|
|
|
|
Home | 500 YouTube Videos, 25 topics in 2 parts | Video page Cancer to last topic science | VIDEOS YouTube on Economic-political Issues | Documentaries, Most view on YouTube, What I've learned | Concise: Diets, health, weight, insulin resistance, and type 2 diabetes | Part 1: Cardiovascular disease causes | Part 2: CVD Myths: Fats, sugars, cholesterol, and Statins id2.html | Part 3:: Carbohydrates: types, tables, role in NAFLD & MeS | Part 4 Fats role in CVD | Rancid Polyunsaturated and Trans-fats are Bad | Part 5: Healthful Lifestyle, Diet, Supplements, & Drugs | Part 6: Ill-health pandemic: conditons, causes, and dietary fixes | Atkins Low Carb Diet with modifications | Diabetes meds, bad medicines | Evidence for Alternate Day Fasting--Cures diabetes | Terms used in dietary articles | Pharma's tobacco science, diet, Inuslin Resistance, diabetes | Best Healthful Supplement for seniors | Fasting cures type 2 diabetes
|
|
|
Recommended Healthful
|
Pharma's tobacco science, diet, Inuslin Resistance, diabetes
|
|
|
Since writing this article, I have in 2020 researched the history of the treatment of diabetes, and found that it had been
managed with a low carb diet, and those who followed the diet with type 2 diabetes lived as long as those who weren't diabetic.
I have wrote an historical chapter on diabetes for the book I am writing on the conditions associated with the western
diet, at http://healthfully.org/rbook/id9.html 9/9/2020 On the video page there is lectures confirming that diabetes Meletus can be managed by diet without drugs
at http://healthfully.org/rh/id7.html
A lesson on how pharma tweaks the
basic
science behind Insulin Resistance to treat signs instead of causes, and the dietary
fix 7/27/15
Pharma
profits from the Western-diet health disaster.
Instead of sending the right message about diet, pharma educates doctors
on the cluster of conditions and signs caused by the effects of the Western
diet. It is not in pharma’s financial
interest to inform doctors about the dietary fix to those conditions. The
article below is about how pharma has manipulated the information about the
satellite of conditions made common by the Western diet.
AS Atherosclerosis
|
|
N3
Omega 3 fatty acids
|
CVD
Cardiovascular disease
|
|
N6
Omega 6 fatty acids
|
HT
Hypertension
|
|
MeS
Metabolic syndrome[1][1]
|
IR
Insulin resistance
|
|
NALFD Non-alcoholic
fatty liver disease
|
KOL
Key opinion leader
|
|
T2D
Type 2 Diabetes
|
MI
Myocardial infarction
|
|
TC
Total Cholesterol
|
Part 1: Wiki’s tweaks by pharma’s KOLs on diet
related conditions
For those who want to know of the actual process leading to the obesity and diabetes pandemics
and how this has been spun by pharma.
For those who when told they are Insulin
Resistant (IR), or have Metabolic
Syndrome (MeS)[2],
Non Alcoholic Fatty Liver Disease (NAFLD), Type-2
Diabetes (T2D, NIDDM,
Non-Insulin Dependent Diabetes Mellitus), this article is for you. There are
pharma’s drugs; they aren’t a fix
because they don’t treat the cause,[3]
and there is a dietary fix that is not mentioned. Nine out of ten of physicians
repeat pharma’s
spin rather than the correct dietary fix--why. If you wish to know of bad pharma then
attend Prof Marcia
Angell’s
President’s
Lecture—link. If you wish to read about diet and/or the
science behind it, then click on link. And for a library of quality- documentaries
on diet, bad pharma, and their tobacco science, then click on this link. What follows is about the spin, what I call
“tobacco science” which is generated to promote profits. Once exposed,
the best fix to the
Western-diet health disaster is revealed.
