Part 1: CVD Myths:
Fats, Sugars Cholesterol, and Statins
8/3/14
The differences between fats
and cholesterol: For
saturated fats to cause CVD they
must pay a role causal role in oxidation of LDL or the inflammation response, but
they don’t. The same is true of
cholesterol; both are bystanders found in plaque along with calcium, cell
debris, muscle cells, fibrous connective tissue, and macrophage. Moreover, diet
has only a modest effect upon
their serum levels (the complex role of diet in CVD is developed in Part 3 & Part 4.
A number of population studies confirm this.[1] Guidelines on diets recommend low fat and low
cholesterol. Part 3 will show why low-fat diet
promotes CVD. Fats fit in with pharma’s
“bad cholesterol” model, but cholesterol is a sterol (a modified steroid) not a
fat—not structurally similar, nor converts to fats. For cholesterol “Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA)” Wiki. “Fats are triglycerides: triesters of glycerol and
any of several fatty acids, “Although the words "oils", "fats",
and "lipids" are all used to refer to fats, technically “fat”
is a subset of lipid” Wiki. Triglycerides are three
fatty acids bonded at
each COOH (organic acid group) to each of OH (alcohol) group on glycerol with
the loss of H2O— in below stick structure of a triglyceride, the red, blue,
& green are fatty acids, and black is the glycerol to which they are bonded.
The black quite different structure
below is cholesterol.
[1] The Women’s Health Initiative (WHI) diet wing, a major NIH
study found no benefit for the low fat cohort, though the intervention was
designed to reduce total fat intake to 20% of calories, and at year 6 resulted
in “Low-density lipoprotein
cholesterol levels, diastolic blood pressure, and factor VIIc levels were
significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%, respectively…. Over
a mean of 8.1 years, a dietary intervention that reduced total fat intake and
increased intakes of vegetables, fruits, and grains did not significantly
reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved
only modest effects on CVD risk factors, suggesting that more focused diet and
lifestyle interventions may be needed to improve risk factors and reduce CVD
risk.” Note bull shit finder: the
modest effect on CVD was 2% (CVD (HR,
0.98; 95% CI, 0.92-1.05”), clearly insignificant. BS in
the conclusion section is common in Pharma influenced studies. Thought leaders
use the conclusion to support
their points, and doctors seldom read the article, but rather the
conclusion. That JAMA, Journal of the
American Medical Association, allows this distortion is one more proof of who
runs the show.
Cholesterol
molecule (above)
AS Atherosclerosis
|
|
N6 Omega 6 fatty acids
|
CVD Cardiovascular disease
|
|
MeS Metabolic syndrome[1]
|
IR Insulin resistance
|
|
NALFD Non-alcoholic fatty liver disease
|
KOL Key
opinion leader
|
|
T2D Type 2 Diabetes
|
N3 Omega 3 fatty acids
|
|
TC Total Cholesterol
|
Dietary cholesterol does not cause CVD: Most
dietary
cholesterol is esterified, and esterified cholesterol is poorly absorbed. Moreover
nearly all of the cholesterol is synthesized in the body.[2] “The body also compensates for any absorption
of additional cholesterol by reducing cholesterol synthesis[9] Cholesterol synthesis can also be turned off
when cholesterol levels are high. HMG-CoA reductase [what statins block]
contains both a cytosolic domain (responsible for its catalytic function) and a
membrane domain.” Wiki. Thus dietary cholesterol does not affect blood
cholesterol level. Production is
regulated through a homeostatic mechanism involving the SREBP protein which is
activated when the cholesterol level is low and turned off when high. “SREBP
pathway regulates expression of many
genes that control lipid formation and metabolism and body fuel allocation” Wiki. “Despite
the common belief that high cholesterol is a significant risk factor for
coronary artery disease, several independent population studies in healthy
adults have shown that low total cholesterol is associated with cardiovascular
and non-cardiac mortality, indicating
that high total cholesterol is not a risk factor in a healthy population”
BMJ 10//22/13.
Pharma
misses the causes (prevention is not in their business plan) and treats high TC with
statins, and other drugs for
the consequences of metabolic syndrome.
The official push for low saturated fats & low cholesterol diet is
based on a wrong assumption, an assumption that promotes consumption of sugar, starches,
and unhealthy fats, whose main source are processed (manufactured) foods (see part
3
and Part
4). Follow
the dollars.
Natural
dietary fat does not cause high TC or CVD: “According
to the
[started in the 50s] Farmingham Heart Study, people who consumed the most cholesterol in their diet did
not have any higher blood cholesterol levels than those who consumed the least
amount…. For most people—though not all—the effect of dietary cholesterol on
serum cholesterol is insignificant” (Bowden & Sinatra 31).[3] So why are the high fat & high
cholesterol diets touted as a major risk factor for CVD? One reason is that
plaque (atheroma) in part contains cholesterol and looks like fat.[4] Another reason is that in the 65 to 70 age
group 72% of those who have a MI have elevated cholesterol; but by the age of
65, 70% of men & 39% of women have elevated cholesterol. Moreover most of
those with elevated
cholesterol have other important risk factor such as HT, AS, and high sucrose
diet. Another reason is in the
1950s rabbits fed a cholesterol-rich diet developed AS. But these results were
not repeated in animals such as rats and baboon that are not herbivores. Prof.
Ancel Keys’ notice low rate of CVD in
Mediterranean countries and did a study of their diet. In his Seven-Country
Study (1951) he
concluded that high TC caused CVD.
