  For the discovery of the metabolism of glucose Otto Meyerhof received the Nobel Prize in Physiology or Medicine in 1922. In 1947, Bernardo Houssay (for his discovery of the role of the pituitary gland in the metabolism of glucose and the derived carbohydrates) as well as Carl and Gerty Cori (for their discovery of the conversion of glycogen from glucose) received the Nobel Prize in Physiology or Medicine.[28]   

The different tastes and sweetness waited for the advancement in the chemistry of sugars. And tastes is not a good method of identification.   Glucose which is only 74 to 80% as sweet as sucrose.  Fructose is rated at 1.17 to 1.75.[29] Fructose is not normally found in the urine, but is in the blood the 3 hours following a meal with sugar The chemistry of sugars delayed the understanding of the role of pancreas and blood sugars, moreover the PP wasn’t discovered until the 1960s and subsequently its role in diabetic pathologies 2 decades later.  .

In 1791 Johann Peter Frank, a German physician, developed a yeast test to detect sugar in the urine; this gradually replaced taste tasting.  In 1788 Thomas Crawley linked the pancreatic dysfunction to diabetes.  Then John Rollo (d. 1809), a military surgeon in the Royal Artillery, he described 1798 the low-carb dietary management of diabetes mellitus.  Gradually the high fat and high protein became the standard treatment.      

A century after to Rollo work--if not early--physicians were determining the severity of adult diabetes by the amount of sugar in the urine over a 24-hour period.  It was crystalized, dried and weighed; under 200 grams was mild, and over 500 grams severe.[30]  This early start on diagnosis and also managing diabetes with diet was given a scientific foundation by the work of Claude Bernard (1813 to 1878)[31] through his work on the functions of the pancreatic juices and the glycogenic functions of the liver, and topics related to diabetes mellitus—a rival of Louis Pasteur in importance.  Among his contributions were the discovery that blood sugar levels were affected by a starch like substance released by the liver, which he named glycogen, and also that the liver absorbed sugar from the blood.  He developed the idea of homeostasis with the use of the current medical science, thus going beyond Hippocrates.  He contributed much in his Introduction to the study of experimental medicine (1865).

 In 1869 Paul Langerhans (1847-1888), a German medical student published a paper describing clumps of cells in the pancreas, which he thought were limp nodes; they were named after him. Others had shown the removal of the pancreas from a dog caused diabetes. 

Insulin received its name before it was discovered in 1889. In Germany, Oskar Minkowski and Joseph von Mering observed that total pancreatectomy in experimental animals leads to the development of severe diabetes mellitus.  This experiment supported the speculation that a mysterious substance produced by the pancreas is responsible for metabolic control.   Insulin was named before it was isolated.   

Dr. Moses Barron published in 1920 an article that described his experimental closure of pancreatic duct by ligature. This procedure prevented the trypsin—a digestive compound--from hydrolyzing the protein insulin secreted by the beta cells (and others hormones).[32]  Since the pancreas produces a number of substance, each from specialized cells (alpha islet cells glucagon. beta islet cells insulin, delta islet cells somatostatin, and PP cells pancreatic polypeptide) this formed another obstacle, that of obtaining with the chemistry of their day (before column chromatography).[33]  Each islet would yield several chemical in the production of insulin, glucagon, somatostatin and pancreatic peptide. 

The separation was beyond the chemistry of the two physicians attempting to isolate the hormone that digested glucose.  Doctors Charles Best and Frederick Grant Banting obtained the assistance of the biochemist James Collip.  This was done at the University of Toronto with the support of J. J.R. Macleod, Professor of Physiology.

It wasn’t until November of 1921 that insulin was isolated from beef and pork pancreas obtained from a slaughter house.  In the spring of 1922 Banting set up a private practice using the extra to treat t1d patients.  Banting and Macleod were awarded the Nobel Prize in Physiology in 1923, and they split their cash prize with James Collip and Charles Best.  Note, Fredrick Grant Banting is a distant cousin of William Banting, the funeral director to the Royal Household.  His book Letter on Corpulence (1863) is still in print and bant and Bantingism have become an English and Swedish words.

Insulin was only used for t1d--not used for t2d, but for a few exceptions.  The main dietary management of t2d remained low carbs.  “Those managed with low-carb diet lived as long as those without t2d.”  wrote Dr. Elliott Joslin.   The low carb diet very gradually reduces IR, and thus moderately the risks for CAWD.  Our drugs to manage t2d increase the risk for CAWD.  I hear the cash register in the background.

The European literatures on low carbs goes back at least to 1797 when Dr. John Rollo published An account of 2 cases of diabetes mellitus with remarks as they arose during the progress of the cure . . .  In 1898 Dr. Richard Thomas in his Diabetes Mellitus and its treatment wrote, “that all carbs should be cut off”.  He went on to write “Ever since Rollo published his book on diabetes in 1797, and pointed out the value of restriction of the carbohydrates in the food, it has been acknowledged that of all forms and methods of treatment this dietetic one is the most important.”  

And, yes, IR was common, sugar was inexpensive by 1810 because of selective breeding of sugar beets and sugar cane.   The condition of affluence gradually became common as the diet changed, and within a century t2d was common. 

Two U.S. physicians dominated the research on type 1 diabetes in the U.S. and the understanding of it from about 1913 and for the next decade for Frederick Allen, and Elliot Joslin for about 4 decades for both types of diabetes.  In 1918 Joslin’s book provided a table by insurance company for normal weight for 4 age groups according to inches and small, medium and large frames.  Each entry as age groupings increased in years, the normal weight increased.  This phenomenon of increased weight above the youthful norm is strongly associated with increasing insulin resistance—see the work of Joseph Kraft--bibliography.  In 1:3 are figures which show that paleo peoples with age, their weight goes down because muscle, cartilage, and bone mass declines.  To go up instead of down with ages entails an overall for the group of increasing insulin resistance which causes weight gain.  Historical figures show that there is a steady increase of t2d, obesity, morbid obesity, and overweight.  Increasing insulin resistance is the norm in the U.S.   

Frederick Allen at Harvard University ran a series of experiments, mainly on dogs, in which he removed their pancreas to produce t1d.[34]  Allen published in 1913 Studies Concerning Glycosuria and diabetes, a 1179-page tome covering his several hundred experiment on animal on metabolism related to diabetes and even more space devoted to case histories, mostly t2d.  It featured 1,200 item bibliography.  (The work can be read at Google Books for free.)  This and subsequent works made him one of 2 leading authorities on diabetes mellitus. 

Out of this research and case histories Allen developed the near zero carbohydrate starvation diet for t1d.  He thought the previous attempts failed because the fat content in the diet cause ketoacidosis—the drop in blood Ph. sufficient to cause often terminal acute reaction.  Allen used a liquid diet focused on avoiding glycosuria (sugar in the urine) and acidosis (low fat).  Allen in 1921 set up a clinic in Morristown, New Jersey for those with early onset diabetes (t1d).  When sugar began to show up in the urine, calories were lowered. Calories average around 600 daily, depending on weight of patient, all of whom were children.     

Following Allen’s writing on starvation treatment, Joslin set up a boys-camp for t1d.  Of his first 1000 cases before insulin Joslin wrote, “I tried to let the four hundred fatal cases tell their useful lesson through the six hundred living.” [35]  Living with t1d had the price of being at the camp under supervision of nurses, and the stress of starvation, and waiting to die.  Though t1d was tragic with children wasting and most died in the first year, the literature focused on t2d, for whom the course was slow, and it could be managed with diet.  As one of the two leading authorities on diabetes in the U.S.--along with Eliot Joslin--Allen received a limited quantity of insulin in 1922 following its successful purification.  It took until 1923 for mass production of insulin.  Insulin was used for those with t1d and those who failed to manage t2d with diet. 

Dietary management of t2d:  Mary Enig noted that “. . . before the discovery of insulin, the only treatment of diabetes was a diet containing a large amount of fat.” [36]   Elliott Joslin’s 3rd diabetic patient was his mother in 1900.  Out of concern he travelled to Germany to learn their method for what we now call type 2 diabetes.  Joslin wrote:  

Naturally, I went to Strassburg to learn from Naunyn, the Nestor[37] of diabetes, how to treat her.  Following his method and with a relatively low-carbohydrate, high fat diet, which I can truthfully say I never knew her to break, the 6 percent sugar soon disappeared and she lived healthfully and cheerfully for 13 years with her diabetes, which was as long as she was expected to live without it.[38]

Notice the low carbs, high fat for adult treatment for t2d, for his mother and millions others world-wide with t2d.  The literature was focused on the adult form which could be treated.  For t1d, except for the attempts of Frederick Allen, little could be done for the quickly fatal juvenile t1d.  In contrast t2d was treated successfully with diet. 

           Joslin’s experience treating t2d including his mother and aunt and the setting up for nurses a special training in the treating of mainly t2d at the New England Deaconess Hospital. This experience lead to his writing 1918, A Diabetic Manual for the Mutual Use of Doctor and Patient, which with new editions remained the standard authoritative source on diabetes in the U.S. for the next 60 years—last edition (14th) in 2005 under the title of Joslin’s Diabetes Mellitus.  The later editions focused on both forms of diabetes.

In Elliott Joslin’s 1918 book on the treatment of type-2 diabetes, he attributed the cause of diabetes to excess sugar.  Between 1800 and 1810 the average consumption of sugar by individual in the U.S. was 11 pound a year, but between 1910 and 1917 it was 73 pounds. . . . with showing this figure for 1916 to be 90 pounds.” [39]

Elliott also thought for several reasons that fats also contributed to the development of t1d and t2d.  But for several reasons many—if not most-- of the physician continued with the low carb diet rather than the balancing of carbs to glycosuria.  Joslin’s recommended diet:  one gram of protein per kilogram of thin weight, and fat at about 30% of calories or less with carbs contributing the major source of energy.  The belief of sugar as cause was buried along with Joslin’s mother who took “6 teaspoons of sugar”—above--as too the pre-insulin undernutrition diet of calories was 70% fat , 22% protein,[40] and 8% carbs.  What caused the switch, at least in the U.S? 

          Joslin’s 2nd book on diabetes for physicians and type-2 diabetic patients is a version of his first book published 2 years before which focused on the science of diabetes mellitus and his clinical experience, The treatment of diabetes mellitus whose last and eight edition was in 1946.  By 1916 his view on carbs and fats changed because of the usually fatal ketoacidosis.


3-Oxobutyric acid KetoEnol.svg

                          Diacetic acid (acetoacetic acid)            acetoacetate  

          The main cause was his (and others) belief that diacetic acid is responsible for diabetic ketone acidosis (DKA): it was believed that the metabolism of fats produces diacectic acid (now commonly called acetoacetic acid) changed the blood’s PH.  The chemistry was faulty, diacetic acid doesn’t appreciable lower Ph.  Diacetic acid is unstable and exist in its quite stable conjugate base,[41] acetoacetate.  The acetoacetate is converted to Acetyl-CoA and enters the mitochondria where it is then covert to oxaloacetate which enters the Krebs cycle.  This error in fat producing diacetic acid from fats and thus a cause for DKA is the main cause, at least during the pre-drug era, for come up with the complicated dietary management. 

I have come to believe the cause of DKA is the dysregulation of the buffer systems which control Ph.  With extreme insulin resistance of the diabetes, many of the hemostasis systems function poorly. 

The acetoacetate form entails that fatty acid metabolism doesn’t cause DKA (#8) for those with t1d and LADA.  The ketone bodies accumulation with t1d and LADA is at 3 times the amount of those on a ketogenic diet.  The lack of insulin causes the higher accumulation of ketone bodies in the bloodstream.  It isn’t this 3-fold excess of ketone bodies that lowers the Ph. of blood sufficiently to cause DKA but the Ph regulatory systems.  Those with t2d (excluding LADA) produce sufficient insulin to prevent DKA.   Joslin in his books followed the science of his day and believed fats caused DKA in those with t1d. 

The work of Professor Bloor and Dr. Gray in Boston and that of workers at various other laboratories has provided us with a reliable indicator for the tolerance of the patient for fat by means of the estimation of fat in the blood. . . . The patient is gaining a tolerance for carbohydrate, and the continued omission of fat beneficial in counteracting the last vestige of acid poisoning, or preventing the appearance of acid poisoning. [42]

Joslin did a bit of mental juggling to account for those of good health who are on a ketogenic diet, such as the Eskimos, those who used the ketogenic diet to prevent or reduce epileptic seizures, for popular weight loss low carb diets, such as promoted by William Banting, Letter on Corpulence (1869) which is still in print a 150 years later, and for the success of the low carb diet to manage adult onset diabetes. 

Eliot Joslin wrote of an adjustment period to his low fat, moderate carb diet. 

The acid intoxication (acid poisoning, or technically termed acidosis) of normal individuals, easily to be produced within three days by the omission of carbohydrates from the diet. . .  When however, the healthy body is gradually accustomed to live upon a diet low carbohydrate, acidosis is avoided.  The same course of events takes place in diabetics.  . . .  This did result when years ago we physicians doing the best we knew, deprived patients of their carbohydrates in order to make them sugar-free, and at the same time, in order to enable them to maintain their weight, we markedly increased fat and protein to make up the calories omitted as carbohydrate.  . . .  we now know better.[43]

Besides DKA with its high mortality Joslin and other though pathogenic the appearance of cloudy blood samples of those on a high fat, low carb diet.  The blood when insulin is low contains free fatty acids, most of which are saturated fats.  Since after taking of blood, refrigeration (ice boxes) was used for preservation of the blood, the saturated fats cooled and gave the blood sample a cloud appearance.  Those on a normal western diet back then with 40 to 50% of calories from fat would, their blood would have significantly lower amount of free fatty acids and thus would frequently appear clear after cooling.  This difference in diet led most in the U.S. researchers to believe that the high fat diet and diacetic acid were the cause of DKA and a major risk factor for t2d—though rare.  This belief resulted their recommended of low-fat diet. However, since a high carb diet caused glycosuria (sugar in the urine) a middle path was best devised, and Joslin adapted that approach and ignored what worked for his mother and aunt; he added much more carbs to the recommended diet.     

The treatment of newly diagnosed t2d relied upon testing the urine for sugar.  The severity of t2d was measured by the amount of sugar in a 24-hour period:

Case 295     680 grams a day, A Severe Diabetes

Case 1147   300 grams a day, A Moderate Diabetic

Case 653     174 grams a day, A Mild Diabetic[44]

Treatment started with very low carbs to eliminate the sugar from the urine, thus fats replacing carbs.  Then there was the process of restoring of carbs to the diet and testing the blood weekly to see at what amount sugar again appeared in the urine.  Such testing required strict adherence to the diet during the testing period, and then making it part of their lifestyle.  Adherence was a problem since t2d is without side effects until glucose is quite high.  For those with severe t2d, “tolerance is less than 20-grams carbohydrate, fasting should be practiced one day in seven.” [45]  Most of them had symptoms, their adherence was better. 

Joslin was aware of the benefit of fasting for the most refractory cases.  One patient once under the care of a Dr. Randall of Topsfield Mass, but now under Joslin’s care, case # 1062:  who contracted diabetes twenty-six years ago, . . go without food, save broth, for several days in succession, and that she would follow his advice.  Her severe symptoms of diabetes subsided at the end of four years.  Her tolerance on June 1, 1916, reached 116 grams of carbohydrate.” [46]  How popular fasting was in Joslin’s area for t2s I don’t know; however, fasting for health was far more common compared to today. 