Wikipedia has become a source for
pharma to spread their spin; not at all surprising given that pharma frames the
discussion of the topic that promote their profits. Again and again pharma’s
Key Opinion Leaders
(KOLs)[4]
simply ignore the fix, and proceed indirectly to promote pharma’s drugs by elevating
bystanders to causes. This
pharmaceutical approach fails to reduce morbidity or mortality. Pharma has through
their KOLs spun medical
textbooks, medical-university classes, mandated continuing-education classes for
doctors, and medical journal contents. This article is about pharma’s spin in
Wikipedia on the above conditions listed in the first paragraph. For example
Wikipedia’s article on NAFLD has 2
sentences about soft drinks and fructose, but missed/ignores the role of fat deposits
in the liver in the liver as a result of the liver’s metabolism of fructose[5]
(“may cause increased deposit of fat
in the abdomen”. Not may,
there is only 1 cause, fructose). On MeS
more of the same: “The
metabolic syndrome can be induced by overfeeding with sugar or
fructose, particularly concomitantly with high-fat diet.” Sugar is 50%
fructose. More spin: fats
are not causal, and the experiment evidence shows that high fructose diet at 9
weeks has a much greater effect on insulin resistance then glucose. On Insulin resistance the science improves, but “Fructose is
metabolized by the liver into triglycerides, and, as mentioned above, tends to
raise their levels in the blood stream”. However, feeding rats a high
fat diet
produces, results not applicable to humans[6]
and high blood fatty acids does has not been shown to cause CAD.
“Therefore, it may contribute to insulin resistance through the same
mechanisms as the dietary fat.” But fat doesn’t contribute
to IR.
More spin the article on type-2
diabetes:
primary causes are obesity and overweight, lack of physical activity,
stress, and urbanization. In the
subsequent paragraph comes sugar-sweetened drinks, and fructose isn’t mentioned.
The article on obesity doesn’t mention fructose or refined carbohydrates, and there are but 2
sentences on sugar. “Diet quality can be improved by reducing the
consumption of
energy-dense foods, such as those high in fat and sugars, and by increasing the
intake of dietary fiber.” This is the wrong message, since fat is not
the problem as Eskimos prove. The
article on the obesity
epidemic makes no
mention of fructose, sugar, or refined carbs.
Pharma
and food manufacturers are very good at influencing the production of
information. Reading Wikipedia leads to
the wrong conclusions.
Wikipedia
doesn’t mention government’s role in
the diabetes and obesity pandemics. It
started with a government commission making a political rather than scientific
choice. Industry then used those who
believed in unhealthy fats and dietary cholesterol to get that message out
through government and corporate media.
The low-fat dietary recommendation issued by the FDA in 1977 was to
replace fat with carbs. Saturated fats
make foods taste better, thus industry responded by enhancing flavor with sugar
and transfats. The government’s change
in the food pyramid and the farm subsidies for grain made manufactured foods
cheap, and thus permitted the growth of the Western diet in and abroad; thus obesity
MeS pandemics.
Wikipedia
and in general the food literature
needs to place to address the problems.
Government created the problem, government needs to step up with the
fix. Public health emergencies like
with cigarettes worked. We had
legislative action to get out the message that cigarettes kill, banned
advertising on television, and through increased taxes dissuaded people from
smoking. Government needs to do the same
with sugar added, low-fat, refined-carbohydrate, rich foods. And our government
needs to provide the food
manufactures with incentives to increase saturated fat[7]
and lower refined carbohydrates.
Part 2, The process leading to insulin
resistance (not spun by KOLs):
Fructose is metabolized only in the liver. About 80% of fructose is used to synthesize
through acetyl CoA into fat in the liver where some of it is stored. About 20%
is converted in the liver to glycogen. Selection
as to which is mediated by insulin. A
meal high in carbs and fructose will result in some of that fat being stored by
hepatic (liver) cells. (Fructose is slowly
cleared from the blood at a significantly slower rate than glucose). Depending on diet (high carbs and sugar),
exercise, and sex hormones IR
develops in the liver and progresses into non-alcoholic fatty liver disease (NAFLD) which is
clinically similar to alcoholic
fatty liver disease (AFLD). With NAFLD,
IR develops in the fat and muscle
cells. Another contributing factor is
that fructose is 15 times in vivo more reactive that glucose (7.5 x 2)--the “2”
because of its slower clearance than glucose.
Blood sugars can latch on to certain amino acids in proteins (glycation) and thereby impede their functions.
When fructose in sufficient numbers latch on to endothelia cells that
line the walls of arteries, through glycation it causes endothelia dysfunction
(like carbon monoxide from cigarettes).