The results received wide press & used to support the new dietary
recommendation of lowering fats from 42% of calories to less than 30%. Based
on his study, Keys promoted the
Mediterranean diet. “Critics pointed out that Keys had data for 22
countries, but selected data from just 6. (As an example,
Keys excluded France, a country with a high fat diet and low rates of
heart disease.) Keys cheated;” at Diet Heart
Publishing. However, years later Keys reversed his
position and stated in 1997: “There’s no
connection whatsoever between cholesterol in food and cholesterol in
blood. And we’ve known that all
along. Cholesterol in the diet doesn’t
matter at all unless you happen to be a chicken or a rabbit” Bower supra
33. This was confirmed in the diet
component of the Women’s Health Initiative (WHI) diet section, fats: “there was no significant reduction in the risk of coronary
heart disease, stroke, or cardiovascular disease,” Wiki. Following
the pattern of marketing studies, researchers were selected to run clinical
trials that had proved their usefulness to pharma in the past. And the
panel for clinical guidelines “were
selected to include experts who would predictable say that … all level of blood
cholesterol in the United States are too high and should be lowered” Bowden 41
quoting Dr. Michael Oliver on the new guidelines of the National Institute of
Health Consensus Development Conference Statement, December 10-12, 1984. This
guidelines state: “The evidence justifies… the reduction of
calories from fat… to 30 percent, calories from saturated fat to 10 percent or
less, and dietary cholesterol to no more than 250 or 300 mg daily.” But
in Lipids 2010 in
a thorough review article on dietary intervention: “Diets
[weight loss] appear to have beneficial lipoprotein effects in individuals with
atherogenic dyslipidemia, compared to high-carbohydrate diets; whereas the
content of total fat or saturated fat in the diet appears to have little effect….
Over the years, data
revealed that dietary saturated fatty
acids (SFAs) are not associated with CAD and other adverse health effects.” “A
meta-analysis of 21 studies considered the effects of saturated fat intake and
found that intake of saturated fat was not associated with an increased risk of
CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki. Low-fat,
low-cholesterol (thus high carbs) is not heart
healthy but unhealthy because of fructose, starches, and unnatural fats-see Part 3
& 4).
[1]
Pharma has added hypertension and high cholesterol-triglycerides. This is more
of pharma’s marketing, and is
irrelevant as explained in Cholesterol Myth and its sequel. Hypertension is a sign of atherosclerosis;
it
can only be healed by body and diet.
[2]
“About 20–25% of total daily cholesterol production occurs in the liver; other sites
of higher synthesis rates include the intestines, adrenal
glands, and reproductive organs” Wiki. Studies
done to show a relationship between dietary cholesterol and AS use rabbits, a
vegetarian, and thus are flawed by design. For example “In contrast with the rabbit, man
responds with only minimal changes of serum cholesterol concentration to
changes of the cholesterol content of the diet.”
[3] Jonny Bowden PhD
& Stephen
Sinatra, MD, The Great Cholesterol
Myth: Why
Lowering Your Cholesterol Won’t Prevent Heart Disease—and the Statin-Free Plan
That Will, Fair Winds Press, Nov.
2012; a national bestseller, has 23 experts who praised the book and are
quoted on the cover & first page, and at Amazon has a 4.8 star rating from
220 reviewers. Getting a fair review of
book is iffy because of heated nature of the topic and many the subscribers to
pharma’s spin. JK finds the book well
supported in the critical
portions on cholesterol’s role; but in spots questionable as to the alternative
approaches to prevention of CVD. A
couple of years before reading this book,
JK had arrived at those same conclusion as to risk of CVD and on some of their
fixes.
[4]
“Atheroma is
an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and containing lipids (cholesterol and fatty acids), calcium and a variable
amount of fibrous connective tissue… in the early stage an
accumulation of mostly macrophages, that have taken up oxidized LKL” Wiki.
|
Natural
dietary fat does not cause high TC or CVD: “According
to the
[started in the 50s] Farmingham Heart Study, people who consumed the most cholesterol in their diet did
not have any higher blood cholesterol levels than those who consumed the least
amount…. For most people—though not all—the effect of dietary cholesterol on
serum cholesterol is insignificant” (Bowden & Sinatra 31).[1] So why are the high fat & high
cholesterol diets touted as a major risk factor for CVD? One reason is that
plaque (atheroma) in part contains cholesterol and looks like fat.[2] Another reason is that in the 65 to 70 age
group 72% of those who have a MI have elevated cholesterol; but by the age of
65, 70% of men & 39% of women have elevated cholesterol. Moreover most of
those with elevated
cholesterol have other important risk factor such as HT, AS, and high sucrose
diet. Another reason is in the
1950s rabbits fed a cholesterol-rich diet developed AS. But these results were
not repeated in animals such as rats and baboon that are not herbivores. Prof.
Ancel Keys’ notice low rate of CVD in
Mediterranean countries and did a study of their diet. In his Seven-Country
Study (1951) he
concluded that high TC caused CVD.
