versus medications 3/3/20
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
American Diabetic Association ATP adenosine
triphosphate B4 fructose,
mitochondrial dysfunction, reduced production of ATP,
reduced autophagy CC
contributing cause CVD cardiovascular
conditions associated with the western diet
DKA diabetic ketone
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
Table 1. US Diabetes Forecasts,
2015 to 2030
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).
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
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,
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
a condition that is virtual unknown among LSPs. 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
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
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
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). 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!
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. 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, 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,
masking the IR by lowering contrary to evolutionary design the blood glucose. So
why is IR so deadly?
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%.  Insulin is what I call a gate way hormone
thus one whose effects are highly regulated. IR is a major CC for CAWD.
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.” 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).
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
stay on just metformin for years; they are on the path to eventual insulin
injections, if they live long enough.
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.”  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).”  Should we expect otherwise
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.
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.” 
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.
William Osler wrote of
managing t2d with low carb diet.
Diabetes, ischemic events, cancer, and Alzheimer’s disease
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
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
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. The effect of ethanol damages the liver and
the pancreas to cause fat accumulation 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
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%. 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. The concordance of identical twins is 70% for
t1d, And for t2d,
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 . . . . epidemiologic studies
indicate that type 2
diabetes appears to result from a collection of multiple genetic defects. . . “
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.
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
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
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. 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.
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
4. Modern health care
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". It has, however, been noted that he advised
tasting the urine for sweetness in other contexts. in western English medicine to Thomas Willis (1621
to 1675) described
the urine of diabetics as “wonderfully sweet as if imbued with honey or sugar.” 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 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
was first isolated from raisins in 1747 by the German chemist Andreas Marggraf. 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.
The different tastes and sweetness waited for the advancement
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.
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. 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)
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.
contributed much in his Introduction to
the study of experimental medicine (1865).
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.
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.
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). 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). Each islet would yield several chemical in the
production of insulin, glucagon, somatostatin and pancreatic peptide.
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
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)
in print and bant
and Bantingism have become an English
and Swedish words.
Insulin was only used for t1d--not used
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
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
a series of experiments, mainly on dogs, in which he removed their pancreas to
produce t1d. 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.”  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
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.”  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:
I went to Strassburg to learn from Naunyn, the
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.
Notice the low carbs, high fat for adult treatment for t2d,
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
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.” 
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,
and 8% carbs. What caused the switch, at
least in the U.S?
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.
Diacetic acid (acetoacetic acid)
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, 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
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
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. 
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
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.
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
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
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
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.”  Most of them had symptoms, their adherence
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.”  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. Many continued to practice medicine according
to experience in the era before guidelines and HMOs.
Managing t2d with Joslin’s diet
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.
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. 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.
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.
Willliam, Clement Bezoid et al, feb 2017, Diabetes
2030: insights from yesterday, today and
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.
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.
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.
 Powell, A, March 2012, Harvard
Gazette, Obesity? Diabetes? We’ve
been set up, and Jason Fung Obesity
Code (2018) P 58.
 Jason Fung, The Diabetes
The lack of reporting of t1d among LSPs entails a connection to the western
diet, and thus likely IR as a CC for t1d.
B, B. Hemmingsen, October 2018, Cochrane
Review, Development of type 2 diabetes
mellitus in people with intermediate hyperglycaemia ('prediabetes')
 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
 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?
Gary Taubes, The case against sugar, 2016,
P 7, using William Olser’s
figures from newer editions of his textbook.
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.
Worse in that the carbs in beer exacerbate the effect of fructose upon the
liver in an additive way.
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.
I.D., M.V. Apte, et al, May 1998, Chronic ethanol administration causes
oxidative stress in the rat pancreas
An average of 3.9 per 15 relatives, over 50% chance that there are 3 of the
aunts, uncles, parents, siblings and grandparents.
Pathologic basis of disease, 6th edition (1999), P 914.
 Henschen, Folke, April 1969, On the term diabetes in the works of Aretaeus
Because of later additions the work is referred to as the Hippocratic Corpus.
 Gemmill, Chalmers MD, Sept,
Greek concept of diabetes
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.
Wiki, history of diabetes March 2020
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
Richard J. Johnson, The fat switch (2012)
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.
Wiki, glucose. March 2020
Wiki, sweetness, 2/20, variation are
from different studies. Sweetness is a
Weight was determined following evaporation; the residue, mainly glucose, was
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
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.
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.
Allen, Frederick MD. In Experimental
studies on diabetes; Series I. 1920;
Production and control of diabetes in dogs, P. 575-586
Dolger, Henry, July 1972, Joslin’s
Diabetes Mellitus. The article is
the title of Joslin’s later editions. which Dolger reviewed.