Though Joslin’s book was the standard on diabetes, others continued with the older low carb diet for t2d.  The most influential text book of the era, by William Osler--considered the father of modern medicine--recommended in his 1923 edition 5% carbohydrates.[47]  Many continued to practice medicine according to experience in the era before guidelines and HMOs. 

Managing t2d with Joslin’s diet never dominated until drugs were found to lower glucose for adult onset diabetes.  Joslin in his book made a negatively commented about physicians giving drugs (he might have been referring to aspirin or another salicylate, they lower significantly glucose in a dose of several grams daily).  He went on to state, “I wish I knew of a good drug for diabetic patients.  It would save me so much time and talk.”  To follow his receipts, calculate the carbs, and in the day before the strip urine test entails more than most t2d patients would follow and consumed more time than most physicians would give.   Another issue is low compliance to his diet, probably no better than today’s with calorie restricted diet and ketogenic diets.  Finally, the low carb diet for t2d permitted a moderate amount of carbs, and thus as with his mother and my aunt an easy life-style change. The recommendation of Joslin was just a competing dietary treatment recommended in both in the U.S. and Germany, thus the norm continued practice to be treating t2d with the low carbs diet. 

The cause for t2d was nearly a century away from being solved and that for t1d has yet to be solved.  The Sugar Association (then known as the Sugar Research Foundation) played a significant role in this delay for the cause of CVD, the blaming of fats for CVD.[48]   They paid 3 Harvard professors to publish tobacco science.  Two of the professors rose to the top, one Fredrick Stare became chairman of the university’s nutrition department; the other D. Mark Hegsted became a USDA official.  The beverage industry had similar activities.  The media of course knows where their interests lies. 

By 1950 much of the major pieces for t2d were known and covered by Merck: 

Damage to the insulin producing cells of the islets of Langerhans, by causes as yet unknown, is responsible for most cases of diabetes mellitus [t2]. . . In certain cases the diabetic state results from increased insulin requirement by the tissue cells to maintain normal carbohydrate metabolism. . . contributor factors are known.  Excessive consumption of sugar and fat. Heredity is apparently important . . . . Pancreatitis hemochromatosis, pancreatic tumors, and trama. . . .It is estimated that between 1 and 2% of the U.S. population  are diabetics. . . .  The liver in uncontrolled diabetes mellitus often is enlarged and fatty.  When symptoms do exist they are so mild that they do not cause the patient to seek medical advice.[49]    

[1] Rowley, Willliam, Clement Bezoid et al, feb 2017, Diabetes 2030:  insights from yesterday, today and future trend

[2] Virtually entails:  There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or "other specific types of diabetes").” Wiki, type_2_diabetres, Feb 2020. 

[3] To repeat myself on this important fallacy:  Vision a bell curve, then vision a population taking a mild poison such as a statin or a sedative for depression.  The bell curve moves to the left; and this includes those at the far right of the curve.  The fallacy lies in cherry picking those of the 10 or 20% on the right of the curve before treatment, and then claim that since they are at the right of the center after a period of treatment, say a year, have benefited from the treatment.  Even those who have come out better after treatment than they were before hadn’t benefited:  Without treatment, they would, they will have also done better, even more than treated. 

[4] Shaneyfelt, Terrence, Robert Centor, JAMA 2009, Reassessment of Clinical Practice Guidelines Go Gently Into That Good Night.  Title of one section of the article: Best guidelines influence can buy: how it happens. 

[5] Powell, A, March 2012, Harvard Gazette, Obesity? Diabetes? We’ve been set up, and Jason Fung Obesity Code (2018) P 58. 

[6] Jason Fung, The Diabetes Code,

[7] The lack of reporting of t1d among LSPs entails a connection to the western diet, and thus likely IR as a CC for t1d. 

[8] Richter, B,  B. Hemmingsen, October 2018, Cochrane Review, Development of type 2 diabetes mellitus in people with intermediate hyperglycaemia ('prediabetes')

[9] Madsen, KS, Y CHI, et al, Dec 2019, Cochrane Review, Metformin for prevention/delay of type 2 diabetes mellitus (T2DM) and associated complications in persons at increased risk for development of T2DM

[10] Hemmingsen, B, Sonne Pelck, et al, Cochrane Review, Oct 2016, Can the glucose-lowering drugs insulin secretagogues prevent or delay type 2 diabetes mellitus and its associated complications in persons at increased risk of this disease? 

[11] Gary Taubes, The case against sugar, 2016, P 7, using William Olser’s figures from newer editions of his textbook.   

[12] Taubes supra P 8-9. 

[13] First case was diagnosed by Auguste Deter in 1901 in a 50-year old women.  She died in 1906.  During the next 5 years 11 similar cases were reported.  It was classified as a subtype of senile dementia in a psychiatry textbook of 1910.   

[14] Worse in that the carbs in beer exacerbate the effect of fructose upon the liver in an additive way. 

[15] Somer, JB, G. Thompson, et al, Sept 1980, Influence of ethanol on pancreatic lipid metabolism   A major cause of pancreatitis is heavy alcohol use, which promotes accumulation of fat. 

[16] Norton, I.D., M.V. Apte, et al, May 1998, Chronic ethanol administration causes oxidative stress in the rat pancreas

[17] An average of 3.9 per 15 relatives, over 50% chance that there are 3 of the aunts, uncles, parents, siblings and grandparents. 

[18] Robbins Pathologic basis of disease, 6th edition (1999), P 914.

[19] Robbin supra 917.

[20] Henschen, Folke, April 1969, On the term diabetes in the works of Aretaeus and Galen

[21] Because of later additions the work is referred to as the Hippocratic Corpus.

[22] Gemmill, Chalmers MD, Sept, 1972, The Greek concept of diabetes

[23] Eknoyan, Garabed, Judt Nagy, April 2006, A history of diabetes mellitus or how a disease of the kidneys evolved into a kidney disease.  Paracelsus is considered the father of modern anatomy. 

[24] Wiki, history of diabetes March 2020

[25] He played an important part in the history of anatomy, neurology, and psychiatry and was a founding member of the Royal Society.  He was pioneer in the research of the brain, nervous system and muscles

[26] Richard J. Johnson, The fat switch (2012)

[27] Type one, childhood diabetes, was quite rare, and most died within months of becoming symptomatic. It didn’t make the medical literature for it was unlikely that a physician would see more than one child.  

[28] Wiki, glucose. March 2020

[29] Wiki, sweetness, 2/20, variation are from different studies.  Sweetness is a subjective rating. 

[30] Weight was determined following evaporation; the residue, mainly glucose, was weighed.

[31] Bernard made many major contributions to science medicine and physiology.  His first major contribution was on the pancreas which shed light on the cause of diabetes mellitus.  He demonstrated the glycogenic role of the liver.  He discovered the vasomotor system in 1851.  He developed the concept of homeostasis and popularized vivisection.  He made significant advances in the adoption of scientific methods including blinded studies.  These ideas and other were the theme of An Introduction to the study of experimental medicine (1865). 

[32] In the pancreas trypsin  is the proteolytic form of trypsinogen thereby preventing self-digestion of the pancreas.  Activation of the trypsin in the pancreas leads to a series of event that result in pancreatitis. 

[33] A glass tube column several feet tall is packed with a powder such as silica gel, to which solvent is poured through to form a slurry.  An Eluent of a solvent with the mixture to be separated is then poured at the top of the column.  This eluent will pass through the slurry in the column to form separate layers depending on the affinity of the compounds to the slurry.  This permits the layers within the column to be separated.  I have done this in the late 1970s with the assistance of biochemistry Prof. Richard Barnett who had done original research using column chromatography during the late 1940s through the 50s which were published.   

[34] Allen, Frederick MD. In Experimental studies on diabetes; Series I. 1920; Production and control of diabetes in dogs, P. 575-586

[35] Dolger, Henry, July 1972, Joslin’s Diabetes Mellitus.  The article is the title of Joslin’s later editions. which Dolger reviewed.

[36] Dr. Enig, Mary, Eat Fat, Lose Fat, 2006 P 143.  Enig (1931 – 2014) An international expert on fats that did major research on fats, and was a leading critic of the tobacco science that natural fats caused CVD. 

[37] Wise Greek senior, who went with the army to troy in the Trojan war, as related in the Iliad.

[38] Diabetes Manual, Tenth Edition (1959), Elliott P. Joslin, P 21. Earlier editions had a different tile (below).  

[39] Elliott Joslin, MD, 1918, A Diabetic Manual for the mutual use of Doctor and Patient, First Edition, P 18

[40] The amino acids, given the starvation, was not metabolized for ATP, but used for essential hormones, receptors, and other essential bioactive compounds.  I find it amazing how many ways the body resists death.   

[41] A conjugate base is the result of an acid donating a hydrogen ion to and organic acid, and thus because of its hydroxyl group is now a base (often with a Ph. above 7).  The base form has a half-life of 130 hours, the acid form of 140 minutes at 39 degrees centigrade a nearly 60 times longer base form. 

[42] Joslin, supra 96. 

[43] Joslin supra 103

[44] Supra Preface

[45] Supra 97

[46] Supra 104

[47] Osler William, McCrae T: The Principles and Practice of Medicine. 1923, New York, Appleton and Co. The diet contained approximately 5% of energy from carbohydrates, 20% from protein, and 75% from fat.   A similar diet recommendation by Frederick Allen in Total dietary regulation in the treatment of diabetes, No. 11, 1919 (available at Books.google.com for free). 

[48]  Kearns, CE, LA Schmidt et al Sept 2016, JAMA, Sugar industry and coronary heart disease research:  a historical analysis of internal industry documents.  Gary Taubes’, The case against sugar develops the role of that industry’s association and Prof. Stare’s role in promoting the safe, empty calories myth and their role in influencing U.S. government’s actions.  . 

[49] Merck Manual 8th Ed 1950, P. 268-269. 

5. Dietary low-carb management of t2d, Merck 1950-61:  extreme low carbs go back at least to the 18th century of adult onset diabetes for western medicine, and probably 3-thousand years or more based on references to urine and diet in surviving fragments from Greece, India and Egypt.  Choosing practices within my lifetime, I picked up my 1950, Eight Edition of the Merck Manual and read their diabetes section.  In the 1950s there was one diabetes in two forms:  either juvenile or latent adult:   

One of the earliest decision the physician must make is whether diet alone will suffice or whether insulin is needed in addition.  Often the obese elderly patient after weight reduction can get along with dietary supervision alone. . . .  Dietary measures:  The diabetic diet is a regularly ingested  “normal diet” with the exception that the more rapidly absorbed carbohydrates[1] and food containing them in large amounts must be eaten sparingly (see Diets). . .  regularity helps prevent overloading of carbohydrate-disposal mechanisms and consequent hyperglycemia. . . . There now seems to be no reason to believe that adult diabetics cannot under proper care, live as long as nondiabetics and carry on relatively normal activities. . . .  In well controlled cases [i.e., blood sugar normal or nearly so], there are fewer complications.[2]    

The medical consensus was that elevated blood glucose was relatively benign until it became symptomatic above 11 mmol/L.  Merck manual was following that consensus, but as drugs came to the market, it followed the new, better treatmentnew and worse phrase is never attached to the new drug on the block, and Merck U.S. is the 7th largest pharmaceutical companies in the world.  Merck is subsidiary of the German Merck which was founded in 1668.  The Merck Manual of Diagnosis and Therapy is the world’s best-selling medical reference.  So have modern miracle medicines and the guideline-generated standard-of-care that improved the lot of the diabetics?  Is new drugs better than diet?  If you were diabetic, would you chose diet or drugs? 

          Drugs came on the scene, other than aspirin, with sulfonylureas, discovered in 1942.  When testing it as an antibiotic, it was found in a high dose to induce hypoglycemia in animals; it increases the release of insulin.  Increasing insulin increase weight gain, IR, and the other CAWD (though of course pharma ignores these side effects and addresses them when needed with tobacco science).  By 1961, 10 Edition of the Merck Manual, 4 insulins had replaced dietary management (drug table P 365)—in Europe sulfonylureas were the treatment of choice.[3]  So what happened to the diet? 

Not surprisingly by the 10th Edition of the Manual  “In general, the fat in the diet of normal- weight diabetic patients varies from 50 to 120 Gm./day and the carbohydrate from 150 to about 250 Gm” P 331-332.  This diet promotes insulin management of both type of diabetes mellitus.  Critics like Gerald Reaven were critical on the focus on carbs and the  glycemic index:  “Raven also disparaged the glycemic index for putting the clinical focus on blood sugar whereas he considered insulin resistance their disease.  Reaven insisted, was to restrict all carbohydrates.”[4]  He was marginalized on role on insulin resistance and sugar in the development of diabetes.  

Gerald Reaven (1928 to 2018) was an endocrinologist and professor at Stanford University School of Medicine whose work on insulin resistance and diabetes achieved notability including the annual Banting lecture in 1988 titled Syndrome X which focused on what we now call metabolic syndrome, the grouping of cardiovascular disease, hypertension, insulin resistance, impaired glucose tolerance, and abdominal obesity. 

Since the 1950 Merck Manual, Eight Edition, the science behind dietary management has made big steps forward both as how best to lose weight, keep it off, and how to cure t2d with high fat diet and fasting, or bariatric surgery; but our standard-of-care is pharma-generated.  But Merck editors don’t mention the dietary science.  Today it is known that the harm associated with t2d (not counting drug side effects) is from insulin resistance which slowly increases because of the medications.  Given the many regulatory functions of insulin, its excess is driving the diabetic health disaster along with the MTDD that is causal for IR.  Another CC is the higher cellular glucose and its slowed rate of conversion to pyruvate, this increases frequency of turning on the polyol pathway that produces fructose and delays the conversion of fructose to pyruvate thereby increasing fructation.[5]  IR, MTDD, are the two major causes and as a result there is the increased fructation, along with the rest of the B4, and those major cause listed in section 3.  A large body of published studies support that drugs and carbs should be contra-indicated for t2d because the low carbs controls t2d lowes the risks for CAWD. 


5. Low carb diet for diabetes mellitus:  Allow me to repeat what is occurring with t2d:  increasing pancreatic release of insulin by dietary carbs and or drugs accelerate the pathogenic processes by increasing IR.  Excess insulin is a very bad thing (3:5).  Excess insulin affects many homeostasis processes.  In addition, since cellular fructose is metabolized last after glucose, the slowed uptake of glucose because of MTDD entails an even slower uptake of fructose from the blood and delayed cytosol conversion to pyruvate, this increases fructation of proteins and PUFAs transported into the MTD, thus causing a higher rate of MTDD when compared to those without IR.  For these reasons low fructose and other carbs diet for those with IR is a healthful choice.  The damage by overstuffing cells also turns on PP’s production of fructose.  The longer it takes to clear the carbs from the cytosol, the longer it will take to switch to fat metabolism and turn on autophagy, another CC for CAWD and t2d.  The high level of insulin is a major CC for the conditions associated with t2d. 

In addition, insulin has many regulatory functions (3:5) that are affected, another pathway to CAWD.  The once standard management of t2d with a low carb diet ought to be reestablished as standard of care and we should follow Oliver Wendell Holmes, Senior, advice of tossing the drugs into the sea.  He stated that “it would be better for mankind and worse for the fishes.”

          The management of t2d with drugs before the development of glucose meter (available in the late 70s in physician offices and the first home meter introduced in November of 1981) there was a major risk for hypoglycemia both for those on insulin and the other drugs for diabetes.  Monitoring consisted of urine testing.  But urine testing is only moderately associated with serum glucose.[6]  The low fat diet was a major CC for hospitalization and death, and still is for those who don’t frequently monitor their blood glucose or who over indulge in recreational drug or suffer from depression and their treatment with sedatives.      