The results received wide press & used to support the new dietary
recommendation of lowering fats from 42% of calories to less than 30%. Based
on his study, Keys promoted the
Mediterranean diet. “Critics pointed out that Keys had data for 22
countries, but selected data from just 6. (As an example,
Keys excluded France, a country with a high fat diet and low rates of
heart disease.) Keys cheated;” at Diet Heart
Publishing. However, years later Keys reversed his
position and stated in 1997: “There’s no
connection whatsoever between cholesterol in food and cholesterol in
blood. And we’ve known that all
along. Cholesterol in the diet doesn’t
matter at all unless you happen to be a chicken or a rabbit” Bower supra
33. This was confirmed in the diet
component of the Women’s Health Initiative (WHI) diet section, fats: “there was no significant reduction in the risk of coronary
heart disease, stroke, or cardiovascular disease,” Wiki. Following
the pattern of marketing studies, researchers were selected to run clinical
trials that had proved their usefulness to pharma in the past. And the
panel for clinical guidelines “were
selected to include experts who would predictable say that … all level of blood
cholesterol in the United States are too high and should be lowered” Bowden 41
quoting Dr. Michael Oliver on the new guidelines of the National Institute of
Health Consensus Development Conference Statement, December 10-12, 1984. This
guidelines state: “The evidence justifies… the reduction of
calories from fat… to 30 percent, calories from saturated fat to 10 percent or
less, and dietary cholesterol to no more than 250 or 300 mg daily.” But
in Lipids 2010 in
a thorough review article on dietary intervention: “Diets
[weight loss] appear to have beneficial lipoprotein effects in individuals with
atherogenic dyslipidemia, compared to high-carbohydrate diets; whereas the
content of total fat or saturated fat in the diet appears to have little effect….
Over the years, data
revealed that dietary saturated fatty
acids (SFAs) are not associated with CAD and other adverse health effects.” “A
meta-analysis of 21 studies considered the effects of saturated fat intake and
found that intake of saturated fat was not associated with an increased risk of
CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki. Low-fat,
low-cholesterol (thus high carbs) is not heart
healthy but unhealthy because of fructose, starches, and unnatural fats-see Part 3
& 4).
Unnatural
and transfats are a risk factor for CVD: again
we have an example of money trumping science.
Cheap fats mean high profits, and unsaturated fats are cheap. Fields
of corn, canola, and soybean yield
vegetable oil and the waste product is sold as animal feed. The problems arise
in that these oils are
high in polyunsaturated fats. The
unsaturated refers to a double bond on the carbon chain of the fat. This double
bond is the long energy point for
which reactive chemical bond thereto. Fructose
and glucose in a reaction called glycation are common reactants. The product of
this reaction results in a modification of the shape of the unsaturated fat
which inhibit its metabolism, and thus proper utilization. Like transfats, these
modified fat molecules
contribute to CVD, and other health
problems. For a
discussion of rancidification read appropriate section in Part 4. Again basic research lies dormant because of
broken information system.
High levels of cholesterol, LDL, and natural
fats[3]
do not cause AS, “Though few doctors
know this, 20 studies have shown that elderly people with a high cholesterol
level in their blood live longer than those with a low level” Donald Miller
professor of surgery, lecture. Thought cholesterol and fats are found in LDL--being present doesn’t
entail causing. “Because LDL
particles appear harmless until they are within the blood vessel walls and
oxidized by free radicals it is postulated
that ingesting antioxidants and minimizing free radical exposure may reduce LDL's
contribution to atherosclerosis” Wiki. This again is a partial
truth, one uncovered
by reading research nearly a century old on CVD and by reading the literature
on the role of pathogens living
in the artery walls. Most of the damage
to LDL found in the artery walls comes from its function as a receptor for
toxic chemical produced by pathogens.
The role of pathogens in the artery walls and the immune function of LDL
are demonstrated in the journal literature.
Thus the presence of LDL within the muscular portion of the artery walls
and there active transport there are explained by their role in the immune
system, and the oxidative damage referred to above and promoted by pharma as
causal, is in fact mainly a result of toxins produced by pathogens. It also
explains why atherosclerosis is
considered the results of an inflammatory process. For a review of this evidence
go to and also articles. Pharma
should be developing treatments to prevent atherosclerosis, but instead for
reasons stated in Part 1, they lower cholesterol. Cholesterol
is manufactured in a 19 step process from acetyl-CoA and acetoacetyl-CoA
in the malev, neither of which
resemble fatty acids in structure.
Cholesterol, LDL, and natural triglycerides are bystanders because in
the degradation of oxidized LDL which houses them, they are released by the
foam cells (swollen macrophages).
Pharma follows its pattern of selling the disease (high LDL, high TC and
triglycerides), they then
selling the treatments. Thus the
reasonable conclusion is that lowering TC
and LDL won’t reduce CVD, and
because of the essential functions of cholesterol, lowering it will have many
and varied side effects. The 800 pound
gorilla sits upon the side effect, than utters “safe and effective.”
Cholesterol lipoprotein basics: looking
at the many roles of cholesterol (below), clearly dramatically lowering its
level below the norm will have major side effects. Cholesterol is essential
for health, so too
is its transport system that takes cholesterol produced in the liver to cells
throughout the body for vital functions.
Since cholesterol isn’t blood/water soluble, it is rapped in low density
lipoproteins for transport, to cells, and returns to the liver when in excess
as HDL.
”About
15% of blood cholesterol comes from the diet; the other 85% is made from acetyl
CoA by the liver and to a lesser extent by other body cells.[4] Cholesterol is so essential that nearly every
cell in the body can make cholesterol. Lipoproteins
vary considerable in their relative fat-protein compositions, but they all
contain triglycerides, phospholipids, and cholesterol in addition to protein. In
general, the higher the percentage of
lipid (fats) in the lipoprotein, the lower its density; and the greater the
proportion of protein, the higher its density” Marieb, p 856-7. On the basis of
centrifugal separation there are HDL, LDL, and VDL.[5] VLD, LDL, and HDL are produced in the liver.