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.
Wise Greek senior, who went with the army to troy in the Trojan war, as related
in the Iliad.
Manual, Tenth Edition (1959), Elliott P. Joslin, P 21. Earlier editions
had a different tile (below).
Joslin, MD, 1918, A Diabetic Manual for the
mutual use of Doctor and Patient, First
Edition, P 18
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.
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.
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).
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. .
Merck Manual 8th Ed 1950, P. 268-269.
5. Dietary low-carb
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:
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
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.,
normal or nearly so], there are fewer complications.
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 treatment—new
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?
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. So what happened to the diet?
Not surprisingly by the 10th
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.” He was marginalized on role on insulin
resistance and sugar in the development of diabetes.
Gerald Reaven (1928 to 2018) was
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. 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
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.”
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. 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.
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.”  This is a
seminal article calling for the science to dictate guidelines:
12 Points of evidence [bold I consider more important]
1. Hyperglycemia is
the most salient feature of diabetes.
Dietary carbohydrate restriction has the greatest effect on decreasing blood
Point 2. During the
epidemics of obesity and type 2 diabetes, caloric increases have been due
almost entirely to increased carbohydrates
3. Benefits of dietary
carbohydrate restriction do not
require weight loss
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
6. Replacement of carbohydrate
with protein is generally
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)
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.]
11. Patients with type 2 diabetes on
carbohydrate-restricted diets reduce and frequently
eliminate medication. People with type 1 usually require lower insulin.
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].
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
Though the article is focused on
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
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
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.” 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.
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.”  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.”  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.”  Between 50 and 70% of dietary fructose is
utilized by the liver. Moreover, fructose
can increase DNL 5-fold. Allow me to explain again, given the
importance of this topic.
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.”  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. 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 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.
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. ; the remaining 20% have progressed from t2d
to t1d, known as latent autoimmune diabetes in adults, LADA. 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%.”  “Type 2 remission after 2 years was 72% and
36% after 10 years.”  The reduction in lipid droplets in the liver and pancreas
with it reversal of IR entails those organs functioning normally and thus
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
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.” 
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.
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 %).
Similar finding for ectopic
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. 
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 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
On the bright side though is a new
procedure with affects similar to the biliopancreatic diversion uses a liner
and has similar results. 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
extreme caloric reduction following surgery with its increased autophagy
promotes the restoration of pancreatic beta cell functions. 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?
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?  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.
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
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.
studies have indicated ketosis may have anti-tumor effects,
however clinical trials have been limited by small sample sizes and not shown
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
intermittent ketosis is lacking.
Diabetic nephropathy can also be reversed with a
ketogenic diet high in short chain fatty acid which produce 3-hydroxybutyrate. Reversing diabetics with nephropathy should be added
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
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
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
for life-long ketogenic diet and intermittent fasting. The treatment of epilepsy
with ketogenic diet
also confirms its safety.
Homeostasis mechanisms through autophagy explains
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
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:
[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
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
Fasting reverses t2d: Whatever significantly promotes
the metabolism of excess fat in the
liver and pancreas will reverse t2d and IR. 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.
Some of his patients do a much
36 hour water fast.
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.
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.”  Not cured but managing her diabetes with
diet. What if she had combined low carbs
with intermittent or alternate day fasting?
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. 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.” 
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.”  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.
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
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
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
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.”  Drugs for DP are gaining in sales.
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. Disconcertingly many of the authors of diet
books recommend just one or the other.
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
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.
 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
 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
France sulfonylureas were approved in 1948; in the U.S. in 1995. A long delay
is often indicative concerns by
Gary Taubes, Good calories, bad calories
2008 P 197
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
Arlan Rosenbloom, et al, Dec 1976, The
role of urine sugar in diabetic management
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
Dr. Fung, Dr Joseph Kraft, and others hold insulin resistance is the best predictor.
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.
Wiki, insulin resistance, 2/2020
Jason Fung, Diabetes Code 2018 P
97 and 99
 Bizeau. Michael, Michael Pagliassotti,
2005 Hepatic adaptation to sucrose and
fructose. For later confirmation (2:2).
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
M, Robit Kulkami, et al, July 2000, Loss of Insulin Signaling in Hepatocytes Leads
to Severe Insulin
Resistance and Progressive Hepatic Dysfunction
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.
2 Diabetes Etiology
 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,
fat storage in the pancreas using 1H-MRS: importance of diabetic
status and modulation with bariatric surgery-induced weight loss
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.