          The call for the low-carb treatment of t2d resulted in 2015 of a journal article with 29 signatures.  The article has 12 point of evidence that support low carbs the sum total of which is compelling.  It is not known who decides what constitutes evidence-based medicine but we feel that these points are sufficiently strong that the burden of proof rests on critics.” [7]  This is a seminal article calling for the science to dictate guidelines: 

12 Points of evidence [bold I consider more important] 

Point 1. Hyperglycemia is the most salient feature of diabetes. Dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels

Point 2. During the epidemics of obesity and type 2 diabetes, caloric increases have been due almost entirely to increased carbohydrates 

Point 3. Benefits of dietary carbohydrate restriction do not require weight loss

Point 4. Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss

Point 5. Adherence to low-carbohydrate diets in people with type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.

Point 6. Replacement of carbohydrate with protein is generally beneficial

Point 7. Dietary total and saturated fat do not correlate with risk for cardiovascular disease

Point 8. Plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary lipids

Point 9. The best predictor of microvascular and, to a lesser extent, macrovascular complications in patients with type 2 diabetes, is glycemic control (HbA1c)[8]

Point 10. Dietary carbohydrate restriction is the most effective method (other than starvation) [fasting] of reducing serum TGs and increasing high-density lipoprotein [Misses that those with the highest 20% of cholesterol live the longest—Framingham Heart Study, started with 5,209 residents in 1948.  It is still running with the edition of a 3rd generation the descendants of the first generation and their wives.]

Point 11. Patients with type 2 diabetes on carbohydrate-restricted diets reduce and frequently eliminate medication. People with type 1 usually require lower insulin.

Point 12. Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to the effects of intensive pharmacologic treatment [Referring to the failure of intensive glucose lowering as not lowering, but rather increasing comorbidities].[9]

Each of these 12 points has several paragraphs with citations to published evidence and most of the 12 have appropriate graphs and tables.  This seminal 2015 article is focused on dietary management of t2d.  As for the critics, there aren’t any, KOLs avoid confrontations and continue to spew out their poisonous cocktail to patient, their CME classes, their textbook chapters, and their guidelines for the “progressive condition.”

Though the article is focused on diet for t2d, there is much more to understanding the forest.  Topics developed in this book prior on the CC for MTDD: fructation, IR, NAFLD, inflammation of the pancreas, the role of fructose in the polyol pathway to lower glucose, all these support the call for the low insulin thus low carb management and treatment of t2d and t1d. 

Not surprisingly is the failure of ADA guideline to mention lipid droplets in the liver and pancreas, and there is in those guidelines a total failure to recognize the issue elevated insulin caused by the medications which are the main CC for the conditions associated with t2d.  Like the seminal article with its 12 point, I cry out for the abandonment of the drug treatment of t2d and its replacement by a low carb and for some a ketogenic diet.

I think of Gunter, my brother-in-law dead at 53, Ela Fitzgerald who had both her legs amputated below the knees, of Jerry Garcia at 53 and 8 days dead from a heart attack, and my neighbor across the street below the age of 65, she died in 2019from kidney failure after 2 years on dialysis.  Yes, I too cry out for the low carbs like Bernstein, Westman, Volker, and the 26 others in a seminal article published in 40 versions, but not in the big 5 English language journals.  We all know friends and relative that have gone down the drug pathway with the lowered quality of life.  Treating glucose as shown by their examples is a failure. 


7.  Fructose damaging MTD is the starting point:  The question is what is causing the insulin resistance?  The textbook answer: In states of insulin resistance, the same amount of insulin does not have the same effect on glucose transport and blood sugar levels.”[10]  Then follows a list of associated factor; but I am not asking what is associated with IR such as age, obesity, sedentary lifestyle, etc., or the downstream effects of IR, such as reduced uptake by cells of glucose, increased release of ROS.  I am asking what is going on in the cell that causes the increased ROS and other contributory pathogenic changes.  The answer is described at length in 2:4:  fructose damaging the MTD through fructation of the proteins and PUFAs imported into the MTD when it is sufficient to have a cumulative effect that is beyond the various repair mechanism for the MTD.  The damage to the mtDNA eventually reach a critical mass and mitophagy and fusion passes on to future generations the mutated mtDNA.  This is the main cause, while PUFAs lower sex hormones, low antioxidants are less significant contributing causes. Though not as of now researched, I would add MSO and RCP as CC for MTDD.  Bad medical science produces bad answer and illness. 

          This decline in glucose metabolism caused by the hepatocytes’ load of mutated mtDNA and thus RATP to cause insulin resistance in the liver, and thus a reduced uptake of glucose by the hepatocytes.  Given the role of the liver’s hemostatic functions including the maintaining blood glucose level mainly through the production of glycogen, its breakdown of glycogen into glucose when needed, and its diminished rate of its detoxification functions, and others all contribute to the development of insulin resistance in other tissues, of which the most significant are the myocytes, adipocytes and other tissues with a have high rates of metabolism.   


8.  NAFLD, to IR and fatty pancreas leads to t2d:  Virtually unknown before 1980, nonalcoholic fatty liver disease now affects up to 30% of adults in the United States and other developed countries, and between 70% and 90% of those who are obese or who have diabetes.” [11]  While largely unknown in the 2000s, NAFLD, NAFL and NASH are the leading cause of chronic liver disease as of 2017. . . . People with NAFLD are likely to be asymptomatic − to have no noticeable symptoms − and often have normal laboratory profiles. . . . The diagnosis of steatosis is made when fat in the liver exceeds 5–10% by weight.” [12]  Understanding the route from the liver to t2d entails understanding prevention and the best dietary treatment.  Since fructose has minimal effect upon insulin, and thus blood glucose, the measuring of insulin and glucose promoted the assumption—supported by the Sugar Research Institute—that fructose was harmless.  “It only became apparent by looking at the slow accumulation of fat in the liver. . . .  Replacing glucose with fructose increases liver fat by a massive 38 percent within eight day.” [13]  Between 50 and 70% of dietary fructose is utilized by the liver.[14]  Moreover, fructose can increase DNL 5-fold.[15]  Allow me to explain again, given the importance of this topic.    

            1. As prior mentioned (3:4), fructose causes MTDD first in the liver, because the liver is the most exposed organ via the hepatic portal vein from the intestines.  Reduced rate of metabolism of glucose and subsequent fructose.  “Insulin signaling in liver is critical in regulating glucose homeostasis and maintaining normal hepatic functions.” [16]  With the development of NFALD, the rate of utilization of glucose decreases, and since the liver utilizes up to 30% of glucose, this diminished rate will significantly raise insulin secretion to lower blood glucose.  through Insulin causes conversion of FFA to triglycerides, thus because of MTDD the excess fat is first in the liver, and with IR, fat accumulates throughout the body.[17]   The pancreas is of particular concern since that organ has receptors for fructose.  The net result is the gradual accumulation on the high sugar diet of lipid droplets in the pancreas.  On the basis of the work of Roy Taylor[18] and others it has been shown that the decline in the production of insulin that causes t2d is a result of inflammation of the pancreas brought on by lipid droplets in the pancreas. 

            2. There are other process caused by fructose that promote NAFLD besides MTDD.  Fructose activates the IMP pathway resulting in the production of uric acid and MSO (monosodium urate crystals).  This sharp micro-crystals can damage tissues and cause resulting inflammation and worse.  The fructosylation of the hepatocytes of the proteins and PUFAs transported to the MTD lead to the damage to the MTD that causes the release of ROS and MTDD.  MTDD slows the metabolism thereby increasing the PP making fructose and MTDD extends the time for which fructosylation occurs in the cytosol.  The deterioration of functions of the liver, the deveation from the paleo-normal levels for insulin are major causes  for diabetes and CAWD.


                  9.  Bariatric surgery cures t2d:  About 80% of those undergoing biliopancreatic diversion are cured of t2d.[19]  ; the remaining 20% have progressed from t2d to t1d, known as latent autoimmune diabetes in adults, LADA.[20] The evidence that surgery not only causes a major reduction in weight but also cures t2d is dispositive: “a ten-year remission rate of type 2 diabetes of 36%.” [21]  “Type 2 remission after 2 years was 72% and 36% after 10 years.” [22]  The reduction in lipid droplets in the liver and pancreas with it reversal of IR entails those organs functioning normally and thus reversing IR.[23]

                            The failure to remain drug free is because of the message: carbs are good, fats bad, and sugars are empty calories.  As their ability to consume more food is restored many of them are back on the pathogenic western diet.  Their weigh regulatory system again functions to restore their weight gradually and again they go down the road again to IR in the liver, fatty liver, and general insulin resistance.  Again I must gripe about the crapolla of bad the KOLs and the wrong message given these patients by physicians and dieticians.

                  On top of that the KOLs have the wrong theory for the cause and for the “remission”:  the KOLs hold that the remission is caused by the dysregulation of hormone secreted in the stomach to which the surgery corrects: “Bariatric surgery is a hormonal surgery in these procedures, for which the alteration in gut hormones develops as a result of the procedure's restriction and malabsorption.” [24]  This gut-hormonal theory entails remission is temporary because as the stomach gradually grows to adjust to the quantity of food the hormones from the gut increase and the patient develops t2d a second time.  Secondly based on this it is held that the remission is not caused by weight loss.  This implants the idea that if an obese diabetic lost most of his excess fat he would still be diabetic.  The KOLs of course ignore important facts about the metabolism of excess fat in the pancreas and liver and that half of bariatric patients are cured in the first two months before significant weight loss.  They got it wrong, and they ignore the studies that prove it. 

                  Bariatric surgery is associated with a significant reduction in the weighted incidence of a number of histological features of NAFLD including steatosis (50.2 and 95 %CI of 35.5–65.0), fibrosis (11.9 and 95 %CI of 7.4–16.3 %), hepatocyte ballooning (67.7 and 95 %CI 56.9–78.5) and lobular inflammation (50.7 and 95 %CI 26.6–74.8 %).[25]

                  Similar finding for ectopic pancreas fat:

                  Recent literature suggests that ectopic fat deposition in the pancreas may contribute to endocrine and exocrine organ dysfunction, such as type 2 diabetes (T2D), pancreatitis or pancreatic cancer. . .   PTGC (pancreatic triglyceride content) was significantly higher in type 2 diabetic subjects (23.8±3.2%) compared with obese (14.0±3.3; P=0.03) and lean subjects (7.5±0.9%; P=0.0002).  An improvement in insulin resistance. . . . Pancreatic fat increased with T2D and drastically decreased after the bariatric surgery. This suggests that decreased PTGC [pancreatic triglyceride content] may contribute to improved beta cell function seen after the bariatric surgery. [26]

                  Restoring t2d by pathogenic high-sugar diet does explain why some do and other done’t get t2d for a second time. Unfortunately, I do not know of studies tracking sugar consumption following surgery.  Looking under the wrong tree entails not tracking diet.  The term remission is inappropriate, since they have been cured, and the subsequent acquiring of diabetes a second time is not the reappearance of a dormant condition (not remission) like herpes, but the travelling down the same dietary pathway that caused the first bout of t2d.   Insulin resistance, sugar, leptin, fatty pancreas and liver[27] are all ignored.  Again they have the research community looking under the wrong type of tree, what Prof. Ben Goldacre calls framing the topic.  We got drugs that promote illness, and the dietary fix marginalized.

                             Not wishing to repeat what was covered in the previous chapter which was on weight reduction, you can visit 6:3, 6, which while on long-term weight loss for those having bariatric surgery, that subsection provides the evidence for the curing t2d.  In that section are two long-term following of patients who had biliopancreatic diversion (Roux-en-Y bypass), and that this type of procedure has superior results.  This option which is more expensive, slower recovery from the procedure, is not being paid for by insurance companies, and the procedure has been replaced by less expensive, less invasive, and less effective procedures. 

                            On the bright side though is a new procedure with affects similar to the biliopancreatic diversion uses a liner and has similar results.[28]  On the dark side is the lack of oversight for devices with horrendous consequence; e.g., heart valve replacement, J & J’s knee replacements, patches following surgery to name three high profile failures of the 2010 decade, each harmed tens-of-thousands of patients.  The question remains how safe is the procedure, will the insurance companies pay for this procedure given that they profit illness, especially from Medicare recipients.    

                  All bariatric surgeries because of extreme caloric reduction following surgery with its increased autophagy promotes the restoration of pancreatic beta cell functions.[29]   Does this finding of subsequent to surgery, extreme low carb diet extend to fasting for those with t2d?  Can one cure not just t2d with diet and insulin resistance without surgery?



                  10.  Curing t2d with ketogenic diet or fasting:   Aalternate-day fasting and to ketogenic diet avoid the yo-yo diet and maintain their weight loss (6:3, 7-8).  Could they also like bariatric surgery (#9) reverse t2d IR? [30]  Fasting and the ketogenic diets turns on autophagy.  The low insulin level increases the duration of autophagy and from this comes the variety of benefits as the body rights the upside-down ship. 

Very-low carbohydrate diets inducing ketosis have shown to be effective in weight loss although superiority over caloric restricted diets continues to be debated [by KOLs and dupes].  Ketosis can improve markers of metabolic syndrome through reduction in serum triglycerides, elevation in high-density lipoprotein as well as increased size and volume of low-density lipoprotein particles. These changes are consistent with an improved lipid profile despite potential increases in total cholesterol level. 

Seizures  Ketosis induced by a ketogenic diet is a long-accepted treatment for refractory epilepsy.] It was first used in the 1920s and is now widely implemented for pediatric and adult patients. 

Neurological diseases: In addition to its use for epilepsy, ketosis is being investigated in other neurological diseases due to its proposed neuroprotective effects including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), autism, headache, neurotrauma, pain, Parkinson's disease, and sleep disorders.

Cancer: Preclinical studies have indicated ketosis may have anti-tumor effects, however clinical trials have been limited by small sample sizes and not shown conclusive benefit.

Other conditions: There is emerging evidence for the use of ketosis in other conditions such as type 1 diabetes, non-alcoholic fatty liver disease, acne and polycystic ovary syndrome, however evidence quality is limited by small sample sizes.

The safety of ketosis up to two years is supported by studies of people following a strict ketogenic diet for epilepsy or type 2 diabetes without adverse events.  However, literature on longer term effects or intermittent ketosis is lacking.[31]

Diabetic nephropathy can also be reversed with a ketogenic diet high in short chain fatty acid which produce 3-hydroxybutyrate.[32]  Reversing diabetics with nephropathy should be added to this list of benefits, along with a reduction in the other risks for conditions associated with the western diet.  The ketogenic diet supplies the fat; while fasting it is the adipose tissue’s that is metabolized.  If the fat is rich in short chain fatty acids (the economical source is coconut oil) the salubrious effects are possible greater than fasting (supra Poplowski). Both fasting and keto diet turn up autophagy sufficiently when they become a life-style they significant lower risk for CAWD.    

The above issue of safety in the Wiki article concerning longer ketogenic diets (also fasting) is waved as the standard warning, like that of drug side effects on TV advertisements; however, the risk from ketogenic diet and fasting is very low, and the benefits very high; while the drug alternative, the benefits are low and fleeting and the side-effects high. 