VLD contain excess triacylglycerol and cholesterol that are not required by the
liver for synthesis of bile acids. LDL
is the major blood carrier of cholesterol (approximately 1,500 molecules, 20%
by weight). LDL receptors on cells
transported into cells where a vesicle then forms in which the cholesterol is
hydrolyzed to form cholesterol esters.
Now within the cell, the cholesterol can be used for membrane
biosynthesis or stored in its esterified form.
HDL functions to transport cholesterol back to the liver for subsequent
transport or biosynthesis. Note it is the LDL rapping that is subjected to
glycation and oxidation, not the cholesterol that causes the formation of
plaque—thus cholesterol is a bystander in the process. Because nature
does nothing in vain, the lowering LDL and
cholesterol is a bad idea.
Principle
functions of
cholesterol:
Converted
to bile in the liver and stored in the gallbladder. The bile dissolves fats
in the digestive
track for intestinal absorption along with vitamins A, D, E, and K. Up to 1
gm of cholesterol is used in this
process.
Absorption from the intestinal track of
fats
Absorption from the intestinal track of
vitamins A, D, E, and K
Precursor molecule in the synthesis of
vitamin D
Precursor molecule in the synthesis of
androgen steroids including the hormones testosterone, estradiol, progesterone
Precursor molecule in the synthesis of
adrenal gland hormone cortisol and aldosterone:
Cortisol
(hydrocortisone) produced by the adrenal gland is the main glucocorticoid
under normal conditions and its actions include mobilization of fats, proteins,
and carbohydrates and enhances the activity of other hormones including
glucagone, catecholamines, activates anti-stress and anti-inflammatory
pathways, plays an important role in the conversion of glycogen to glucose. During
human pregnancy plays important roles in fetal development. Cortisol reduces
bone formation, calcium
absorption in the intestines, and transports potassium out of cells and the
exchange for sodium ions. Cortisol
counter acts insulin, raises free amino acids in the serum, acts as
antidiuretic hormone, stimulates many copper enzymes, affects reproductive
system, stimulates hepatic detoxification.
Aldosterone effects are on
the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption
of sodium and
increased excretion of both potassium (by principal cells) and hydrogen ions
(by intercalated cells of the collecting duct)--Wiki.
Myelin sheath usually around
only the axon of a neuron. It is essential
for the proper functioning of the nervous system.
Cholesterol is an essential constituent of myelin.
Demyelination results in diverse
symptoms determined by the functions of the affected neurons. is the loss of the myelin sheath
insulating the nerves, and is the hallmark of someneurodegenerative autoimmune diseases, including multiple sclerosis. Dysmyelination has
been implicated in a number
of human diseases including schizophrenia.
Statins lower TC but don’t prevent MI. Statins lower TC
about 30%, but have no significant effect on ischemic events. This is the conclusion I drew from Braunwald
textbook[6] section on statin. An
article in Therapeutics letter
came to the same conclusion doing a meta-analysis using some of the same major
clinical trials: “This cardiovascular benefit is not reflected in 2 measures of
overall health impact, total mortality and total serious adverse events. Therefore, statins have not been shown to provide an overall
health benefit in primary prevention trials.”
And repeated in JAMA in a meta-analysis of 11 studies that included the
clearly cooked Jupiter and xTNT Studies[7]. Assuming for good
reason there is major positive bias, which is the
industry norm; the statins are significantly negative. However, those in the
top 5% risk group for MI slightly reduce their risk.
If
they followed lifestyle changes, they would benefit much more than from a
statin. Statins have a significant
negative effect upon quality of life, especially among those above the age of
65, and it is counter-indicated for those above 75 because of increased death
due to decreased Q10 and ATP—yet still frequently prescribed. Side effect
fall into two groups those
apparent to patients, and those on a cellular level. Inhibition of the mevalonate pathway causes the varied
side effects. In my article on statins fourteen are listed:
19 NEGATIVE EFFECTS: One, ED,
it lowers
testosterone , and nitrous
oxide thus causes ED; a similar
effect upon women for the steroids are synthesized from cholesterol. Two, COX-2 inhibitor, just like Vioxx, which
increased heart attacks (MIs) over
300%[8]. The American Heart
Association warns:
“accumulated evidence that non-steroidal, anti-inflammatory
drugs [COX inhibitors], with the exception
of aspirin, increase risk for heart attack and stroke”--promote atherogenesis. Three, blocks production of
Q10, which enters LDL and inhibits oxidative damage that causes atherogenesis, and. Four, Plaque instability: “Vulnerability
of
plaques to rupture and thrombosis is
of greater clinical
relevance than the degree of stenosis they cause” (Corti et al., 2003). “Statins
affect plaque stability in a variety of ways. The meta-loproteinases degrade
extra-cellular matrix components and thus “weaken the fibrous cap and destabilize the
lesions” -- Goodman and Gilman pharmacology, 11th Ed, p
950. Rupture of plaque causes over
80% of MIs. Statins inhibit
secretion MMP-1, 3, & 9 from SMC, and microphages make plaque less
stable. Five, reduction in ATP: Q10 is
needed for the conversion of APD to ATP (adenosine-5-triphosphate), the
source of energy for muscles contraction.