Wiki, Bariatric surgery Jan 2020
 Courcoulas, Anita, Susan Yanovski, et al, Dec 2014, JAMA
Surgery, Long-term Outcomes of Bariatric Surgery: A National Institutes of Health
 Gumbs, AA, IM Modin, et al, April 2015, Changes in insulin resistance following bariatric
surgery: role of caloric restriction and weight loss
 Wiki bariatric surgery Jan 2020
 Bower, Guy, Tania Toma, et al,
April 2015, Bariatric Surgery and Non-Alcoholic
Fatty Liver Disease: a Systematic Review of Liver Biochemistry and Histology
 Gaborit, B, I Abdesselam, et al, July 2014,
fat storage in the pancreas using 1H-MRS: importance of diabetic
status and modulation with bariatric surgery-induced weight loss
 Gumbs, AA, IM Modin, et al, April 2015, Changes in insulin resistance following bariatric
surgery: role of caloric restriction and weight loss
Escalona, March 2014 Duodenal-jejunal bypass liner
to treat type 2 diabetes mellitus in morbidly obese patients
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
 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
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.
 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
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
Krista, Marc Hellerstein, July 2007,
Alternate-day fasting and chronic disease prevention: a review of human and
Jason Fung, The Diabetes Code P 199,
 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
 Jackson, Ivor, Margaret McKiddie, et al,
Feb 1969 Effect of fasting on
glucose and insulin
metabolism of obese patients
Fung, Jason, The diabetes code, (2018)
Fung supra 203, This process is not a
bad thing, see #13
 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
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
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. . . . 
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
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
Aspirin also lowers glucose among its
many benefits (see http://healthfully.org/rc/id3.html under diabetes heading). A
high dose of uncoated aspirin cured t2d.
Their average standard carbohydrates of the 8 in the clinical trial was
25% of calories.
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
“Rheumatic fever and diabetes rarely coexist” (Reid supra). The
same applies to rheumatoid arthritis.
Though I ate the western diet, I had
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. 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.
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. To be a fit senior for most requires
strenuous regular activity decades prior.
I am sad over how short physicians’
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
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
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
in part was responsible for the claim by Joslin and others claiming that fats
promote t1d, 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. 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
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%.
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? All other cells have MTD which can metabolize
ketone bodies. And what about the Eskimos?
I smell the methyl amine of rats
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;
but those who are diabetic, the hypoglycemia occurs too rapidly to permit
metabolic and hemostasis adjustments.
With the natural adaptation, 5 levels of switching
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, 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.” 
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). History has little force for continuing a
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
Treating the sign, glucotoxicity, instead of the cause IR:
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. The low fat diet became the standard again by
the 1960s with about 3 grams of carbohydrate to 1 of fat recommended. 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
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
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.”  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
review with 29 signatures, in Nutrition, Jan 2015, and there are 33 version
published (listed in Googlescholar.com). The dietary guidelines didn’t
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
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
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;
why are their case histories terrible different than Joslin’s mother and my
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.
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
15. Drugs for treating t2d,:
(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,
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.
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
[tolbutamide] "expanded the total market by bringing under medical care
diabetics who were formerly not treated.” 
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
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;
there by limiting diet treatment in the 10th
Edition to at most
10% of what is clearly stated as in prior 2 editions. 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
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:
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 
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
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, 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!
drug metformin?: Is the apple rotten? What about the 4th most
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.”  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. 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. 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
The Cochrane library failed to
find significant advantage to treating pre diabetics with metformin.
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.
that a slight advantage that is not statistically significant is treated as
though it is significant. 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).
started on metformin, it is highly
unlikelyu that one will ever be able to stop it without intensive lifestyle
Metformin deserves special attention
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
Metformin, however, has so little effect
on fasting glucose and HBA1c that the current blood test is not sufficiently
sensitive. The lack of a known mechanism of action could
be because there is none, or none that are significant. Alternative it has been
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.
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.”  “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 dose‐dependent
manner by effects on mucosal and serosal glucose transfer.”  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. . . “ 
So which explanation would you prefer, the Wikipedia or the journal article
with the mechanism for poor glucose absorption?
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.” 
Starting on a drug that is cheap and fails is a lead into a drug that works and
is patented. Possible like with
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
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, 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.
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.] “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.”  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 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
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 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). 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. 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
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.”  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
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
The reality is that pharma isn’t
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 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.
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)
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
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
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
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.” 
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. 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
Their 2019 update guidelines are over
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
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
expense.] To maintain weight loss, such
programs must incorporate long-term comprehensive weight-maintenance
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.
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
patients with diabetes aged 40–75 years
and >75 years without ASCVD, use moderate-intensity statin in addition to
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
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.