Endothelia dysfunction is a risk factor for ischemic events including
heart attacks and strokes (see atheroma, pathogens, and cholesterol myth and Australian government’s
documentaries on the dietary villains and the cholesterol myth). Based
on
incontrovertible scientific studies the actual process leading to CAD starts
with IR in the liver. This is
quite different that the spin the paragraphs above and the article below.
Part 2. Journal article by KOL:
So how does pharma and their KOLs deal with this dietary evidence? Simple,
they ignore it. Since pharma controls the teaching process,
the generation of treatment guidelines, and has captured the regulatory system,
we have a healthcare nightmare. If you
doubt the ugly picture I have painted, watch the documentaries and lectures by
professors which I have collected with links at (http://healthfully.org/rh/id7.html). As
Harvard Professor Marcia Angell puts, “what can the 800
pound gorilla do? Pretty much anything it wants.” The 800 alludes
to the global sales of $800
billion per year industry. The critics
are buried under the avalanche of misinformation, and marginalized by the
corporate media. Pharma’s power to ruin
careers sends a chilling message to the medical community. It limits the content
of criticism.[8]
The
article below is a well-argued piece dressed in tobacco science. Strong
evidence of industry authorship is
found in that there are 4,783 citations of this article, and it has 9 different
journal versions—revealed by scholar.google.com. Pharma relies upon
ghost writers to get their message out.
KOLs
attach their names to the ghost written articles—see Prof. Ben Goldacre’s Bad
pharma 2013 pages 287-299 for the evidence. The article below is part
of pharma’s effort
to expand the market for their diabetic drugs to include those with insulin
resistance--see,
and,
and.
[9] Pharma sell the condition insulin resistance,
then the drugs which are supposed to prevent its progression to MeS and T2D. Prof. Marcia
Angell--and others—call this “disease mongering”. Long-term clinical trials
have failed to find a statistically significant benefit at this stage for
treating IR to prevent T2D and CAD’s acute consequences.
For a cohesive analysis of the evidence and the issues Dr. Jason Fung’s
YouTube lectures are excellent—for links. However
physicians are encouraged through guidelines to lower the bar for T2D based
upon the surrogate endpoints of fasting serum glucose and HBA1c.
Under some circumstance this includes
treating aggressively IR. This
again is the wrong message, because the
drug course leads to a chronic deteriorating condition. The right message is
a low refined-carb diet
with strenuous physical activity.
[2] Metabolic syndrome is a cluster of signs
which are associated with the conditions of coronary artery disease,
atherosclerosis, which include Insulin resistance, obesity, and type-2
diabetes. Pharma has added to MeS
the bystanders: high cholesterol
(hyperlipidemia
also called dyslipidemia), high triglycerides (fats) and hypertension. However,
these three are not causal, but
rather signs of underlying conditions.
They are like the fever associated with influenza. Cholesterol and fat
found in plaque are signs
of an immune response to pathogens,
and hypertension is a sign of atherosclerosis.
Treating fever does not cure the underlying influenza, nor does treating
hypertension, high blood cholesterol, and triglycerides reduce morbidity or
mortality—though KOLs teach otherwise.
As taught doctors treat the bystanders, and the results aren’t worth
their side effects.
[3] High blood glucose is not the problem, but
rather a sign of the problem which is a fatty liver that has mucked up the
metabolic control system. Fatty liver is
caused by excessive fructose in the diet.
The fix is to metabolize liver fat by an extremely low carb diet.
[4] In
medicine a doctor becomes a KOL only through providing services for
pharma. The selection process determine
prominence.
[5]
Fructose is metabolized only in the liver where it becomes fatty acids (fat)
and glycogen. However, fructose at most contributes to only 20-30 for glycogen—at—the rest comes from
glucose. Glycogen is the storage form of
glucose--under 3 kg are stored. This fat
from fructose accumulates in the liver cells (hepatocytes). When in excess,
it adversely affects various
processes in the liver. This results in
insulin resistance in the liver. Insulin
promotes fat storage; thus high liver insulin entails increased fat storage in
hepatocytes. The fatty liver with a
high carb diet causes insulin resistance in the rest of the body.
[6]
Rat (and rabbits) is primarily a vegetarian.
Rats have not evolved for a high fat or high cholesterol diet; man
has. The Eskimo and certain African
tribes eat a very high fat-cholesterol diet, yet their lipid profiles are
normal and they don’t suffer from CAD.