“ATP is often called the ‘molecular unit of currency’
of intracellular energy transfer including
muscle contraction and for
chemical reactions. ATP
transports chemical energy within cells
for metabolism”--Wikipedia. A
reduction of
40% in CoQ10 is accepted.[9] Six, The heart muscle under stress needs more
ATP, not less. This is why pharma
excludes the elderly and those with coronary
heart failure (CHF) from trials.
Thus, “the mean
age of ME/CFS patients
dying from CHF are 2.5 years younger than the control group.” CHF
death rate has tripled since
1989. In a review of statins on depletion of Q10 concludes:
“As the potency of statin drugs increases and as the target LDL
cholesterol level decreases, the severity of Q10 depletion increases and
heart-muscle function declines. This tragic
scenario may very well be prevented by using supplemental Q10 with all HMG
CoA reductase inhibitors [statins]” and,
and.
Thus “Lower
cholesterol, poorer outcome in CHF
patients.” Pharma
ignores Q10 side effect.
Seven, All Statins
inhibit
the rate controlling enzyme HMGCR of
the mevalonate pathway. “This pathway
generates a range of other products in
addition to cholesterol, including coenzyme Q10, heme-A, [dolichol], the production of dimethylallyl
prophosphate (DMAP), &
isopentenyl pyrophosphate
(IPP), which serve as the basis for the
biosynthesis of molecules used in processes as diverse as terpenoid synthesis, protein prenylation and isoprenylated proteins which have pivotal roles in cell
biology and human physiology and potential relevance to benefits as well as
risks of statins. Drugs, such as the statins,
stop the
production of mevalonate by inhibiting HMG-CoA
reductase” Wiki. “The Mevalonate pathway is important for, cell
membrane maintenance, hormones, protein anchoring,
and N-glycosylation. It is
also a part of steroid biosynthesis” Wiki.
“Dolichols are isoprenoids synthesized from mevalonate. They are vital to the process of Glycoprotein formation in
the endoplasmic reticulum of cells. In
this capacity it is critical to the
formation of the Glycoproteins involved in neuro-peptides,
cell identification, cell messaging and Immune defense.
Reduced bioavailability of dolichols can affect every cellular process in the body”
Wiki.
And this is only a partial list.
Eight, Cholesterol is essential
for life.
“It is the
precursor for the biosynthesis of
steroid hormones, bile acids,
vitamin D, and is an essential component of cell membranes for proper
permeability and fluidity. Effects
include pancreatic and hepatic dysfunction, ED,
diabetes[10],
muscle weakness and myopathy (muscle disease). The myelin is a cholesterol
base coating around nerve cells[11]” (Wiki). Nine,
Cognitive, the
reduction Q10 & cholesterol for the myelin sheath causes cognitive
decline--especially in the elderly where
it often leads to an incorrect diagnosis
of Alzheimer’s
disease and of neuropathy. Ten, Causes
Parkinson’s and Alzheimer’s diseases. These conditions are associated with low
level of cholesterol—at Uffe p 56. Eleven Causes cancer a
confirmation of earlier animal studies—summary
of cancers, and. Twelve Stimulates
atherosclerosis and heart disease
by blocking the vital CoQ10,
heme A, vitamin K2 (the
cofactor for matrix Gla-protein activation) and biosynthesis of selenium
containing proteins, one of which is vital glutathione
peroxidase—at
2015. This article states that
“statins stimulate atherosclerosis and heart failure”, and then provides the
mechanisms. Thirteen Causes Interstitial lung
disease is similar to emphysema in that it is a progressive condition that
affects alveolar epithelium and other tissues.
Of FDA reported side effects, it is 1/40th. Fourteen, Causes cancer in
animal studies, and thus in humans, at. Fifteen, Polyneuropathy, damage affecting
peripheral nerves, features weakness, numbness, pain, etc. is 26 times more
common after 2 years on statins compared to general matched population—at. Sixteen Side effects
account for the poor
compliance in the elderly (75% stop
within 2 years). Poor compliance also occurs with
elite athletes. Seventeen
treats the wrong cause, cholesterol doesn’t cause ischemic events
or atherosclerosis but rather infective agents (and) living in the tunica intima;
thus statins are ineffective. Three out
of
4 major studies of secondary prevention (ALL-HAT, ASCOT, & PROSPER) failed to
find life extension from statins
(Table 42-78, Braunwald’s Supra, p
1085). This table stands in opposition
to the “safe & effective”
claim (p 2286), which is
pharma’s mantra, a mantra supported by their marketing studies and guidelines.
Junk science is the norm (p 3) on
TNT trial. Eighteen, Primary prevention of high risk no benefit huge meta-study found,
in JAMA. Nineteen, drug interaction with
serious side effects are common, considering that over half of senior in their
6th decade have taken statins, and seniors average age 72 average 6
drugs according to a hospital emergency admission study (polypharmacy).
Statins have serious side effects most of which come on gradually and there are
drug interactions; both are often assumed to be part of the illness. There is
no incentive or requirement for a physician to report a suspected side
effect, which is sent to the manufacturer, who then sits on the information
sent by the doctor. Eventually the
manufacturer makes comments on reported side effect and sends them in to the
FDA, often denying that their statin was the cause. Knowing this,
seldom does a doctor consume
his time to send a report of a suspected side effect. And patients knowing
the faith their doctor
has in statins and the limited time for an office visit, he often doesn’t give
the negative news about side effects.