Paleo people supply the answer as to long-term lack of adverse effects of the ketosis and intermittent fasting.  The Eskimos diet and health were studied in their natural environment before the western diet was introduced, and thus they are proof of the safety of life-long ketogenic diet.  Many of the paleo people regularly go without food when travelling distances and when hunting.  The mammalian examples provide more evidence for life-long ketogenic diet and intermittent fasting.  The treatment of epilepsy with ketogenic diet also confirms its safety.

Homeostasis mechanisms through autophagy explains why both ketosis and fasting are recuperative.  The excessive lipid droplets in the liver and pancreas that causes inflammation are flagged though signalling to turn on autophagic processes during extended periods of fasting, and during ketosis.  Since the only difference between a ketogenic diet with its 5% carbohydrates and fasting is the rate of fat metabolism and not the degree of autophagy, the two should come to the same recuperative effect.  Thus both ketogenic diet and water fasting have been used for a variety of conditions including dementia, cancer, diabetes, and epilepsy.   The carbs during a ketogenic diet merely reduce the livers need for glycogenesis to supply the erythrocytes with the essential glucose for their metabolism.  Thus as to benefits there should be little difference between the two.   

Ketogenic diet reverses t2d:  Given our understanding of the process, the condition of the pancreas, the history of treatment with low carb diet, and the evidence from bariatric surgery, all these supports that a ketogenic diet can reverse t2d. In a trial on point: 


The LCKD [ketogenic diet] improved glycemic control in patients with type 2 diabetes such that diabetes medications were discontinued or reduced in most participants. Because the LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication.[33]

Again the trail is thin as to studies on point, but with the biological basics the path is clear.  Given the evidence for the wide range of benefits of the ketogenic diet, it will manage t2d drug free and gradually reverse t2d and at the same time through the promoting of autophagy and avoiding the side effects of drugs and significantly reduce the risks for CAWD.     

Fasting reverses t2d:  Whatever significantly promotes the metabolism of excess fat in the liver and pancreas will reverse t2d and IR.[34]  This is the approach used by Dr. Jason Fung in his clinic in Toronto with repeated success, using both alternate day fasting and low carbs. 

Fasting allows us to naturally empty the sugar from our body (the sugar bowl).  Once empty any incoming sugar will no longer spill out into the blood, and we will no longer meet the criteria for diabetes.  We will have reversed the disease. . . .  In my Intensive Dietary Management program, we often start with a thirty-six-hour fasting period three times per week for type 2 diabetes.  During the eating periods, we prescribe a low-carbohydrate high-fat diet. . . .  Some people will do a classic water-only fast, others a modified-fat fast, and still others a bone broth fast.[35]    

Some of his patients do a much longer than 36 hour water fast. 

          A personal comment on fasting:  as before mentioned given the risk of cancer at about 50%, I certainly want to reduce my risk.  I do once or twice a year a longer water fast.  Since I am at my youthful weight and in my 7th decade, I have experienced hitting the wall (lack of energy), which last for hours as the adipose hormone leptin reduces metabolism and other processes as the body undergoes a metabolic switch.  To avoid this, I do a modify fast with fats, cheese and meats.  I once used bell peppers with fats, but since the bacteria in the small intestines use enzymes to break down fiber, and thereby the gut absorbs 50 to 70% of the glucose, I have switched to proteins and fats. 

In 1916 Elliott Joslin in his case studies reported a lady “who contracted diabetes twenty-six years ago, . . go without food, save broth, for several days in succession, and that she would follow his advice.  Her severe symptoms of diabetes subsided at the end of four years.  Her tolerance on June 1, 1916, reached 116 grams of carbohydrate.” [36]  Not cured but managing her diabetes with diet.  What if she had combined low carbs with intermittent or alternate day fasting? 

The results of fasting are rapid as to its effect upon IR.  In an experiment on 7 untreated t2d who fasted for 3 days their fasting glucose while on a standard dies was 196, at 3 days it was 127mg/dL.[37]  More on point is the treatment of 13-obese diabetics unmedicated who fasted from 17 to 99 days for obesity. “All patients showed improvement in glucose tolerance, with abolition of previous mildly diabetic curves in five patients, irrespective of subsequent weight gain.” [38]   

 Dr. Fung commenting on his clinical experience: “How long it takes to reverse the disease depends on the intensity of the fasting regimen and the length of time you’ve had the disease.” [39]  I believe it is determined by a number of factors:  age, degree of insulin resistance, amount of fat in the liver and pancreas, basil metabolism, and lifestyle, and overall health, thus as Jason Fung says everyone is different.  

The dawn phenomenon (dawn effect):  A couple of years ago a friend with t2d tried to manage her condition with a low carb diet.  Monitoring her blood glucose with drugs, she was alarmed at the rise in glucose.  I had no answer as to why this occurred and she discontinued her low carb diet.  Since then she has gained 25 pounds and pain in her legs and is stoically stuck in the quick sand of drugs.

On my second reading of The diabetes code, (Jan 2020) P 203, I found the answer.   Since in the dawn-hours blood sugar is at a low point, the body in preparation for activity releases epinephrine, which causes the liver to breakdown glycogen to release sugar.  Cortisol is also released: 

In the early fasting state, cortisol stimulates gluconeogenesis (the formation of glucose), and activates antistress and anti-inflammatory pathways. Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose-1-phosphate and glucose.  This is done through its passive influence on glucagon.] Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for  epinephrine to have an effect on glycogenolysis.

This effect is frequently noticed for those with t2d because of blood monitoring:

These hormones are secreted in a pulsatile manner, peaking in the early morning then falling to low levels during the day.  In nondiabetic situation where there is no need to manage blood glucose artificially, the DP [dawn phenomenon] is a normal occurrence, but most people miss it because the magnitude of the rise is very small.  In about 75 percent of type 2 diabetics, however it shows up as a noticeable spike in blood glucose levels early in the morning. . . . Like the overinflated balloon, the liver puts forth prodigious amounts of sugar in order to relieve itself of this toxic sugar burden.  [40] 

To put it another way, evolution is for our health, the release of sugar during a ketogenic diet or fasting when diabetic is a good thing for our liver and us.  One last comment, incongruously, pharma with their toxic glucose theory holds “plasma cortisol possible contributes to the pathogenesis of dawn phenomenon in NIDDM in patients.” [41]  Drugs for DP are gaining in sales. 

The combination approach:  This is a “no brainer”, like take a water soluble antioxidant and a fat soluble antioxidant. Combining fasting and ketogenic diet improves the degree and rate of management of t2d and its reversal.  It turns up in the long term autophagy more either one alone.  This combination permits the patient to sculpture the management of t2d.  The combo also improves MTD functions, which increases the rate of pyruvate metabolism and thus glucose.[42]  Disconcertingly many of the authors of diet books recommend just one or the other.

The critics:  This simple and obvious way to reverse t2d and improve the health of those with t1d has its moneyed critics with their tobacco science, social engineering, guidelines, and marketing.  One of their standard moves is to fiend protecting the public.  One ways to recommend the supervision of a physician when changing diet--a burden upon the patient and a way to reduce the number of those to try the dietary management and fix. 

For Intermittent fasting and alternate day fasting doesn’t need the aid of a physician. The battery operated glucose monitoring blood testing for those trying the dietary fix is sufficient to prevent hypoglycemia.  For the fix effects upon non-diabetic medications the local pharmacist for free.  Moreover, the physician will criticize the dietary fix and thus dissuade some of those who would otherwise have made the healthful choice.  For long-term water fasting taking supplements for potassium, sodium, magnesium, vitamin is advisable and available over-the-counter and through Amazon.  To see a well-meaning physician is likely to do more harm than good. 

[1] Those with a high glycemic index.  The insulin index which once I relied upon falls short in that with carbohydrates certain amino acids will significantly raise insulin, but taken without carbohydrates they don’t.   

[2] Merck Manual, eight editions, 1950, pgs. 268-9; the 9th Edition, 1965 essentially repeats that message p. 331.  The 10th Edition, 1961 refers to diet, but with the sulfonylurea drugs entering the market, the dietary approach is just mentioned in passing.  By 1980, the Goodman and Gilman’s the pharmacological Basis of Therapeutics, Sixth Edition makes no mention of the dietary, drug-free alternative.  Upon finding that KOL stamp on contents of the 6th Ed., my 38 years of faith in Goodman & Gilman quality was shattered.  I thought that in the Keynesian economic era, that the medical science was of the highest standard because lives and quality of life depended on it, and that the best of science was collected into medical textbooks.  I mistakenly thought it all changed with the Reagan pro-business economics.  No, pharma was being pharma all along, as a 1960s NEJM summary article explains    

[3] In France sulfonylureas were approved in 1948; in the U.S. in 1995.  A long delay is often indicative concerns by the FDA. 

[4] Gary Taubes, Good calories, bad calories 2008 P 197

[5] The KOLs position is that there is little of the end-product fructose, and sorbitol accumulates to cause excessive osmotic pressure.  They call the polyol pathway the sorbitol pathway (2:5, 2-4).   

[6] Malone, John, Arlan Rosenbloom, et al, Dec 1976, The role of urine sugar in diabetic management

[7] Feinman, Richard D, Richard K Bernstein, Eric C Westman, Jeff S  Volek, total 29 authors, Jan 2015, Nutrition,  Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base  FULL  But when bought by pharma as the ADA is, there is no debate, just the same repeated casuistry  is printed,, see their guidelines (#13).

[8] I, Dr. Fung, Dr Joseph Kraft, and others hold insulin resistance is the best predictor.

[9] Feinman, Richard D, Richard K Bernstein, Eric C Westman, Jeff S  Volek, total 29 authors, Jan 2015, Nutrition,  Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base  FULL.

[10] Wiki, insulin resistance, 2/2020

[11] Harvard Heart Letter  Harvard Medical school    September 1, 2011, Abundance of fructose not good for the liver, heart

[12] Wiki non-alcoholic_fatty_liver_disease, Nov 2018

[13] Jason Fung, Diabetes Code 2018 P 97 and 99

[14]  Bizeau. Michael, Michael Pagliassotti, Sept 2005 Hepatic adaptation to sucrose and fructose.  For later confirmation (2:2).

[15] Fach, David, Kaori Minehira, et al July 2005, Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men

[16] Michael, M, Robit Kulkami, et al, July 2000, Loss of Insulin Signaling in Hepatocytes Leads to Severe Insulin Resistance and Progressive Hepatic Dysfunction

[17] Social CC to the probability of the obesity, diabetes and other CAWDs.  Contributes to a population fructose consumption and the percentage who will gain weight.  Some social groups such as the affluent in the US, university instructorzs, and those in theater have greater peer conditioning to maintain a youthful weight.  

[18] Taylor, Roy, April 2013, Type 2 Diabetes Etiology and reversibility

[19] Knop, Flip, Roy Taylor, August 2013, Mechanism of Metabolic Advantages After Bariatric Surgery:  It’s all gastrointestinal factors versus it’s all food restriction.  I hold it is IR and entopic fat, and the 20% who fail to improve have progressed to t1d.  This doesn’t entail an immune attack upon beta cells but could be the result of the gradual apoptosis with replacement of the beta cells.  Which process has yet to be determined.  See for more on current science Gaborit, B, I Abdesselam, et al, July 2014, Ectopic fat storage in the pancreas using 1H-MRS: importance of diabetic status and modulation with bariatric surgery-induced weight loss

[20] Of course given the sugar addiction of most of the obese, the failure of physicians to convincing warn their patients that sugar started the process leading to obesity and t2d, and their recommendation to limit fats, these 2 contribute to the failures of both resulting in their regaining weight and 2nd bout of diabetes.

[21] Wiki, Bariatric surgery Jan 2020

[22] Courcoulas, Anita, Susan Yanovski, et al, Dec 2014, JAMA Surgery, Long-term Outcomes of Bariatric Surgery: A National Institutes of Health Symposium

[23] Gumbs, AA, IM Modin, et al, April 2015, Changes in insulin resistance following bariatric surgery: role of caloric restriction and weight loss

[24]  Wiki bariatric surgery Jan 2020

[25] Bower, Guy, Tania Toma, et al, April 2015, Bariatric Surgery and Non-Alcoholic Fatty Liver Disease: a Systematic Review of Liver Biochemistry and Histology

[26] Gaborit, B, I Abdesselam, et al, July 2014, Ectopic fat storage in the pancreas using 1H-MRS: importance of diabetic status and modulation with bariatric surgery-induced weight loss

[27] Gumbs, AA, IM Modin, et al, April 2015, Changes in insulin resistance following bariatric surgery: role of caloric restriction and weight loss

[28] Munoz, R, A Escalona, March 2014 Duodenal-jejunal bypass liner to treat type 2 diabetes mellitus in morbidly obese patients

[29] KOLs commonly claim that changes in regulatory hormone produces better blood glucose levels.  Thus, they are ignoring pancreatic and liver inflammation, lipid droplet, and the restoration of beta cells.  See Wiki bariatric surgery Jan 2020

[30] Antoni, Rona, Kelly Johnston, et al, March 2014, The Effects of Intermittent Energy Restriction on Indices of Cardiometabolic Health, and Westman, Eric, William Yancy, et al, Dietary treatment of diabetes mellitus in the pre-insulin era (1914-1922) published in Prospective in biology and medicine, Johns Hopkins University Press, winter 2006

[31] Wiki, ketosis, Jan 2020.  A summary article at Michalsen A, C Li, Dec 2013, Fasting Therapy for Treating and Preventing Disease - Current State of Evidence supports the same conclusions. 

[32] Poplawski, Michal, Jason Mastaitis, et al, April 2011, Reversal of Diabetic Nephropathy by a Ketogenic Diet—FULL.   Coconut oil is the common source of 3-hydroxbutyrate.  This article misses that the measurement of glycation includes fructation, and that of the differences between HSPs and LSPs as to nephropathy, t2d, and CAWD.  Also misses RATP and RRA, both of which promote an assortment of neurological conditions. 

[33] Yancy, William, Jarjorie Foy, et al, Dec. 2005, A low-carbohydrate, ketogenic diet to treat type 2 diabetes.  In the 16-week trial 1/4th of volunteers (BMI 42, average age 58) discontinued their medication, and 36% reduced it, and 14% no change.  Weight was reduced 6.6%.  Since there wasn’t weekly measurement of triglycerides during the 16 weeks, compliance affects results.  At the end of the trial triglycerides decreased 42%.  A1c was down 16%. 

[34] Varady, Krista, Marc Hellerstein, July 2007, Alternate-day fasting and chronic disease prevention: a review of human and animal trials

[35] Jason Fung, The Diabetes Code P 199, 201, 202

[36] Supra 104

[37] Nuttall, Frank, Rami Almokayyad, et al Feb 2015, Comparison of a carbohydrate-free diet vs. fasting on plasma glucose, insulin and glucagon in type 2 diabetes

[38] Jackson, Ivor, Margaret McKiddie, et al, Feb 1969   Effect of fasting on glucose and insulin metabolism of obese patients

[39] Fung, Jason, The diabetes code, (2018) P 200

[40] Fung supra 203,  This process is not a bad thing, see #13

[41] Atiea, JA, SM Aslam, et al, July 1990, Early morning hyperglycaemia "dawn phenomenon" in non-insulin dependent diabetes mellitus (NIDDM): effects of cortisol suppression by metyrapone

[42] Descamps, O, J Riondel, et al, Nov 2005, Mitochondrial production of reactive oxygen species and incidence of age-associated lymphoma in OF1 mice: effect of alternate-day fasting

11. Supplements and exercise:  The sex hormones (a supplement for the seniors) among their many salubrious functions is the partial regulation of lipoprotein lipase (LPL) which is essential for the metabolism of fats; and these sex hormones controls fat disposition: 

One reason men get fatter above the waist as they age is that they secrete less testosterone, . . [which] suppresses LPL activity on the abdominal fat cells . . . .  In women the activity of LPL is high on the fat cells below the waist, which is why they tend to fatten around the hips and gut, and low on the fat cells of the gut.  After menopause, the LPL activity in women’s abdominal fat catches up to that of men. . . . [1]   

A senior by taking natural hormone replacement from a compounding pharmacy (6:2) can reduce excess lipodystrophy.  Gary Taubes (Chapter 9) Why we get fat goes on to describe the experiments of George Wade on rats where he removed the ovaries.  It provides an animal model on the importance of estradiol.  The same applies to testosterone. 

