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Two Changes in content
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The cholesterol myth. Numerous critics have pointed out that cardiovascular
disease is not caused by higher levels of blood cholesterol or fats. Pharma
promotes the cholesterol myth and ignores the major causes.
-
Major cause of cardiovascular disease is pathogens living
within the middle layer of artery walls. It initiates the immune response which
involves LDL, and white blood cells. Reactive chemicals such as simple sugars
and carbon monoxide can potentiate the process resulting in the formation of plaque within the artery walls and it leaking
out to cause an ischemic event. These chemical damage the endothelial cells that line the interior artery walls.
For confirmation from journal articles on primary role
of infective agent enter into http://scholar.google.com/ terms such as bacteria
+ atherosclerosis or go to http://healthfully.org/rl/id8.html and id9 for
collection of articles
CoQ10 a powerful antioxidant and co factor in the Krebs cycle (citric acid
cycle) that produces the energy molecule ATP. Aspirin protects the mitochondria thus increase production of ATP.
Aspirin the best
cardiovascular
protector -- 3 pgs. http://healthfully.org/rc/id17.html 7/23/21
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AS Atherosclerosis
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|
MeS
Metabolic syndrome
| |
CVD
Cardiovascular disease
|
|
MI
Myocardial Infarction
| |
KOL
Key opinion leader
|
|
T2D
Type 2 Diabetes
|
This is one of several recently updated
articles on cancer and aspirin. aspirin http://healthfully.org/rc/id3.html aspirin’s cancer protection http://healthfully.org/rc/id18.html Aspirin inhibits atherosclerosis http://healthfully.org/rc/id17.html Cancer
Basics & Chemotherapy http://healthfully.org/rc/id16.html Cancer
http://healthfully.org/rl/id4.html
Pharma which
runs clinical trials and continuing education classes for physicians does so for marketing purposes. Their information on truly healthful drugs such as estrogen and aspirin is based on tobacco (marketing) science.
On how pharma controls the practice of medicine in our corporatist government and
others. The articles explains why doctors give junk drugs in a clear and balanced way--Junk treatments. A perverse system produces perverse results.
There is a long list of chemicals touted
as good for health. Over and over again
we hear hype about safe and effective
drugs. About 5% are very effective. Among
those healthful and effective drugs is
aspirin. I have pasted a sample taken
from a large body of journal
articles which show that aspirin
prevents or ameliorates many major chronic
conditions by its effect upon the bodily systems. I wrote a
summation of its benefits and history in “Aspirin” and a
rebuttal to pharma’s assault. For
background as to how pharma operates using tobacco
ethics read “Marketing
Science”, which details
pharma’s control of the practice of medicine. Realizing that daily 325 mg of aspirin would cut in half their
bottom line, pharma uses tobacco science
to drum into doctors and the public that aspirin is dangerous and ineffective,
then pitches their patented drugs. A chorus of marginalized scientists have exposed bad pharma (see video library), but with
little affect. The article below is on
how aspirin prevents cardiovascular disease (CVD).
Pharma frames the topic of aspirin to greatly
exaggerated the risk of ulcer (see rebuttal), and
exclude its benefits. Cardiovascular
disease (CVD)[1]
which accounts for half of all deaths is a caused by atherosclerosis (AS).
The doctors hear pharma’s tobacco science that “demonstrates” that CVD starts with high serum LDL, triglycerides
and cholesterol. As a chorus of marginalized
critics demonstrate this is false totally false, see, and. What follows is supported by thousands of
medical journal articles; just search http://scholar.google.com/ to find
them. There are 3 major causes of
AS and
thus CVD. Most significant is pathogens colonizing inside the artery walls, the layer labeled the tunica media. “Infection
with microorganisms is considered a pathogenic factor in atherogenesis. Several
studies have shown the presence of a
broad spectrum of bacterial species in atherosclerotic plaques, which could
trigger local inflammation. Because T cells [a type of white blood cells]
contribute to atherosclerotic plaque inflammation, we studied the
responsiveness of human plaque derived T-cell cultures to bacteria of different
species” at. “A
rapidly-expanding volume of research is implicating common infectious
agents—including the respiratory but Chlamydia
pneumoniae, the ulcer-causing Helicobacter
pylori bacteria, herpes viruses such as cytomegalovirus, and Herpes simplex
and even dental
infections—as playing a direct role in the instigation and progression of CVD….