Seldom does the FDA act upon side effects. This system is broken!
The
results for statins are dismal: “A
meta-analysis of predominantly industry sponsored data reported that in a low
risk group of people aged 60-70 years taking statins the number needed to treat
(NNT) to prevent one cardiovascular
event in one year was 345. … In this
group [patients who had suffered an MI] the NNT is 415 for mortality over one
year. This doesn’t mean that each
patient benefits a little, but rather that 414 will receive no prognostic
benefit [only side
effects].” And it gets worse, because
pharma would have selected in their pool those not suffering from congestive
heart failure, for they would have fared much worse on statins, which increase
significantly the mortality rate from a heart attack. And there are many other
doggy ways in which
their study is biased such as wash out period, giving the drug to a selection
population not on other heart medications such as for hypertension, and what
other way will produce favorable
results. Moreover, those studies with
negative results are not published. So,
why do doctors have faith in statins? As stated in part 1, the 800 pound gorilla has replaced
evidence based medicine with expert based medicine, and the gorilla owns the
clinical trials and provides the thought leaders. These thought leaders repeat
the mantra “safe
and effective” which is also repeated in cardiology textbooks and guidelines.
Secondly the thought leaders teach that plaque formation is strongly correlated
with the TC, LDL blood levels, and
the 30% average reduction in TC is
entails a corresponding reduction in ischemic events, which is confirmed by
their marketing studies, which minimalizes side effects, of course. All this
is fed to physicians in continuing
education classes given to promote drugs.
Peer-pressure, clinic administrators, and the need to follow guidelines
market statins and promoting the cholesterol myth. Corporations have taken over
the health-care
system.
Why does the FDA allow this: As
stated on page 2, the FDA functions as an extension of pharma? This failure
to supervise in the public’s
interest is not covered in corporate media; but it is published elsewhere. See
for example the article Consumer
Report article FDA: From Watchdog to Lapdog? Prof Marcia Angell in her book The
Truth About the Drug Companies, chapter 12, gives a detailed history of
Congress passing
pharma-friendly legislation and its affects upon the FDA. Allowing off
label prescribing of drugs opens the doors wide, which averages
over 50% of
sales. Merck tested Mevacor (the first
statin) on a very select population of those with familial hypercholesterolemia (FH,
about 1 in 1,500). They
have a genetic defect which causes their cholesterol to be several times above
the norm.[12] The surrogate end point lowering TC was used for FDA approval. Moreover, “there
are no interventional studies that directly show mortality benefit of
cholesterol lowering in familial hypercholesterolemia patients” Wiki, That
is why
Merck for Mevicor’s used
the surrogate endpoint lower TC.
Once approved, their marketing department went to work. All this is permitted
by a very dysfunctional
FDA—see Consumer Report article.
New Guidelines for cholesterol:
the
future will bring more of the same, ever-lowering standards for treatment
guideline, dismal results, more me-too-drugs (patented knock-offs), and FDA
approval. Now pharma, based on
AstraZeneca’s Jupiter Study, has lowered the guideline bar: “US recommendations for low density lipoprotein cholesterol
concentrations could put most of the Western world's adult
population on statins. This is the
message from the American National Cholesterol
Education Program published last year.1… Recently,
Getz et al calculated that in Norway, one of the healthiest nations in the
world, about 85% of men and more than 20% of the women over age 40 would be
classified as high risk using this criterion.”2 The
BMJ article then listed the known
side effects of statins, quite different than the safe sales mantra. But our
physicians won’t hear of side effects
in pharma’s continuing education classes, nor will the public from our
corporate media. “The government’s
obsession with levels
of total cholesterol, which has led to the overmedication of hundreds
of millions of people with statins, has diverted our attention from the more
egregious risk factor of atherogenic dyslipidaemia” BMJ. However, pharma has made such a mess of the causal process
for CVD that bystanders are accused of being causes, this is the case with dyslipidaemia. High serum fat level (dyslipidaemia) is a
result of a high sugar diet—see last section.
The Western diet is the cause of the rise in CVD and obesity. It is a
result of the high combination of
high fructose and high glucose.
New cholesterol drugs:
Several block-buster statins have gone off patent—Lipitor costs now a $1 a day. Thus pharma has
been working on new molecular entities to lower cholesterol. Several of them
are in in phase III trials
(trials used for FDA approval). New
major class of drugs, instead of blocking
synthesis, act upon the cholesterol regulatory mechanism. “Alirocumab is a human monoclonal antibody designed for the treatment
of hypercholesterolemia. This therapeutic is
also known by the codes REGN727 and SAR236553.
It was discovered by Regeneron Pharmaceuticals and
is being co-developed by Regeneron and Sanofi” Wiki.