Estradiol and testosterone differ only by one functional group, moreover, the level of one influence the level of the other through about a 10% rate of conversion.  Both function to increase metabolism and through testosterone’s androgenic effect muscle mass.  Both also function to reduce ROS damage to the MTD.  Thus these hormones lower serum glucose and thereby reduce the degree of IR.  Yes, the sex hormones are salubrious and thus a target for bad pharma.  I have been taking topical testosterone, high dose since 2004 from a compounding pharmacy.  

Aspirin also lowers glucose among its many benefits (see http://healthfully.org/rc/id3.html under diabetes heading).  A very high dose of uncoated aspirin cured t2d.  Their average standard carbohydrates of the 8 in the clinical trial was 25% of calories.[2] 

High dose of uncoated aspirin—typically 3.5-grams ad a day--was the gold standard of rheumatoid arthritis treatment and used for other conditions to lower inflammation.  It had been noted in the literature that “Rheumatic fever and diabetes rarely coexist” (Reid supra).  The same applies to rheumatoid arthritis.   

Though I ate the western diet, I had done far better than my associates.  A major part of this I attribute to aspirin.  I had taken on doctor’s advice starting in 1992, 2.5 grams a day of coated aspirin for chronic back pain.  After 3 years I reduced it to Uncoated aspirin at .7  grams taken daily until 2016, not for my back which was without major episode, but because aspirin in the higher dose lower the cancer risk by 50%, and has been shown to reduce at about 50% those having been treated for stages I, II, and III breast cancer from a relapse with metastatic breast cancer.[3]  Aspirin up-regulates the apoptosis system for abnormal cells (see http://healthfully.org/rc/id18.html).  Like with the sex hormones and neurosteroids, aspirin is a target for bad pharma.  The use of low-dose and coated aspirin, and the exaggeration of the risk of stomach bleeding are all part of pharma’s attack.

Vitamin C ought to be added since the diabetics have low ascorbate in their cells.  Vitamin C among its 8 essential factor, includes its role in the folding of collagen.  This could explain a number of risk factors for diabetics.  If diabetic, I would add 3 to 5 grams of sodium or calcium ascorbate to the liquids I was drinking throughout the day, not one dose because of it low rate of absorption due to gastric regulation.     

Exercise stimulate an increase in number of MTD thus increases the rate of metabolism of glucose, thereby lowers insulin.  With regular physical excretion, insulin resistance is reduced.  Exercise also increases autophagy.  This is particularly important for senior, given the evidence in support of the role of diminished MTD function in aging.  Two studies of senior runners, one at Stanford University the other of a New York runners club:  the mortality rate were 1/3 those of the general population and over an 8-year delay for a major health event.[4]  To be a fit senior for most requires strenuous regular activity decades prior.  

I am sad over how short physicians’ and public’s memory is for what was standard treatments.  Go to the journal articles, the evidence is there—as I have done at healthfully.org.  The evidence for both hormone replacement and aspirin is beyond refutation.  It is as Prof. Ben Goldacre writes: “It is amazing how quickly a good drug become bad one once off patent.”  We are a social animal and industries exploit that.     


12.  Confusion from the past, on ketoacidosis and hypoglycemia:  Two major life threatening risks were associated with the early (before 1936) insulin injections, and one with the injection hypoglycemia.  Insulin is metabolized in the liver thus has a short half-life, and there wasn’t a digital device for measuring blood glucose until the 1980s.  The two life threatening conditions were hypoglycemic shock and diabetic ketoacidosis (DKA).

There is significant confusion over ketosis and ketoacidosis.  Ketosis is elevated ketones caused by the metabolism of fats during starvation, ketogenic diet, or fasting.  It Is about 1/3rd the level of a type-1 diabetic in ketoacidosis.  Diabetic ketoacidosis (DKA) is a life-threatening condition caused by low blood pH (7 and below).  Before insulin it was nearly always fatal for those with t1d.  DKA can also can be caused by alcohol, medications, and toxins.  Today with early treatment DKA death rate is under 5%.  With DKA there is hyperglycemia, dehydration and metabolic acidosis, and sometimes also hyperkalemia (potassium) and hyponatremia (sodium).   Elevated ketones from a ketogenic diet does not cause DKA.  DKA is caused by the near total lack of insulin, and is treated with the injection of insulin (infusion of sodium bicarbonate to increase PH is of questionable value).  Those properly diagnosed with t2d produce sufficient insulin to not progress to DKA, though those with LADA (occurs when t2d progress to t1d) are at risk for DKA.  About 20% of end stage t2d have progressed to LADA; they are producing very little insulin.  DKA in the USA results in about 135,000 hospital admissions yearly and about 3,000 deaths. 

Ketoacidosis is caused dysregulation of the body’s buffering system for which bicarbonate is a vital component.  The narrow range of Ph. Is especially important for protecting tissues of the central nervous system.  Acidosis and alkalosis can prove fatal.  I doubt that diacetic acid is a major CC, rather that there is much more to failure of the buffering system.  The journal trail if thin, and I have bigger fish to catch. 

A second function of bicarbonate which is release by the pancreas in response to the hormone secretin to neutralize stomach acids in the intestine.  That acidosis occurs with t1d when the body’s system permits the Ph. to dip to 7 or slightly below.   Something is amiss, but what I haven’t as yet found, if such evidence has been published.

The false connection of ketosis with DKA in part was responsible for the claim by Joslin and others claiming that fats promote t1d,[5] and also for the inclusion of carbs in the diet of those with t2d.  Elliott Joslin blamed the increase in sugar for t2d (#2). The published animal experiments in 1913 by Frederick Allen supported Joslin’s conclusion for maximizing carbs until sugar was found in the urine, and thus less saturated fats in the diet of those with t2d.[6]  I failed to find this simple connection in reading Allen’s work. Others prior had assumed a connection of fats to t1d.  Allen and others were critical of that connection.  With the development of insulin and a lack of monitoring of blood glucose, there was no need for an extremely low carbohydrate diet with its low dose of insulin.  Insulin seemed to the physician a safe and healthful treatment for t1d, and higher amounts as better, but not too much to cause hypoglycemia.     

The early insulin (before 1937) had a short half-life; this resulted in a significant risk of DKA—more commonly called today acetoacetic acid.  The lack of blood monitoring entailed balancing the dose of insulin with the meal and physical activity.  DKA, because of improve treatment, had in the 1930s a mortality rate of about 25%. 

Urine testing for glucose doesn’t reveal current blood glucose; there is a delay before kidney excretion of excess glucose and its accumulation in the bladder.  Too much insulin resulted in hypoglycemic shock, which sometimes is fatal.  Only those with deep pockets could afford a full-time nurse specially trained for diabetes patients.  Things improved in 1936 with the development of a longer lasting insulin.    

While hypoglycemia is assumed to affect neurons or other brain cells that require glucose for their metabolic functions because supposedly some types of brain cells cannot depend upon ketones when glucose is low—yet which type of cell hasn’t been demonstrated.  Moreover, hypoglycemic shock affects more than the brain (fainting). These other effects included palpitation, tachycardia, sweating, pallor, and nausea, which counts against the lack of glucose for the brain claim.  Erythrocytes lack MTD, thus they can’t metabolize ketones, but can metabolize glucose in the cytosol.  Hypoglycemia affect the erythrocytes ability to deliver oxygen, which clearly affects the brain and other cells—thus explaining the other effects above of hypoglycemia.  Why should a type of brain cells which has MTD not be able to metabolize ketones (fats) like every other cell type but erythrocytes?[7]  All other cells have MTD which can metabolize ketone bodies. And what about the Eskimos?  I smell  the methyl amine of rats promoting glucotoxicity. 

The reason the person on a multiple day water fast avoids and also those on a ketogenic diet avoid hypoglycemic shock is that they go through 5 stages of the Randel cycle, an adjustment process;[8] but those who are diabetic, the hypoglycemia occurs too rapidly to permit metabolic and hemostasis adjustments.  With the natural adaptation, 5 levels of switching[9] during fasting the mechanisms for glycogenesis is turned on to supply the most common cell in the body, the erythrocytes. is less than half the serum glucose level of what causes in a diabetic hypoglycemic shock (6:3, 8).  Other CC could be a defect in calcium signalling,[10] or other causes that I haven’t come across.  Pharma uses the risk of hypoglycemia for the inclusion of carbs in the diet 6 times a day; it promotes drug sales and keeps the patient in the fat storage mode due to elevated insulin, thereby blocking the blocking weight loss with its improved health.  I believe it is false that a type of brain cells requires glucose for all the above reasons.  

Note while fasting the blood glucose level will drop to about half that of normal, (~3.2) but without the symptoms of hypoglycemia that occurs with diabetic, this is because of the natural metabolic shifts (5 listed by George Cahill Senior of Harvard) which don’t occur for the diabetic:  PHASES OF STARVATION: In the transition from the fed to the fasted state, a sequence of metabolic alterations occurs, listed as follows with their approximate duration: 1) Gastrointestinal absorption of substrate 1-6 hours 2) Glycogenolysis 1-2 days 3) Gluconeogenesis first week 4) Ketosis 3-4 days onward 5) Diminishing gluconeogenesis and increasing cerebral ketone consumption second week onward.” [11]

As covered in Section 1, the insulin levels of the Kitavans (1:3) is much lower.  A better path for those with t2d is to lower insulin by lowering carbs and avoiding diabetic medications.  Even better is attempting to reverse IR and reset the WRS so as not to have to go down the pathway taken by those on the Biggest Losers (6:3, 3) for which water fasting, intermittent fasting, and ketogenic diet is what I would try if I were diabetic.   

All this confusion resulted in carbs being included in the diabetic diet; it benefits pharma.  However, until drugs other than insulin obtained wide usage in the 50s, t2d was managed with a low carb diet.  Then pharma gradually changed that practice from diet to drug for the management of t2d.  Those who supported the dietary approach were and are marginalized—remember the 29 signers of article presenting 12 reasons to change the guideline (#5).[12]  History has little force for continuing a better treatment. 


      13. Homeostasis and don’t upset the apple cart:   In the beginning were the Greeks and Romans most influential was Galen. They rested upon the Greek foundation, and the work of Hippocrates and his followers.  He strong recommended dietary fixes, and recommended allowing the body to heal in most cases without intervention of drugs.   Their observations proved that autophagy is the best fix.  Galen and other subscribed to this approach. 

      Over and over again I find media marketing hawking new drugs wonders, miracles foods, fad diets, and an equally long list of what to avoid.  Everything but what works best for the healthy, a low sugar diet with 2 meals a day.  And for those with major medical issues or high risk, longer fasting and a keto diet


14. Treating the sign, glucotoxicity, instead of the cause IR:  With the onset of drugs that lowered glucose, all this changed to low fat again and thus much more carbs than before drugs—more carbs, more drugs.  Conveniently, the theory that fats caused diabetes became accepted and to it was added lipid hypothesis as the major cause for CVD. 

Glucose had been used for over a century to detect and measure the severity of t2d through collection of urine---the taste of blood was also used.  With focus already well establish upon glucose as a marker for t2d, the choice to focus on the sign glucose by pharma fits their pattern of profits first.  Their business ethics explains their failure to research for a way to reverse t2d, and pharma opposes treatments that weren’t highly profitable.  The decision to frame the cause of the comorbidities of t2d on glucotoxicity was a business decision made by an industry that promotes illness.   

As shown in #5, fructose damaging MTD is the starting point to IR in the liver and from there IR in other tissues, etc.   Again we have key opinion leaders, including  Elliot Joslin, recommending what favors pharma, and ignoring over a century of successful low carb treatment, including his mother and aunt.[13]  The low fat diet became the standard again by the 1960s with about 3 grams of carbohydrate to 1 of fat recommended.[14]  This focus fits in with the movement to treat cholesterol which gained momentum in the 1970s with the introduction of cholesterol lowering drugs and the war on fat clogging lipids, which benefited both food manufacturers and pharma.  Science has been buried by an industry ran by its marketing department.  So is the issue glucotoxicity , or is it a sign of MTDD and insulin resistance—or both?

The logic of low carbs and thus low drugs is compelling, though ignored by nearly all physicians and dieticians; they continue to recommend low fat (thus high carbs).  Again we have a case of the science and critics being marginalized.  Few journals will publish works that contradict the established recommendations: “A reconsideration of the role of thigh-fat, low-carbohydrate diet for the treatment of diabetes mellitus is in order.” [15]  The example of Richard K. Bernstein M.D. (1934) who has t1d, his clinical experience with t1d and t2d, and his book (which I read), Dr. Bernstein’s diabetes solution, all support the ketogenic diet, as too his good health (he is on YouTube), and there are over 15 journal articles including Dietary carbohydrate restriction as the first approach to diabetes management:  critical review and evidence base—a review with 29 signatures, in Nutrition,  Jan 2015, and there are 33 version of it published (listed in Googlescholar.com).  The dietary guidelines didn’t change.       

Time to consider again what was and should be now.  A parallel situation with my aunt Bertha similar to Joslin’s mother.  She developed t2d after WWII and lived a full life without drugs.  She lived until her 6th decade when arrhythmia was suddenly fatal.  What about the fatsoes of the past from Henry the 8th (1491-1547) onward?  Note: portly Romans and Greeks are virtually unknown, and their medical writings lack descriptions of type 2 diabetes.  In latter times, surely some who had the conditions of the affluence obesity and diabetes.  There was little interest before 1700 in English for t2d.  It is as though such people weren’t under the care of physicians.  Or was a few fortunately like William Banting[16] and my aunt Berth managing it with diet and living a full life?    

Why is the past so different than since the 1970s when treatment with pills causes a spiral of increasing IR leading to end-stage t2d with its insulin injections?  The UK has 70,000 amputation of legs a year.  My brother-in-law’s leg wouldn’t heal and was scheduled for amputation when he died of heart failure in the hospital at the age of 53 in 2006.  This is similar to what happened to Jerry Garcia of the Grateful Dead, who had end-stage diabetes.  He was in a drug rehab facility in 1995 when he was found dead from a heart attack, also age 53.  My neighbor 3 months ago (Sept 2019) died from kidney failure, for the last 2 years she was on dialysis.  Tracy, my former officer manger, now managing for my lead installer who took over the business.  She is nearly blind; she has been diabetic for about 30 years.  My real estate agent of 3 years ago, a wonderful lady, has end stage diabetes—she looks it.  Both ladies are on over 100 units of insulin.  Why has end-stage diabetes become common; and why are their case histories terrible different than Joslin’s mother and my aunt Bertha? 

End-stage diabetes is really end-stage insulin resistance.  Yes, the issue isn’t hyperglycemia but extreme hyperinsulinemia (3:5, 2-6).  This didn’t occur when dietary management was successful and the norm, now the norm is drugs.  The insulin injections are a result of failure of the standard of care.  The combination of low fat diet and drugs that increase insulin resistance is deadly.  We all know diabetics who died early and others who quality of life is poor and are waiting to die.

