Dr.
XXXX I find you first among authorities on obesity, diabetes, and how to
reverse them. I have a
medical website since 2004, 11 years of university studies in science and
philosophy, over 4 years of full-time investigation into issues associated with
diabetes, I counsel several diabetic to follow your dietary management of type-2
diabetes, and I strongly recommend that they buy your two books, watch your
lectures, and become your outpatient. My
examination of journal articles and books, prior to discovering your lectures
on YouTube, has lead me to the same major conclusions as yours. Your work was
one more confirmation of my hypothesis
to which you added important details and evidence. Recently I have come across
in my research of
the diabetes pandemic the role of low ascorbate which causes defective collagen
that causes diabetic angiopathy and thus the comorbidities associated with diabetes.
What
is your opinion thereon? Assuming the
correctness of my piecing together the evidence and that you too are aware of
this analysis, do you recommend supplementation, which supplementation and what
dose? Do you check with your patients
for low ascorbate in tissues that store very high levels rather than serum
ascorbate?—serum ascorbate reflects dietary intake.
As you know pharma
which is in the
business of treating illness, and this leads them to create a guideline protocol
for treating a chronic with patented drugs.
Their fiduciary model causes the industry to prefer treating 1) symptoms,
2) down-stream abnormalities, 3) to create chronic conditions through their
medication, and 4) not to cure the condition.
In my search of the results of their tobacco science, I have come across
in May that diabetics have reduced amounts of ascorbate, that the measure of
serum ascorbate only reflect recent dietary intake, that to uncover this
shortage requires doing an assay of tissues/cells which store ascorbate such as
lymphocytes, that ascorbate is essential involved in 7 biosynthesis processes, of
particular importance is the production of collagen, that the production of defective
collagen is very possible the major causal factor in the development of
diabetic angiopathy, and the development of diabetic angiopathy is the major
cause for the comorbidities associated with diabetes; thus low cellular
ascorbate is what physicians ought to be treating and scientists researching. Given
that the tight management of serum
glucose has failed in clinical trials to produce a reduction in the comorbidities
associated with diabetes, the causal explanation that the diabetic’s higher
level of serum glucose with its higher rate of glycation and the production of advanced
glycation end products (AGE) is suspect.
Other evidence goes to debunk the putative key role of the pharma-favored
role of serum glucose with its profitable tight management of serum
glucose. One journal article entitled Age-dependent
increase in ortho-tyrosine and methionine sulfoxide in human skin collagen is
not accelerated in diabetes. Evidence against a generalized increase in
oxidative stress in diabetes (J Clin Invest. 1997 Aug 15; 100(4): 839–846) doubts the role of glycation. Below is part of that article’s
abstract. The article found that
oxidative stress—looking at skin samples--is not the cause of uniquely high for
the diabetics, and thus not the cause for collagen vector in the pathologies associated
with diabetes. There are hundreds of
articles, 85% before the year 2000, that are on low ascorbate and its
consequences, of which some favor pharma’s oxidative stress theory caused by
low ascorbate, while other stress a much different role of ascorbate and
collagen. Unfortunately I have not found
a seminal article that pieces together the journal articles, I have copied about
a dozen such articles—see attachments.
I
could pursue the topic further, but for the other demands of research and
goals. I am gathering together my
research into a single volume like Prof. Peter Gotzsche recent books. Assuming
the correctness of this line of
analysis ascorbate or diabetics of supplements, like that of taking CoQ10 if on
a statin. Do you advise increasing
ascorbate intake, and how much?
From abstract (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC508256/): “We
show that ortho-tyrosine and methionine
sulfoxide are formed in concert with Nepsilon-(carboxymethyl)lysine and
pentosidine during glycoxidation of collagen in vitro, and that they also
increase with age in human skin collagen. The age-adjusted levels of these
oxidized amino acids in collagen was the same in diabetic and nondiabetic
subjects, arguing that diabetes per se does not cause an increase in oxidative
stress or damage to extracellular matrix proteins. These results
provide evidence for an age-dependent increase in oxidative damage to collagen
and support previous conclusions that the increase in glycoxidation products in
skin collagen in diabetes can be explained by the increase in glycemia alone,
without invoking a generalized, diabetes-dependent increase in oxidative stress.”
The plasma and tissue concentration of ascorbic
acid (AA) is reduced in diabetes. This study was designed to investigate the
mechanism and significance of this phenomenon. The low plasma AA concentration
of diabetic rats can be normalized by dietary AA supplement (20–40 mg/day), a
dosage approximately equal to the maximal synthetic rate of this substance in
the rats. Treatment of diabetic rats with this regime prevented the decrease in
activity of granulation tissue prolyl hydroxylase (PRLase), an AA-dependent
enzyme required for maintaining the normal properties of collagen. The
decreased plasma AA concentration and granulation tissue PRLase activity in
diabetes can also be normalized by the
aldose reductase inhibitor tolrestat. We conclude that in diabetic animals
there is a true deficiency of AA that may be responsible for some of the changes
of collagen observed in diabetes.
Treatment with AA or an aldose reductase
inhibitor may prevent some of the diabetic complications with underlying
collagen abnormalities.
From my notes:
Dietary myo-inositol
supplementation was effective
in normalizing plasma AA levels
aldose reductase inhibitor tolrestat.