Another is “PCSK9
has medical significance because it acts
in cholesterol homeostasis. Drugs that block PCSK9 can lower low-density lipoprotein cholesterol
(LDL-C)” Wiki. “PCSK9 inhibitors,
in late-stage testing at Pfizer, Amgen
Inc, and
a partnership of Sanofi SA and Regeneron
Pharmaceuticals Inc. PCSK9
are antibodies designed to block
a protein whose natural
function is to maintain the presence of LDL in the bloodstream” Reuters. Another
is “Juxtapid from Aegerion Pharmaceuticals';
and Kynamro from Sanofi and Isis Pharmaceuticals. Aegerion's Juxtapid[13]
has been the early standout despite an annual treatment price tag that is more than $119,000
higher than Kynamro”
Motley
Fool. Given
the size of this trial and
duration (16,000 patients with CHD, lasting
3.7 years) and thus cost, pharma knew that the FDA would accept the surrogate
endpoint of lower cholesterol. Otherwise
pharma would have had a trial of under a 1,000 patients and ran it
short-term. Obviously AstraZeneca
expected a positive outcome, and phase III trial, for the raw data must be
submitted to the FDA. With the revolving
door and those working for the FDA can moonlight for pharma, the only risk
pharma faced was deadly side effects in great numbers. Having passed that
hurdle, these new drugs failed to save lives in clinical trials. So the FDA
notified pharma that these drugs
must only pass the surrogate endpoint of lowering cholesterol: “everyone
knows that better endpoints come
from lowering cholesterol.” “Members
of an experimental class of cholesterol-lowering drugs could get U.S.
regulatory approval based on their ability to lower "bad"
cholesterol, and may not need to show that they reduce the risk of heart attack
and stroke, the Food and Drug Administration said on Thursday. The statement
eased industry concerns that the agency would require more onerous
"outcome" studies before approving the drugs, known as PCSK9 inhibitors.”
Reuters. This
is another example of tag-team
drug oversight. Only a fool would take a
drug that lowers cholesterol but doesn’t prolong life and prevent heart attacks.
That person (or society) would be paying for
a drug that only offers serious side effects.
And it gets worse, as pointed out prior, positive spin is the norm for
journal publish articles generated from phase III trial. A major study of neuroleptic
drugs found that
Positive bias averaged 32% (range 11 to 69%) in a total of 74 journal articles.
Yes, statins and these new molecular entities work, just read the
tobacco science in the journals. A series
of articles are hitting the press and the studies they are based on are being
taught by pharma’s KOLs—for more.
So what is the cause
of CVD?
The pharma generated literature holds that CVD consists of atherosclerosis
in the
coronary arteries and other arteries, and that leaking young plaque from within
the artery walls cause myocardial factions (MI).
They also hold that atherosclerosis is an inflammatory process; however
pharma and their key opinion leader ignore the role of pathogens. The role of
pathogens in the artery walls and the immune function of LDL are demonstrated
in the journal literature. Thus the
presence of LDL within the muscular portion of the artery walls and there
active transport there are explained by their role in the immune system. They
are actively transported by the
endothelia cells to absorb the toxins generated by pathogen. These pathogens
also explains why a high
number of white blood cells are within the artery walls. These processes explain
the entire process
leading to the formation of plaque within the artery walls, in the same way
that explains the formation of a boil in response to pathogens. In fact the
young, unstable atheroma within
the artery wall resembles a boil. For a
review of this evidence go to
and also articles. There are a number of contributing factors
for this process. The two main ones are
those which causes metabolic syndrome,
namely a high sucrose (fructose) diet compound by high glucose mostly from
starches (carbohydrates). This
combination cause fat storage in the liver which when accumulates in the liver adversely
affects its metabolic controls.
Uncorrected over several year this will result in insulin resistance[14]
which often progresses to endothelial
dysfunction in the arteries, and the conditions grouped by pharma as metabolic
syndrome, which includes atherosclerosis, CVD, hypertension, obesity, and for
some high Total Cholesterol (TC).[15] Other major contributors to cardiovascular
disease include rancidification of polyunsaturated fats, transfats, reactive
products of metabolism including glycation by glucose and fructose.
Why
the rise in CVD? The
cause is obvious, just
look at the numbers, it is the Western diet.
And it is not the fast foods, sedentary lifestyle, but the one two punch of
fructose and glucose. Fructose mucks up the liver by being
converted to fat in the liver the place where it is metabolized. The high carb
(glucose) Western diet results
in high insulin which is secreted to lower the glucose. Insulin sends a message
to cells for to store
fat and burn glucose; this causes an excess accumulation of fat in the liver,
and this overtime mucks up the liver’s metabolic regulatory functions. Fatty
liver, typically a 40% or greater
accumulation of fat in the liver, is now estimated at 30% of the US population
as of 1999 by the NHANES
study, and is labeled Non-Alcoholic
Liver Disease (NAFLD). The excess fat is stored
in hepatocytes
(liver cells), and thus affects their performance. One result of this
is that the body becomes
less responsive to insulin, and from that there is a clear causal relationship
to obesity, CVD, diabetes and other
chronic conditions. Yes it takes
both fructose and glucose. The Japanese eat a high carb diet consisting
of white rice and noodles, which accounts for up to 85% of calories, yet they
consume only 14 grams of sugar, and they have a very low rate of CVD. Click
on link for a detailed discussion
of this topic. This is not new science,
just that food manufacturers and pharma wants us to chase the wrong causes.
What
is be done: To
ask pharma and their doctors is to ask for
drugs. It takes both high fructose and
high glucose to bring on NAFLD and insulin
resistance which Thus the obvious life-style change is that of diet: avoid
sugar (like the Japanese), lower carbs,
and eat more saturated fats and green-leafy vegetables. Depending on current
health there are a
number of paths. The best choices have
been described in concise form at
and a longer form at. In the following: Part
3, a review of the evidence concerning carbohydrates; in Part 4, a review of fats. The final section, Part 5, is on life-style changes,
supplements, and drugs that reduce the risk of CVD and AS. Part 6 is a listing of key points, a
glossary of terms, and a guide to the first 4 Parts by subject headings and
listing which page they are on, with a link to an easy-to-print posting of the
first 5 Parts. Part 7 is a guide on healthful videos and
books.