Glucotoxicity is based upon upsetting the apple cart; viz., by creating the wrong villain and pushing the “science” that supports it.  Pharma claims that comorbidities associated with t2d are because of the moderately higher level of serum glucose compared to the normal level of fasting glucose of 550 m/mL , the western standard.  Fasting glucose becomes symptomatic at above 1100 m/mL.  This level was used as the diagnostic point for t2d because of the diminished product of insulin caused by pancreatic inflammation caused by excessive entopic lipid which effects the production of insulin by the beta cells.  However, in 2018 the level was lowered by the ADA guidelines that now treats pre-diabetics with drugs for diabetes based on low quality industry funded or government funded studies.[17]          

          There is glucose toxicity covered prior in this work; it is not a major cause for the comorbidities of t2d.  Its toxicity comes from elevated glucose turning on the polyol pathway that makes the reactive fructose.  A high carb diet is not pathogenic; but add beer or sugar to it, and it is.  Of course the KOLs and dupes claim that it is elevated glucose and have articles on the pathways and genes that cause the health issues associated with t2d.  The evidence throughout this book is dispositive.


15. Drugs for treating t2d,: 


Tolbutamide (Orinase) a sulfonylurea

The trail for dietary management gets thin.  The 9th edition Merck Manual (1956) moves away from dietary control of t2d, and by 1961 there is a list of drugs: “Several orally administered drugs, including the sulfonylureas, tolbutamide and chloropropamide, which chemically are related to the sulfonamides and the guanidine derivatives, e.g., phenformin are effective in lowering blood sugar” P 312-313.  By 1961 oral drugs were recommend for all t2d cases including mild t2d P 313.  They were not recommended for t1d.   

The most effective of the new drugs, the sulfonylureas, entered the U.S. market in the late fifties.  Sulfonylureas increase the release of insulin from the beta cells—a bad thing since it increases insulin resistance in the target cells; thus hastens the development of t2d.  Sulfonylureas increase the risk for the important endpoints in long-term studies.  They also by lowering serum glucose increase the risk of the sometimes fatal insulin shock caused by hypoglycemia. 

As for metformin the most prescribe of the drugs for a new patient with t2d, as stated in (#16), it is a gate way drug, not effective in lowering blood glucose, and it causes nausea, thus making it easy for the physician to offer another drug, likely patented. 

The 3rd choice in the Merck 1961 was tolbutamide a sulfonylurea. 

Upjohn's formulation [tolbutamide] was preferred when the Lilly formulation demonstrated evidence of toxicity in parallel trials at the Joslin Clinic. Lilly pulled carbutamide and halted development, leaving the field open for Upjohn to market its new treatment. In 1956, Upjohn filed for approval from the Food and Drug Administration. Jeremy A. Greene found the application's size – 10,580 pages in 23 volumes with 5,786 cases reports – was necessary to "render visible the relatively small improvements provided in less severe forms of diabetes." Orinase, [tolbutamide] "expanded the total market by bringing under medical care diabetics who were formerly not treated.” [18]  

Even to this day the dietary recommendation is a sham.  It is not low carbs, but low fat, thus its fails the patient but not pharma.  The recommendation in the normal diet for both  t1d and t2d, is the avoidance of large portions of food that rapidly raise glucose.  For t2d there is a section on oral hypoglycemic agents (P. 312-3 Merck Manual 10th Edition).  For t2d the obese are advised to lose weight (which almost always fails), and below that in Merck’s heading 2. “Mild nonobese diabetics usually can be controlled without insulin.  If this is not possible on the adequate diet which maintains ideal weight, insulin or one of the oral agents may be given”-- end of section, P 313.  This is a major revision from the previous 2 editions which clearly recommended diet as first choice.  Moreover, in all 3 editions it is a normal high carb diet with 2 restrictions: to limit fats and large portions of rapidly digested carbs.  This is hardly a suitable diet, since low fat entails more carbs.  The diet is not designed to cure t2d,  Since  up to 90% of t2d are overweight;[19] there by limiting diet treatment in the 10th Edition to at most 10% of what is clearly stated as in prior 2 editions.[20]  The diet with carbs will increase the use of insulin for both t1d and t2d as well as drugs for both.  “The diabetic diet is a regularly ingested ‘normal diet’ with the exception that the more rapidly absorbed carbohydrates and foods containing them in large amounts must be eaten sparingly . . .  to avoid hyperglycemia (Eight Edition P. 273, and repeated in the 9th Edition, P. 331, but not the 10th Edition). 

The BMJ has a summation article on diabetes drugs approval and pharma’s business plan.  I highly recommend it, and have pasted it at http://healthfully.org/rh/id15.html, or punch the search engine Bad medicine: the way we manage diabetes, Des Spence, April 2013.  Dr. Des Spence describe the guideline process. 

From his article  “The drug industry’s business plan for diabetes follows a familiar pattern:


  • (1) Conduct questionable research and control the original data.

  • (2) Schmooze the politicians, health regulators, and patient groups to suggest under-treatment and need for “urgent action.”

  • (3) Recruit tame diabetologists, massage them with cash, and get them to present at marketing events that masquerade as postgraduate education.

  • (4) Pay doctors to switch to newer drugs in dubious international post-marketing “trials.”2

  • (5) Seek endorsement from the National Institute for Health and Care Excellence to bully doctors to treat diabetes aggressively with drugs.3 [21]


The article meets publication standards of 2013, however, each of the leading English   journals over the last 10 has--but for possible the BMJ--shut the door on what offends industry.   I fear the same might have happened in the last year with the BMJ.  What follows on the drug treatment is evidence for Pharma’s successful business model.  As of 2010, there were 11 types of drugs for diabetes,[22] and since then several more.  I wondered why the best-selling of the drugs, off patent metformin, holds that position?  What is the evidence?  We need to know! 


16.  Wonder drug metformin?:   Is the apple rotten?  What about the 4th most prescribed drug with 81 million U.S. prescriptions in 2014? 

I have when possible to relied upon mode of operation in evaluating a drug, but The molecular mechanism of metformin is not completely understood.  Multiple potential mechanisms of action have been proposed.” [23]  Knowing how it works allows me though the journal articles to see if it is possible significantly effective.  The lack of mechanism, greatly increases the likelihood that there isn’t a mechanism, and the claims of effectiveness are all marketing.[24]  Next. I attempted to research the long-term side effects of metformin, and I only came across industry articles on the standard side effects nausea, diarrhea and flatulents.  I wanted to see if its slight effect upon glucose was worth its side effects.

The normal pharma pattern is to not look for those horrific side effects like stroke and cancer.  I found benefits for cancer and liver cirrhosis survival, lower blood glucose, HBA1c, IR, and a lack of weight gain (but those studies are compared to other drugs that causes weight gain adverse events and scientific fraud in articles is the norm).  The lack of weight gain is because of its negative effects upon the digestive system:  eat less when nauseas and having diarrhea.  Moreover, serious side effects seldom show up in a younger population and short-term trial.  This is the usual pattern for a  blockbuster, journal articles that claim benefits and adverse events not found.[25]  Journal articles weren’t helpful in evaluating metformin.  Article after article found it lowered IR, ROS, reduced the risk for progressing to t2d, cancer, CVD, weight loss, lower fasting glucose.  I will save you from a list of other drugs that follow the journal pattern of marketing.  To find out of metformin’s long-term effects would require the opening up of the data banks

          1. The Cochrane library failed to find significant advantage to treating pre diabetics with metformin.

          2. In general, the reporting of serious side effects was sparse. Few participants died and we did not detect a clear difference between the intervention and comparator groups. We also did not detect an advantage or disadvantage of metformin in relation to health-related quality of life. Our included studies did not report on non-fatal heart attacks, strokes or complications of diabetes such as kidney or eye disease. [They shouldn’t since these are issues with end-stage t2d; and they have been excluded from the trials.]   Few studies estimated the direct medical costs. When compared to diet and exercise, metformin was more expensive. When compared to intensive diet and exercise, metformin was less expensive.

      1. Note that a slight advantage that is not statistically significant is treated as though it is significant.[26]  Add to this the failure to receive the raw data and the average of over 30% positive bias, and it is very likely that metformin promotes t2d, not prevents it. 

          This still leaves me with the nagging thought, why metformin, why is it promoted, now off patent, like statins?  My best guess would be (1 the promotion of managing serum glucose.  The patient taking this off-patent drug is likely to request a different drug, one that is easier on the digestive system and more effective at lowering glucose.  Metformin thus is a gateway drug.  (2) I suspect like statins there are major pathogenic consequences (those for statins are listed at http://healthfully.org/rc/id6.html). “Once started on metformin, it is highly unlikelyu that one will ever be able to stop it without intensive lifestyle changes.”[27]      

Metformin deserves special attention with the new standards soon over 30% of adults will be taking diabetic medication, and metformin is the gate way drug.  This is another case like with hypertension, no physical symptoms, yet a “condition” being treated with drugs.  After a year on the drug and a failure to lower glucose, the physician rolls out a patented diabetic medication to be added for treatment or replace metformin with a drug that has less side effects, and, of course, is more effective.  By then most patients are sufficiently worried about their t2d and have sufficient faith in their physician who gave them an off patent drug, that they will add a second drug to manage blood glucose. 

Metformin, however, has so little effect on fasting glucose and HBA1c that the current blood test is not sufficiently sensitive.[28]  The lack of a known mechanism of action could be because there is none, or none that are significant.  Alternative it has been proposed that:

Biguanides [metformin, dimethylbiguanide, is the only marketed one of that class of drugs] can lower fasting levels of insulin in plasma. Their therapeutic uses derive from their tendency to reduce gluconeogenesis in the liver, and, as a result, reduce the level of glucose in the blood [thus lower insulin].  Biguanides also tend to make the cells of the body more willing to absorb glucose already present in the blood stream, and there again reducing the level of glucose in the plasma.[29]

This Wikipedia statement by a KOL claims that metformin lowers insulin by increase cellular absorption of glucose. But a more likely explanation accounts for nausea and diarrhea, the reduced absorption of glucose, with the intestine bacteria causing those side effect.  These results indicate that metformin had a significant effect on the digestive tract, and that metformin treatment exerted an inhibitory effect on intestinal glucose absorption in the rat.” [30]  “The inhibitory effect of metformin on both the mucosal and serosal glucose transfer mechanisms was greatest in the middle portion of the small intestine. The results suggest that metformin decreases intestinal glucose absorption in a dosedependent manner by effects on mucosal and serosal glucose transfer. [31]  Animal studies indicate that metformin can cause intestinal glucose absorption to be delayed and occur more distally along the tract. animal studies have also shown that metformin increases glucose utilisation by the intestine, particularly anaerobic glucose metabolism. . . “ [32] So which explanation would you prefer, the Wikipedia or the journal article with the mechanism for poor glucose absorption? 

Gluconeogenesis occurs to replace vital stores of glycogen, which among other things is stored for emergencies such as preventing hypoglycemia which can cause a cascade of events due to the lack of glucose for the erythrocytes.  Secondly, the amount of glucose replacing glycogen daily used is a small percentage of the daily amount of dietary glucose.  The average diabetic uses very little glycogen (prolonged exertion reduces stores, and most are sedentary).  So, if the claim of blocking production (not supported by the Wikipedia article) is correct, metformin would have minimal effect on the glucose markers. 

          This brings me back to the question of how good is metformin?  Quoting the lecture of Prof. James McCormack citing Hirst and Farmer footnote blow:   “Metformin monotherapy reduces A1c ~ 1.1%, doubling the dose from 1000 to 2000 mg/day ads 0.25% to 0.3% additional change in A1c.” [33] Starting on a drug that is cheap and fails is a lead into a drug that works and is patented.  Possible like with claritin,[34] the delay in FDA approval was because of the weak evidence for its benefits.  There is a gap of 38 years since its introduction in France, 1957 and the United States 1995

This brings me to the next fact that in a number of trial the tight management of glucose results in a worse outcome.  There are 2 reasons, one is that stuffing cells with glucose turns on polyol pathway with its fructose production.  Second is that most treatments increase insulin and thereby increasing IR.  The cells being overstuffed with glucose then respond by withdrawing more of the insulin receptors on its surface.  Since IR is a better marker for CAWD, better than blood glucose,[35] with increased IR and insulin higher blood level the dysregulations of leptin and others increases.  Not surprising a review of the many functions of insulin, including IGF1 & 2, and leptin, compared to glucose, insulin is the gorilla in our blood.

From the lecture by James McCormack (on YouTube), as A1c goes up a digit from 5 to 6, 8 to 9 and so the risk of adverse event goes up about 2% over 10 years.  Those with t2d have a 10-year risk of CVD of ~ 20%.   The risk of dialysis lifetime risk goes up from about 1% to with A1c of 7 or less to about 2%, with 11 A1c and a 6% risk of peripheral neuropathy.  Blindness lifetime risk with diabetes start at near zero for 7 and 4% for A1c of 11.   Fifty-five percent of diabetics are under 7% A1c.  For metformin there is but only the UKPDF study; it found a 7% reduction in cardiovascular endpoints over 11 years; however, a subsequent meta-analysis found no benefits.  And UKPDF compared metformin to other drugs, not placebo.  Sulfonylureas showed only a 3% reduction in retinal photo coagulation, all of the other types of drugs have not been studies in the chart McCormack showed.  Given the sizes of those studies none were statistically significant.  In a meta study of metformin, 12 studies, 9,500 on metformin and 3,500 on conventional drugs, changes in CVD, mortality, MIs strokes, heart failure peripheral vascular disease, amputations and microvascular disease, all results were insignificant, [and worse if you consider the built in bias for pharma funded studies.][36]  “In 2013, the level of evidence for the clinical efficacy of antidiabetic drugs is disappointing and does not support the millions of prescriptions written for them.” [37] Without dietary management as the placebo group [the best therapy], all results of clinical trials are inconclusive. Preferable an active placebo such as atropine to reduce breaking blind.  

The manufacturer of the drug testing their product against the worst drug, or made worst by being too low a dose, this is marketing not science; this is what we have with few exceptions.  Again, I remind you the strong case concerning clinical trial made by Prof. Ben Goldacre in Bad Pharma.

With the new guidelines the standard of treatment is to drug the prediabetic.  McCormack asked: “why are we taking these drugs that don’t make a difference for the reason of lowering risk of major events? And why give 100% of them a drug to prevent at some future date 25% of them receiving a drug for diabetes?”  Remember, that those with t2d are asymptomatic and can be successfully managed with diet.  The benefits of metformin are repeated by physicians as absolutely proven, beyond a doubt.  However, the UKPDS 34 study[38] followed only 134 on metformin followed 11 years, and given the standard 30% industry positive bias (including burying side effects), I certainly would not take this strange, bioactive chemical.  Oh, and don’t forget in the study when metformin was added to sulfonylureas there was a 60% increase in morality (a 6% absolute increase).[39] The use of multiple drugs is the norm after starting out on metformin. 

The dismal results for metformin are extended to others in a study which compared glyburide, metformin and rosiglitazone for newly diagnosed patients.[40]  In the comparison with other drugs, metformin caused less weight gain.  Being made nausea is not the way I want to slow my weight gain. 