[7]
Cheap plant fats that are high in polyunsaturated fats are unhealthy because of
rancidification in the body, and the high amount of omega 6 fatty acids—see fats. Monounsaturated and saturated fats are far
better.
[8]
For example I find it hard to believe that such diligent researches as Prof.
Robert Lustig, Ben Goldacre, and Marcia Angell, science writer Gary Taubes and
Dr. Jason Fung--all with a public presence--don’t know of the cholesterol myth,
They are all on YouTube, links. Finding a publisher is difficult, Prof. Uffe
Ravnskov MD, Dr. Duane Graveline, and Anthony Colpo had to self-publish their
important summary books on the cholesterol myth; however, Dr. Stephen Sinatra,
who has a large public following, found a publisher. Other accesses to the mass
media are barred,
and very little is found in the medical journals on the cholesterol myth.
[9]
The issue of bias in pharma-funded studies is complex and damning—see Bad Pharma
Supra reference to studies
which show that industry funded studies favor the sponsor. A study of 74
journal articles that used the raw data found Positive bias averaged 32%.
|
|
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
Typical of pharma is this sample abstract which is
tweaked. Missing in this case is a diet
high in fructose and other carbs which is the starting point for IR through its
causing NFALD.
The article weaves a tale of how IR
progresses to MeS. For every condition
there are two biological
pathways, one tweaked by pharma, the other usually is found in fragments in the
journal literature, and is based upon laboratory studies, mostly on rats. After
this article (below) is three
appendixes, all of which piece together the complex aetiology of metabolic
dysfunction and the expose the various food manufacturers and pharma-generated
myths.
http://care.diabetesjournals.org/content/14/3/173.short diacare.14.3.173Diabetes
Care March 1991 vol. 14 no. 3 173-194
Insulin Resistance: A Multifaceted
Syndrome
Responsible for NIDDM [T2D], Obesity, Hypertension, Dyslipidemia, and
Atherosclerotic Cardiovascular Disease
Abstract
Diabetes mellitus is commonly
associated with systolic/diastolic hyperten sion, and a wealth of
epidemiological data suggest that this association is independent of age and
obesity. Much
evidence indicates that the link between diabetes and essential hypertension is
hyperinsulinemia. Thus, when hypertensive patients,
whether obese or of normal body weight, are compared with age- and
weight-matched normotensive control subjects, a heightened plasma insulin response
to a glucose challenge is
consistently found. A state of
cellular resistance to insulin action subtends the observed hyperinsulinemia.
With the insulin/glucose-clamp technique, in combination with tracer glucose
infusion and indirect calorimetry, it has been demonstrated that the insulin
resistance of essential hypertension is located in peripheral tissues (muscle),
is limited to non-oxidative pathways of glucose disposal (glycogen
synthesis), and
correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and
essential hypertension can be sought in at least four general types of mechanisms:
Na+ retention, sympathetic
nervous system over-activity, disturbed membrane ion transport, and
proliferation of vascular smooth muscle cells. Physiological maneuvers, such as
calorie restriction (in the overweight patient) and regular physical exercise,
can improve tissue sensitivity to insulin; evidence indicates that these
maneuvers can also lower blood pressure in both normotensive and hypertensive
individuals. Insulin resistance and hyperinsulinemia are also associated with
an atherogenic plasma lipid profile. Elevated plasma insulin concentrations
enhance very-low-density lipoprotein (VLDL) synthesis, leading to
hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from
the VLDL particle leads to an increased formation of intermediate-density and
low-density lipoproteins, both of which are atherogenic. Last, insulin,
independent of its effects on blood pressure and plasma lipids, is known to be
atherogenic. The hormone enhances cholesterol transport into arteriolar smooth
muscle cells and increases endogenous lipid synthesis by these cells. Insulin also
stimulates the proliferation
of arteriolar smooth muscle cells, augments collagen synthesis in the vascular
wall, increases the formation of and decreases the regression of lipid plaques,
and stimulates the production of various growth factors. In summary,
insulin resistance appears to be a syndrome that is associated with a
clustering of metabolic disorders, including non-insulin-dependent diabetes
mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic
cardiovascular disease.
|
|
|
|
|
|
|
|
|
Enter supporting content here
INTERNAL SITE SEARCH ENGINE by Google
|
|
|
|
|