Part 8 is on obesity and its health
consequence; it looks at why we get fat.
Part 9 is a dictionary of terms, Part 10 is on the New Atkins diet, and Part 11 on Alternate Day Fasting. Finally there is
a summation article on healthful supplement for seniors--enjoy the documentary-lectures page, please.
[1] Jonny Bowden PhD
& Stephen
Sinatra, MD, The Great Cholesterol
Myth: Why
Lowering Your Cholesterol Won’t Prevent Heart Disease—and the Statin-Free Plan
That Will, Fair Winds Press, Nov.
2012; a national bestseller, has 23 experts who praised the book and are
quoted on the cover & first page, and at Amazon has a 4.8 star rating from
220 reviewers. Getting a fair review of
book is iffy because of heated nature of the topic and many the subscribers to
pharma’s spin. JK finds the book well
supported in the critical
portions on cholesterol’s role; but in spots questionable as to the alternative
approaches to prevention of CVD. A
couple of years before reading this book,
JK had arrived at those same conclusion as to risk of CVD and on some of their
fixes.
[2]
“Atheroma is
an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and containing lipids (cholesterol and fatty acids), calcium and a variable
amount of fibrous connective tissue… in the early stage an
accumulation of mostly macrophages, that have taken up oxidized LKL” Wiki.
[3] The deviation from natural fats
will be developed in part 3. There you
will find out the recent deviations from natural (high ratio of omega 6: omega
3 fatty acids and the production of
trans-fats through hydrogenation of vegetable oils) cause an assortment of
conditions including CDV. Thus the low
fat diet replaces one unhealthful part of diet (unnatural fats) with a worse
item sugars.
[4] While cholesterol is also
produced by the adrenal gland, intestines, and gonads, they do so for
conversion to hormones and other molecules.
Over 80% of blood borne cholesterol is produced in the liver, some of
which is recycled and returned to the liver via HDL.
[5] VDL consists of approximately
13% phospholipids, 60% triglycerides, 18% cholesterol, and 7% proteins; LDL is
45% phospholipids, 10% triglycerides, 20% cholesterol, and 25% protein, and HDL
20% phospholipids, 5% triglycerides, 30% cholesterol, and 47% protein (Human
Anatomy and Physiology 2nd Ed. Elaine Marieb, 1992, p 856).
[6]
Braunwald, Heart Disease, 8th Ed. P 1085 table. There of the
4 major clinical trials, 3 of
them the placebo cohort had as many major ischemic events as those treated with
statins. This book published by Bayer
ignored the data to conclude the opposite.
[7] For a detailed account of
Pfizer’s TNT Study on how the evidence was worked to lower guidelines for
statins (Lipitor). The Jupiter study “a
major discrepancy between significant reduction of nonfatal stroke and myocardial
infarction, but no effect on mortality from stroke and myocardial infarction…
raises troubling questions concerning the role of commercial sponsors “….
” NIH,
& Wiki.
[8]
A reasonable
assessment of total early deaths from the selective COX-2 inhibitors in the US
would be over 200,000; and a much greater number for the non-selective COX
inhibitors, the NSAIDs—but for aspirin.
Celebrex is still on the market, and though warnings about all COX inhibitors
warning that they
promote CVD, the oft-heard sales
message prevails.
[9] After 3
months treatment of healthy patients with a poor TC using pravastatin or simvastatin, the total
cholesterol and CoQ10 (Q10) were lowered 40%, when
compared to the placebo group. “A
diminution of Q10 availability may be the cause of membrane alteration with
consequent cellular damage”—Journal
of clinical Pharmacology. This finding is
supported in other studies and widely accepted—summary article.
[10]
9% increase in risk of developing diabetes over 4 years, meta study Lancet 2010
based on pharma trials--undoubtedly under-reported.
[11]
The 2nd cause for neuropathy, the
first low Q10. The two are additive.
[12] At that abnormal level the rate
of oxidative damage to LDL out-paces the cleanup process, and typically their
first MI occurs in the 4 decades. But
this doesn’t prove that without other risk factors those with a TC near
350 are at significantly
greater risk.
[13] Juxtapid is a once-daily
capsule taken in the
evening well after a last meal; it works in conjunction with proper diet and
exercise to remove LDL cholesterol from a patient's blood. While it did reduce
LDL cholesterol levels by approximately half during the first 26 weeks of study
in its phase 3 trial, it also comes with a boxed warning regarding liver
toxicity: Juxtapid can cause the accumulation of fat in the
liver, as well as liver enzyme abnormalities. The FDA's approval was given on
the condition [request] that Aegerion run three post-marketing studies
regarding the safety of long-term use of the drug” Fool . Rarely are
requested trial completed timely, and penalties are non-existent.
[14]
Insulin resistance is a condition in which the cells throughout the body became
tolerant to the NORMAL high serum level of insulin which occurs in response to elevated
blood glucose following a meal or a snack. The pancreas as a consequence secrets
even
more insulin to bring the serum glucose level down to the normal range.
[15]
There are other causes, nothing is simple: Reactive chemical both produced
by metabolism
and environmental sources also are causal for CVD, MI,
and related
conditions. Also contributory are unnatural
fats, mainly trans and oxidized polyunsaturated fats. High cholesterol (hyperlipidemia)
given the cholesterol
myth lacks a medical reason for inclusion in metabolic syndrome.
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