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
support of roommate, significant other,
friends, family, and others
daily the documentary and lectures at http://healthfully.org//rh/id7.html
Extended water fasting
Alternate day fasting
benefits of fasting with
under 10% of calories from carbs
low digestible carb snacks
of fats 75% to carbs under 25% of calories (not counting proteins)
replacement after the age of 60 men 50 women (6:2)
work or exercise including weight training—especially if on HRT
non-fasting days no digestible carbs 3 hours before going to sleep
you must nibble something stick to fats, leafy green and other vegetables that
are low in digestible carbs, and proteins such as cheeses.
What’s causing t1d: While it is an autoimmune response
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.
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.
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”. 
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.”  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
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.
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.” 
factors associated with t1d, besides genetic,
are vitamin D3 and its receptor, viral infections, cytokines and chemokines,
and the western diet.” 
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%.”  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.
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
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
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. .
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
experience and publication convincing make support the low carb alternative.
Again consistent with the early work we have the combination
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
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.
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
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.
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.
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,
2009, Dietary fructose and intestinal
barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver
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. 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.
Gary Taubes, Why we get fat, and what to
do about it, (2011)
 Reid, James, A. I. MaDougall, et al, Nov 1957, Aspiring and Diabetes mellitus.
8 treated all were diabetic of 5 years or less.
 Holmes, Michelle,
Wendy Chen et al, March 2010,
Aspirin intake and survival after breast cancer
 Fries, James, Hubert, et al,
Nov 2011 Postponed Development
of Disability in Elderly Runners A
13-Year Longitudinal Study
the cytosol the fatty acids are converted to acetyl-CoA which in the MTD is
converted to acetoacetate (the conjugate base of DKA).
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.
Erythrocytes have two reasons: one for
size going through capillaries, the other to use less oxygen which is carried
George Jr, Oliver Oven, 1968, Starvation and
Georg F Jr., May 1977, Physiology of
acute starvation in man
 Cheng, Bin, Mark Mattson, Dec 1991, NGF
and bFGF protect rat hippocampal and human cortical neurons against
hypoglycemic damage by stabilizing calcium homeostasis
Georg F Jr., May 1977, Physiology of
acute starvation in man
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
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.
Manual, 10th Edition, 1961, P 1810.
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
new Atkins for a new you, 2010,
along with co-authors Stephen
Phinney MD, and Jeff Volek Ph.D. The
authors are on YouTube.
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.
KOLs in guideline have steadily lowered several times the level for t2d (#11 & 12).
Wiki, tolbutamide, Dec 2019. The
story of the first of the first
sulfonylurea, and first pill for t2d.
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?
With the 8th Edition,
there was a complete rewrite, thus the
language was different than the earlier editions.
Spence, Des, April 2013 Bad medicine: the
way we manage diabetes
Bianchi, D, S. Del Prato, June 2011,
Looking for new pharmacological treatments for type-2 diabetes.
Wiki, metformin, Dec 2019
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.
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?
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
for prevention/delay of type 2 diabetes mellitus (T2DM) and associated
complications in persons at increased risk for development of T2DM
Jason Fung, Diabetes Code P 144
Prof. James McCormack, lecture to physicians, YouTube, Metformin—the case of
exaggerating both benefits and harms
Wiki, biguanides, Dec. 2019
 Ikeda Tadasu, Keiko Iwata, et al, April 2000,
effect of metformin on intestinal glucose absorption in the perfused rat
 Wilcock, Carol, Clifford Bailey, Feb 1991, Reconsideration
of inhibitory effect of
metformin on intestinal glucose absorption
 Bailey, CJ, C Wilcock, et al June 2005, Metformin
and the intestine
 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.”
“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.
As Joseph Kraft (bibliography) points out elevated insulin often causes normal
blood glucose level.
PLoS Medicine 2012;9:e1001204
Diabetes Metab, 2014 Feb 3. Pii:S1262-3636
NEJM 2008;359 – Sep 10
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.
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.
Marcia Angell, Harvard Prof.,2004, The truth
about drug companies, P 80
to 93, and on 29 other pages.
 I had applied 1967 to go there but
ended up in graduate school at the University of Manitoba. in philosophy
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?
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.
#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
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
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)
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.
 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
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
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
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
Ozougwu, JC, KC Obimba, et al (Nigeria) June 2013, The pathogenesis and pathophysiology
of type 1 and type 2 diabetes
latent_autoimmune_diabetes_in _adults, Dec
Stenstrom, Gunnar, Andres Gottsater, et al, Dec. 2005, Latent autoimmune diabetes
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
is dead: long live autoimmune diabetes!
Belinda, Richard K. Bernstein, et al, June 2018, Management of Type 1 Diabetes With
a Very Low–Carbohydrate Diet
 Floyd, John, Stefan Fajans, et al, sept 1966, Stimulation
of insulin secretion by amino acids