“From 2004 to 2013, none of the 30 new diabetes drugs that came on the market were proven to improve key outcomes, such as reducing heart attacks or strokes, blinds or other complication of the disease.” [41]  Looking at these numbers as a newly diagnosed patient, I would conclude that the help offered isn’t help. Take drugs that make you sick and shorten your life or lower the intake of carbohydrates, the choice is obvious, but not given the patient.

Drugs to treat glucose are like drugs to treat fever, the problem with t2d is insulin resistance, and with colds a bacteria or virus.  Pharma’s maximization of profits entail over and over again they treat signs of a condition, because to cure a condition is less profitable, and to treat t2d with diet is for them the worse.  I am not claiming that pharma isn’t looking for a drug to lower insulin resistance, but as far as I known they haven’t found one, one that would be effective in preventing the progression from IR to t2d or t2d to morbidity.  Would they market it? that is another question. 

The reality is that pharma isn’t in the business of looking for new molecular entities.  Their research is on me-too drugs.  The basic research for new molecular entities is done by other companies, universities, and the NIH, and with the former 2 pharma buys the rights to the drug, run clinical trials, then market it.  Marcia Angell at length develops the me-too topic topic[42]  The NIH gives a company the new drug, with the stipulation under law that the price shall be reasonable, however, that clause is no enforced.[43]  

Earlier I had mentioned that pharma is maximizing the treatment of glucose, so what are the new guidelines that classifies 10s of millions more as diabetic and recommends treating pre-diabetics with metformin, that is one half of 30% of the adults who now have t2d, many of whom go untreated.  My 2 Canadian friends were put on metformin in the fall of 2019.  I feel morally obligated to devote space to this issue.  This Section is about fixes and dietary management and curing of t2d thus belongs in Section 6.  T2d and insulin resistance are a major of all the CAWD.  By simply limiting carbohydrates to 10% of calories entails that this lower production of insulin for most of the t2d patients is adequate to regulate serum glucose and place those so managed in the group who at the high range of IR and with their morbidity risk factors.  The association Prof. James McCormack found between increase in A1c and pathology is not because of the glucose but because of the degree of medication with its side effects and their exacerbating of the IR.  The new guidelines are treating healthy people with drugs that cause the side effects associated morbidities of t2d.  As Dr. Fung in books and lectures points out, most of those medication increase insulin resistance, and it isn’t glucose but the IR that needs to be managed, which he does through low carb diet and fasting.

Over and over again good treatments are replaced with bad ones.  One point, the UBC professor James McCormack (University of British Columbia)[44] lecture provide a rebuttal to the spin generated by KOLs on the benefits of metformin.  This is what I have up on my video page for his 2015 lecture: 

****** Metformin – the case of exaggerating both benefits and harms, 29 min, 150,000 views Prof James McCormack, UBC   No quality evidence that metformin increases lactic acidosis, reduced renal performance, and does NOT have significant benefits, just less harm than some other drugs.  Very minimal lowering of A1c.  He is skeptical of treating glucose.  A study compared it as to quality of life to that of having a mild stroke.  If your physician told you that any of the drugs for diabetes has no benefits but lowers the quality of life comparable to a stroke, would you take it?  https://www.youtube.com/watch?v=pUOC5d0Siws   Excellent

Again and again we are back to the B4 and IR.  The dupes of pharma don’t understand this; they focus on lowering glucose with drugs.  They believe as told that the risk of a high fat diet outweighs the risks associated with t2d and its drug management.  It is the cholesterol-statin story, only now it is glucose and glucose lowering drugs. 

If I seem angry, it is not at the dupes, but at a system which rewards profits before people, one that is very good at marketing, and it is not truly anger, but sadness over the quality of the golden years and those who are obese decades before those years.  Where I live in a gated senior community there are over 200 seniors, and there are just 3 in good health—drug free and normal lean weight.  I would certain say no to my physician for metformin as I did for a statin, would you?  So what are the new guidelines?


17.     The ADA 2019 guidelines:  The ADA guidance has a long list of science ignored: There is nothing about insulin resistance, fatty liver disease, fatty pancreas, fasting, increasing fat on the low carbs, the weight regulatory system, and the yo-yo diet.  It is more of the same for the last 50 years, and it fails.  Is the ADA dumb, or are they beholding to pharma and food manufacturers?  They recommend bariatric surgery and the Mediterranean diet, yet fail to mention (and the media too) that the Mediterranean peoples eat on an average about half the sugar of Americans, they fail to mention treatment for t2d should start with dietary management. 

I keep wondering how stupid can it get?  Could it be their sponsors: “AstraZeneca, Aventis, Bristol-Meyers, Squibb, Eli Lilly, GlaxoSmithKline, Merck/Schering-Plough, Monarch, Novartis, Pfizer, and Wyeth.” [45]

The sign of the problem is the inability to control the level of serum and cellular glucose as per mammalian design.  So instead of avoiding glucose, they recommendations are to eat more glucose and less fats, the other source of energy.  This is the expert opinion (thought leader also called KOL) system what is repeated over and over again.  The KOLs justify high carbs because the fats are more pathogenic than the carbs for those who are diabetic or prediabetic, and also for the general populace.  I guess the Eskimos still on a traditional diet are the sickest people on this planet.  I guess the introduction of the high carb diet high in sugar is not what has caused in population after population of paleo peoples a health disaster far worse than the affluent nations.  [46]Refined carbs gram-per-gram are as to amount of glucose nearly equal to the unrefined carbs.  A recommendation of avoiding refined carbs has little impact on the sum total of glucose over a 6-hour period between meals.  So what does the ADA recommend?   

Their 2019 update guidelines are over 100 pages, I picked through for what I considered relevant key points: 

Prediabetic A1C 5.7 to 6.4 fasting glucose 100-125 mg/dL (5.6-6.9 mmol/L).   Diabetic 6.5 or greater; fasting glucose 126 mg/dL (7.0 (mmol.L) 

Metformin therapy for prevention of type 2 diabetes should be con­sidered in those with prediabetes, especially for those with BMI ≥35 kg/m2, those aged <60 years, and women with prior GDM [gestational diabetes].  Several pharmacologic agents have been shown to decrease the incidence of diabetes, although none are ap­proved by the U.S. Food and Drug Administration (FDA) specifically for diabetes prevention.  Metformin has the strongest evidence base and demonstrated long-term safety as pharmacologic therapy for diabetes prevention. 

Based on intervention trials, the eating patterns that may be helpful for those with prediabetes include a Mediterranean eating plan and a low-calorie, low-fat eating plan. Additional research is needed regarding whether a low-car­bohydrate eating plan is beneficial for persons with prediabetes.


To achieve weight loss of >5%, short-term (3-month) interven­tions that use very low-calorie diets (≤800 kcal/day) and total meal replacements may be prescribed for carefully selected patients by trained practitioners in medical care settings with close medical monitoring.  [Their insurance won’t cover the expense.]  To maintain weight loss, such programs must incor­porate long-term comprehensive weight-maintenance counseling.

  1. Metabolic surgery should be rec­ommended as an option to treat type 2 diabetes in appropriate sur­gical candidates with BMI ≥40 kg/m2 (BMI ≥37.5 kg/m2 in Asian Americans) and in adults with BMI 35.0–39.9 kg/m2 (32.5–37.4 kg/m2 in Asian Americans) who do not achieve durable weight loss and improvement in comorbidities (including hyperglycemia) with reasonable nonsurgical methods.

  2. For patients with diabetes aged <40 years with additional ASCVD risk factors, the patient and provider should consider using moderate-intensity statin in addition to life­style therapy.  

  3.  For patients with diabetes aged 40–75 years and >75 years without ASCVD, use moderate-intensity statin in addition to life­style therapy.

Pregabalin [Lyrica], duloxetine [Cymbalta], or gab­apentin [Neurontin] are recommended as initial pharmacologic treatments for neuropathic pain in diabetes.  [All major sedatives, highly addictive when taken long-term, more addicting than the opioids, (4:6)]. 

The just listed Lyrica, Cymbalta, and Neurontin are all major sedatives (sleep more and the pain is less) which are more addicting than heroin—though your doctor is taught they are safe and effective.  Need I point out the dollar trail?  Or again the results from using sedatives for pain (4:5, 9d)?    

Only the lowest standard trials have justified treating the prediabetic as Prof. McCormack points out.  That the FDA hasn’t as of Dec. 2019 approved drugs for pre-diabetics is evidence that the ADA used the lowest standard clinical trials.  As Prof. James McCormack said: “It is ridiculous to put the prediabetic on a drug that doesn’t lower the risk of type-2 diabetes for the putative reason that it might reduce his 25% risk of needing drugs to manage his diabetes.”  That reduced risk has not been demonstrated in the better of the clinical trials.  In addition, research indi­cates that low-carbohydrate eating plans may result in improved glycemia and have the potential to reduce antihyperglycemic medications for individuals with type 2 diabetes.  We ought to go back to the back to the pre-drug dietary treatment day.


18. A listing of what is best for dieting for weight loss, managing diabetes, and lowering risk for CAWD (in approximate order of importance):

SOCIAL FACTORS:  building the will power to behave differently

  1.  Enlist support of roommate, significant other, friends, family, and others

  2. Watch daily the documentary and lectures at http://healthfully.org//rh/id7.html


  1. Extended water fasting

  2. Alternate day fasting

  3. Extend benefits of fasting with under 10% of calories from carbs

  4. Intermittent fasting[47]

  5. Very low digestible carb snacks[48]

  6. Ratio of fats 75% to carbs under 25% of calories (not counting proteins)

  7. Hormone replacement after the age of 60 men 50 women (6:2)

  8. Strenuous work or exercise including weight training—especially if on HRT

  9. On non-fasting days no digestible carbs 3 hours before going to sleep

  10. If you must nibble something stick to fats, leafy green and other vegetables that are low in digestible carbs, and proteins such as cheeses. 


19. What’s causing t1d:  While it is an autoimmune response with genetics increasing the risk; however, given that LSPs have near zero rates of t1d, the western diet and fructose-MTDD is likely the major CC in that it promotes the immune response that destroys the beta cells.     

  1. William Osler reported that of the thirty-five thousand patients under treatment at John Hopkins since its inception, only ten had been diagnosed with diabetes.  In the next eight years, 156 cases were diagnosed [mainly t1d].  Mortality statistics were wrote Osler, suggested an exponential increase in those reported dying from the disease—nearly doubling between 1870 and 1890 and then more than doubling again by 1900.  By the late 1920s, Joslin’s epidemic of diabetes had become the subject of newspaper and magazine articles. . . Emerson and Larimore published an analysis of diabetes mortality statistics in 1924, they reported a 400 percent increase in some American cities since 1900—almost a 1,500 percent since the Civil War.[49]

  2. As the sugar went down in price t1d went up (the t2d was not fatal, it was managed by diet).  And this trend continues in some areas more than others: “There is on the order of a 10-fold difference in occurrence among Caucasians living in different areas of Europe, and people tend to acquire the disease at the rate of their particular country”. [50]

  3.           There is more direct evidence through the use of markers for the development of t1d, the GAD, protein tyrosine phosphatase-like protein, and for IA, autoantibodies to insulin.  2,547 children were at increased genetic risk for t2d and 142 developed IA and 42 progressed to t1d.   Information on intake of fructose, sucrose, total sugars, sugar-sweetened beverages, beverages with non-nutritive sweetener and juice was collected prospectively throughout childhood via food frequency questionnaires.” [51]  They were followed for 10.2 years.  Conclusion:  Total sugar intake was significantly associated with an increased risk of progression to type 1 diabetes in children with IA,” (supra Lamb).   “The use of 2 genetic markers in screening for the observational study produce only a low percentage of t1d at 10.2 years follow up. Other study have shown the adverse effects of a high fructose diet upon the liver.[52]

  4. The role of T cells has been studied but what initiates the process is in need of further research. “The challenge for the future is to determine which factors contribute to the loss of tolerance to beta-cell antigens, and to define what measures T-cells can provide to suppress autoreactivity, since it is becoming increasingly evident that T-cells provide a two-edged sword: some T-cells could be pathogenic, but others can regulate the disease process and thus form new targets for immunointervention.” [53]   Among the factors associated with t1d, besides genetic, are vitamin D3 and its receptor, viral infections, cytokines and chemokines, and the western diet.” [54] 

  5. Consistent with the observation of William Osler, the incidence of t1d is rising:  “Across Europe, the average annual increase in the incidence in children under 15 years is 3.4%.” [55]  Finding the process is a drug oriented approach, finding the environmental causes is a prevention approach.  Unfortunately, 95% of the research is focused of processes.  The environmental role, why there is a steady increase in t1d remains unknown.

    It doesn’t stop with youths, given the drug management of t2d, about 20% of those with end-stage t2d, those on high dose of insulin are likely to have LADA, latent autoimmune diabetes in adults.  It is a form of t1d that comes on slowly among those diagnosed with t2d.  It would also explain why for some dietary management of t2d has disappointing results, and the same for those with bariatric surgery.  And like with t1d there are degrees of beta cell destruction, thus a degree of the dependence on insulin to control their serum glucose and mask the symptom of t1d. 

About 80% of all LADA patients initially misdiagnosed with type 2 (and who have GAD antibodies) will become insulin-dependent within 3 to 15 years (according to differing LADA sources). . . .  It is estimated that between 6-50% of all persons, depending on population, diagnosed with type 2 diabetes might actually have LADA.  This number accounts for an estimated 5–10% of the total diabetes population in the U.S. or, as many as 3.5 million persons with LADA[56]

          The research and existence of the condition doesn’t get the attention the numbers would justify.  Pharma is happy lowering glucose with drugs, and the more t2d progress the more drugs.  There is a Wikipedia article and some journal articles: 

Latent autoimmune diabetes in adults (LADA) is a disorder in which, despite the presence of islet antibodies at diagnosis of diabetes, the progression of autoimmune β-cell failure is slow. LADA patients are therefore not insulin requiring, at least during the first 6 months after diagnosis of diabetes.  Prospective studies of β-cell function show that LADA patients with multiple islet antibodies develop β-cell failure within 5 years, whereas those with only GAD antibodies (GADAs) or only islet cell antibodies (ICAs) mostly develop β-cell failure after 5 years. .[57]

          Just what drives the destruction of beta cells is not known, but the association with our high fructose diet, increasing IR through drugs, and the lack among the LSPs create a compelling links to our current treatment and the western diet.  What has gone wrong with the immune system, and which cells, this needs to be confirmed.  It is the B4, it flows from the pattern of other conditions.  The message of Dr. Robert Lustig, that sugar is a slow poison like ethanol, finds supports from many sources. 

          The reliance on drug treatment of t1d with increased carbohydrates to manage the effects of insulin injections is a way of promoting sales and increase the risk factors associated with t1d and side effects caused by the drugs.  The Richard K. Bernstein MD personal experience and publication convincing make support the low carb alternative.[58]   

Again consistent with the early work we have the combination of B4 affecting systems built upon the high fructose western diet. Even without knowing the process which causes the beta cell destruction, the low sugar diet lowers the risks probably to a paleo level where the condition is virtual unknown. 


20.  What caused the children with t1d to waste?  I have come to believe that the wasting of children with t1d prior to insulin injections is to a significant extent caused by the failure to utilize amino acids, since insulin controls the anabolic IGF-1 and IGF-2.  The metabolism of muscle of those children is a way that their body can gain amino acids for various essential functions.  However, the picture is not that simple since leptin, the insulin like growth factors and other hormones are partial control by insulin, these too could be CC for the wasting of those with t1d.  Other causes for the wasting could be elevated blood sugar and damage to the kidneys which excreted the excess sugars.  These patients could still metabolize fat and the toxic effects of extreme hyperglycemia could be avoided by a ketogenic diet, like those used back then and still used to reduce epileptic seizures.  Wasting, I believe, is caused mainly by the failure to build proteins.  Possible some physicians had tried the diet for epileptics on those with t1d before 1923, but that didn’t change medical practices for t1d.



Fructose, not glucose damages beta cells.

We also showed directly that proteins in beta-cells were actually glycated by using an antibody which can specifically recognize proteins glycated by fructose, but not by glucose. . . .  Taken in pancreatic beta-cells by provoking oxidative stress mainly through the glycation reaction, which may explain the deterioration of beta-cells under conditions of diabetes.

Taken together, these findings suggest that exposure of skeletal muscle cells to fructose induced oxidative stress that decreased mitochondrial DNA content and triggered mitochondrial dysfunction, which caused apoptosis.

Pancreatic polypeptide (PP) is a polypeptide secreted by PP cells in the endocrine pancreas predominantly in the head of the pancreas. It consists of 36 amino acids and has molecular weight about 4200 Da

The function of PP is to self-regulate pancreatic secretion activities (endocrine and exocrine). It also has effects on hepatic glycogen levels and gastrointestinal secretions. Plasma PP has been shown to be reduced in conditions associated with increased food intake and elevated in anorexia nervosa. In addition, peripheral administration of PP has been shown to decrease food intake in rodents.[2] PP is secreted by PP pancreatic cells of Langerhans islets. It stimulates the gastric juice secretion, but inhibits the gastric secretion induced by pentagastrine. It is the antagonist of cholecystokinin and inhibits the pancreatic secretion which is stimulated by cholecystokinin. On fasting, PP seric concentration is 80 pg/ml; after the meal, it rises up from 8 to 10 times more; glucose and fats also induce PP's level increase, but on parenteral introduction of those substances, the level of hormones doesn't change. The administration of atropine, the vagotomy, blocks the PP's after-meal secretion. The excitation of the vagus nerve, the administration of gastrin, secretin or cholecystokinin induce PP secretion.




Sub-Lim, Jung, Michele Mietus-Snyder, et al Nature, April 2010,  The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome possible source for the above fructose causing t2d 

Spruss, Astrid, Ina Bergheim, Sept 2009, Dietary fructose and intestinal barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver disease



Removed from #4  I also include the bariatric surgery cure of t2d (#6), role of metformin in promoting drugs for t2d and why metformin was chosen from the over 100 patented drugs to be the first choice for newly diagnoses diabetics, and now prediabetics (#12), In defense of this article it is for physicians and administrators, and too much science would have a much smaller effect on the audience. Their focus of the article is on changing guidelines and how diabetes ought to be managed, and it was effective at that as far as communicating; however, nothing has changed as to drug treatment. Thus if you want less science the article is a good choice, and if you want more science and history, then read on.  

Another reason to keep carbs low is the insulin response to proteins (several of the essential amino acids); insulin; becomes moderately high.[59]  I believe that  (though lacking the evidence) that other hormonal cause the insulin response not to affect blood glucose which is normal, but to promote the utilization of amino acids in the building of proteins for insulin regulates IGF-1 and 2 which promote the synthesize proteins and polypeptides from amino acids.  By keeping carbs low, I am proposing that other regulatory hormones assure that the elevated insulin caused by the amino acids does not shut down autophagy which utilizes the proteins.  If this mechanism didn’t exist, the high insulin caused by the amino acids would cause hypoglycemia.  Nature is very good at maximizing the utilization of amino acids—they can’t be stored—and at preventing a condition, hypoglycemia, which would reduce survival.  If autophagy was turned off those amino acids would not be metabolized.   Details make a big difference for the diabetic, both type 1 and type; there are very significantly benefit from the low-carb diet.  One of those benefits is that a snack or meal without carbs; i.e., of protein and fats, doesn’t shut down fat metabolism and autophagy repairs.


[1] Gary Taubes, Why we get fat, and what to do about it, (2011) P 119.

[2] Reid, James, A. I. MaDougall, et al, Nov 1957, Aspiring and Diabetes mellitus. Of the 8 treated all were diabetic of 5 years or less.

[3] Holmes, Michelle, Wendy Chen et al, March 2010, Aspirin intake and survival after breast cancer

[4] Fries, James, Hubert, et al, Nov 2011 Postponed Development of Disability in Elderly Runners   A 13-Year Longitudinal Study

[5] In the cytosol the fatty acids are converted to acetyl-CoA which in the MTD is converted to acetoacetate (the conjugate base of DKA).

[6] Allen’s Studies concerning glycosuria and diabetes (Harvard University, 1913) changed the prevailing view that diabetes was a problem that involved only carbohydrate metabolism by claiming that all food produced diabetic symptoms of glycosuria and acidosis.  From his work came the starvation diet. 

[7] Erythrocytes have two reasons:  one for size going through capillaries, the other to use less oxygen which is carried for delivery. 

[8] Cahill, George Jr, Oliver Oven, 1968,  Starvation and survival

[9] Cahill Georg F Jr., May 1977, Physiology of acute starvation in man

[10] Cheng, Bin, Mark Mattson, Dec 1991, NGF and bFGF protect rat hippocampal and human cortical neurons against hypoglycemic damage by stabilizing calcium homeostasis

[11] Cahill Georg F Jr., May 1977, Physiology of acute starvation in man

[12] Feinman, Richard D, Richard K Bernstein, Eric C Westman, Jeff S  Volek, total 29 authors, Jan 2015, Nutrition,  Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base

[13] My copy of the 1959 Diabetic Manual, Joslin, for the patient, tenth edition doesn’t not mention low-carb alternative.  I am not implying that Joslin sold his soul for dollars, for as I have looked at the science of his era and the medical issues of ketoacidosis and hypoglycemia (#11), and its role in his developing a way which he believed avoided those conditions; however, his role was promoted by industry by their selection process. 

[14] Merck Manual, 10th Edition, 1961, P 1810.

[15] Westman, Eric, William Yancy, et al, Dietary treatment of diabetes mellitus in the pre-insulin era (1914-1922) published in Prospective in biology and medicine, Johns Hopkins University Press, winter 2006.  Eric Westman MD is author of The new Atkins for a new you, 2010, along with co-authors Stephen Phinney MD, and Jeff Volek Ph.D.  The authors are on YouTube.   

[16] At the advice of his physician, who relied on the work of a French physician, William Banting (1796 to 1878) followed an early version of the Atkins diet.  It was for weight, but also manages t2d.  He was the funeral director to the Royal Household.  His book on dieting, Letter on Corpulence, addressed to the public, 1863, went through a number of editions and remains in print.  Banting and bant has entered the English, and in Swedish banta is a verb for being on a diet.  William is a distant relative of Sir Fredrick Banting, of insulin fame.  Though William might not have progressed to t2d, the record I think is too incomplete to know.    

[17] KOLs in guideline have steadily lowered several times the level for t2d (#11 & 12).

[18] Wiki, tolbutamide, Dec 2019.  The story of the first of the first sulfonylurea, and first pill for t2d. 

[19] Cecil essentials of medicine, 1986, P. 488, There are 6 drugs listed for treatment of diabetes.  Like the Merck of 1961, the diet approach is not stressed, nor designed to succeed.   And it gets worse:  “To diminish the risk of vascular disease, all diabetic patients should be place on a diet low in fat. . . . and with a low cholesterol content. . . .”  P. 490.  The benefits of the drugs are “The complications of diabetes usually take 10 to 20 years to develop.” It goes on to state that tight control of glucose should not be instituted for those with longer life expectancy.  P 490.  I wonder if this message is taught in CME classes for limiting tight control of glucose to exclude from tight control? 

[20] With the 8th Edition, there was a complete rewrite, thus the language was different than the earlier editions. 

[21] Spence, Des, April 2013 Bad medicine:  the way we manage diabetes

[22] Bianchi, D, S. Del Prato, June 2011, Looking for new pharmacological treatments for type-2 diabetes.   

[23] Wiki, metformin, Dec 2019

[24] I am not imply that a mechanism of action entails a better drug, for part of the sales pitch is to “show how the drug rights a biological imbalance.”  The mechanism as with an sulfa drug sheds light on its effects and side effects. 

[25] When examining the use of statins, on the model of how it works, it is a major cause of dementia.  Surprisingly, there are a number of population studies which “show” that statins lower the risk of dementia.  The autopsy studies find to prove it is Alzheimer’s disease in the dead portions of the brain clumps of amyloid and tau plaque (proteins).  (The tau involves abnormal phosphorylation).  I hold that because of the reduction in the production of ATP caused by a 40% reduction in the essential co-enzyme Q10, there is a corresponding reduction in cellular maintenance permitting this accumulation among the elderly.  Odd that pharma would fund studies that conclude a prophylactic effect.  Do they know something, and are doing damage control?  

[26] This slight-of-hand reflects the lower standard applied by Cochrane Collaboration, as made public when Peter Gotzsche was removed from their Governing Board, in a 6 to 4 vote of its 13 members. Sept 2018.  In an interview, Gotzsche wrote in a BMJ article Nov. 2018:  "Cochrane no longer lives up to its core values of collaboration, openness, transparency, accountability, democracy and keeping the drug industry at arm’s length."[  Madsen, KS, Y Chi, et al Dec. 3 2019 Metformin for prevention/delay of type 2 diabetes mellitus (T2DM) and associated complications in persons at increased risk for development of T2DM

[27] Jason Fung, Diabetes Code P 144

[28] Prof. James McCormack, lecture to physicians, YouTube, Metformin—the case of exaggerating both benefits and harms

[29] Wiki, biguanides, Dec. 2019

[30] Ikeda Tadasu, Keiko Iwata, et al, April 2000, Inhibitory effect of metformin on intestinal glucose absorption in the perfused rat intestine

[31] Wilcock, Carol, Clifford Bailey, Feb 1991, Reconsideration of inhibitory effect of metformin on intestinal glucose absorption

[32] Bailey, CJ, C Wilcock, et al June 2005, Metformin and the intestine

[33] Hirst, JA, AJ Farmer, et al, Feb 2012 Quantifying the effect of metformin treatment and dose on glycemic control.  ADA article with support of Pharma, there were 21 versions of the article, and the conclusion follows the pattern of positive bias for a patented drug.  Conclusion: “Evidence supports the effectiveness of metformin therapy in a clinically important lowering of HbA1c used as monotherapy and in combination with other therapeutic agents. There is potential for using higher doses of metformin to maximize glycemic control in diabetic patients without increasing gastrointestinal effects.”

[34] “Claritin was patented by Schering-Plough in 1981, but not approved by the FDA until 1993—after much scientific controversy about whether it is better than a placebo at the low doses necessary to prevent drowsiness.” Marcia Angell, The truth about drug companies, 2004, P 186.  Eventually, the 4% reduction in hay fever was sufficient for a patent, and at its peak the Americans were milked for $2.7 billion annually; adjust for the 20-year real inflation, it is over double that amount—gasoline was about $1 a gallon. 

[35] As Joseph Kraft (bibliography) points out elevated insulin often causes normal blood glucose level. 

[36] PLoS Medicine 2012;9:e1001204

[37] Diabetes Metab, 2014 Feb 3. Pii:S1262-3636

[38] NEJM 2008;359 – Sep 10

[39] And it gets worse, in that the study was unblended thus all non-objective outcomes ae subject to reporting bias, in a number of outcomes during the study multiple points were added to it (pharma’s common way of getting the outcomes they want), there was dropout period, in that 22% of the volunteers dropped out, and as stated before compared to the raw data there always is industry bias in clinical trials and their write-ups.  Finally these findings were never reproduced (thus the difference between these finding and the meta-analysis referred to above.   

[41] Fauber, Hohn, Elbert Chu, Oct, 2014, The slippery slope:  is a surrogate endpoint evidence of efficacy?  And in The slippery slope:  adverse events and runaway diabetes train.    

[42] Marcia Angell, Harvard Prof.,2004, The truth about drug companies, P 80 to 93, and on 29 other pages.

[43] Angell, supra 62-73

[44]  I had applied 1967 to go there but ended up in graduate school at the University of Manitoba. in philosophy  

[45] Gotzsche, Peter, Deadly medicine and organised crime, how big pharma has corrupted healthcare, 2013, P 186. Gotzsche’s book won a BMA (British Medical Association) Medical Book Award, and it has forwards by former Editor-in-Chief of the BMJ, Richard Smith, and Deputy editor of the JAMA, Drummond Rennie.  Need I say more? 

[46] High sugar, honey, dates, and so on were foods for centuries consumed by the affluent, therefore, evolution favored an adjustment to the toxic fructose, an adjustment that only now the paleo peoples and other LSPs are making.  

[47] Both #s 2 & 3 a limited numbers of calories, 500 for elderly and women, 600 for men with very low carbs will not significantly tak the dieter out of fat metabolism through elevated insulin to cause conversion of free fatty acids to triglycerides or shut down autophagy

[48] This would consist of cheese, meets, fish, oils, green –leafy vegetables, nuts, in small portions so as not to significantly raise insulin and thereby shut down autophagy and causes the conversion of free fatty acids to triglycerides.  These types of snacks should be used to extend diet and make repeating of 1, 2, and 3 more likely.  

[49] [49] Gary Taubes, The case against sugar, P. 7-8. What is now called t2d, was adult onset, was maned by diet, and only a few intractable cases would result in hospital admission, of which probably most had progress to LADA (Latant Autoimmune Diabetes Adult), thus the increase in cases were nearly entirely type 1.  Other sources support this conclusion.  Fredrick Madison Allen in his textbook, Studies concerning glysouria and diabetes, and Elliott Joslin (1869-1962) The treatment of diabetes mellitus:  with observations based upon three thousand cases (1923)

[50] Wiki, type_1_diabetes, Dec 2019. Triggers suggested “include dietary agents such as proteins in gluten, time of eeaning, gut microbiota, viral infectioins and bacterial infections like paratuberculosis.” Again the fruits of the wrong trees. 

[51] Lamb, Molly, Brittni Frederiksen, et al June 2015, Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes Autoimmunity Study in the Young

[52] Crescenzo, Raffaella, Francesca Blanco, et al April 2012, Increased hepatic de novo lipogenesis and mitochondrial efficiency in a model of obesity induced by diets rich in fructose

[53] Roep, Bart, March 2003, The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure a seminal article covering attempts to unravel the processes and causes.

[54] Roep, Bart, March 2003, The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure.  The article missed the association with dietary sugar, IR, and MTDD. 

[55] Ozougwu, JC, KC Obimba, et al (Nigeria) June 2013, The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus

[56] Wiki, latent_autoimmune_diabetes_in _adults, Dec 2019

[57] Stenstrom, Gunnar, Andres Gottsater, et al, Dec. 2005, Latent autoimmune diabetes in adults:  Definition, prevelance beta cell function, and treatment. The complexity of issues covering LADA is covered in Rolandsson, O, JP Palmer, March 2010, Latent autoimmune diabetes in adults (LADA) is dead:  long live autoimmune diabetes!

[58] Lennerz, Belinda, Richard K. Bernstein, et al, June 2018, Management of Type 1 Diabetes With a Very Low–Carbohydrate Diet

[59] Floyd, John, Stefan Fajans, et al, sept 1966, Stimulation of insulin secretion by amino acids

Enter supporting content here

On how daily excessive fructose damages the mitochondria and thus is the main cause for the conditions associated with the Western diet--much, much, more than insulin resistance, type-2 diabetes, and weight gain