A review of thirteen published
studies in which researchers went hunting for the organism [Chlamydia
pneumonia] in arterial tissues showed that the organism could be detected in
over half of all atheromas, but in only 5 percent of adjacent, lesion-free arterial
tissue samples” Calpo, The Great Cholesterol
Con, p. 207-8,
at. “Atherosclerosis is now recognized as a
chronic inflammatory disease occurring WITHIN the artery wall and ultimately
responsible for myocardial infarction [MI, heart attack], stroke
and peripheral vascular disease. A
crucial step in atherogenesis is the infiltration of monocytes [a type of white
blood cells] into the sub-endothelial space of arteries where they differentiate
into macrophages and become functionally active. Macrophage accumulation within
plaques is a hallmark of all stages of
AS. Activated macrophages are major
players in all stages of lesion development.
They not only accumulate lipids but also express effector molecules that
are pro-inflammatory, cytotoxic and chemotactic. Furthermore, they secrete enzymes
that degrade extracellular matrix leading to
plaque destabilization and increased risk of rupture [MI]” Current
Vascular Pharmacology, 2009. In
addition to their transport function, LDL and HDL bind and thus clear toxins
produced by bacteria. “A clue is the fact that the lipoproteins constitute an innate immune system
by binding and
inactivating microorganisms and their toxic products through formation of
circulating complexes” at.
Thus LDL--with its contents of cholesterol and triglycerides--along with
white blood cells function to rid the body of pathogens and their toxins within
the artery walls. LDL is not the cause
of the problem, but a response to it, like firemen at a fire. Cholesterol is
packaged LDL for transport
because of its essential functions throughout the body. Thus lowering cholesterol
which is packaged
in LDL is not a good idea. Not
surprisingly statin drugs which lower cholesterol by partially blocking its
synthesis is a bad idea. Statins cause a
lot of issues without lowering adverse events, so warn a chorus of
scientist. Statins block aspirin. It isn’t saturated fats and
cholesterol but he immune response to pathogens results in AS--at.
In summary, the toxins which damage LDL are caused by infective agents colonizing artery walls.[2]
The key role of infectious agent is documented in hundreds of journal
articles. Since plaque is encapsulated
within the artery walls, the best treatment would be either antibacterial or promote
immune functions. Pharma using tobacco
science creates a model for CVD that
promotes drugs such as statins which block the production of
the
vital cholesterol (a bystander, not a cause of AS), antihypertension drugs, and
others. The second most significant causal factor for
AS is glycation: the binding of
monosaccharides—principally glucose and fructose from sugars and carbohydrates—to
artery endothelial cells to cause endothelial dysfunction. This dysfunction
promotes the entering of
pathogens into the artery walls and also weakens the cap which contains young
plaque and thereby allows it to leak which can cause an MI (heart attack). And
glycation in the liver results in liver
insulin resistance that can progress to become type-2 diabetes (T2D).
T2D promotes CVD through
elevated serum glucose which
increases glycation; and through various metabolic effects due to insulin
resistance—see. A third cause of
AS is oxidation coming from metabolic activity and from carbon
monoxide produced by cigarettes. This
too can cause endothelial dysfunction.
The biology behind CVD and AS
is different than what pharma teaches
through their KOLs (key opinion
leaders) as to the causes of AS, CVD,
and MI, and as a consequence what is done to lower the risk.
The evidence for aspirin’s method
of action comes from a number of laboratory studies on
animals. In the Journal
of
clinical Investigation 1979: “The average extent of narrowing of the
lesions was approximately twice as great in the control monkeys. Coronary involvement
was lower in the monkeys
that received aspirin (controls, 13.8±+1.6% vs. aspirin, 4.9±+1.6%).… Morphologically
the lesions were
predominately atheroma with
abundant foam cells…. The
majority of lesions in the monkeys treated with aspirin were predominantly
small, pure foam-cellular atheroma.” Confirming these results in the Chinese
Medical journal 2006 and showing lack of plaque in the aorta for the aspirin
group (p. 1811-13): “The
mechanism of AS suppression by
aspirin in cholesterol-fed rabbits is related to the inhibition of COX-2
expression together with the reduced inflammation
followed by, but not related to the hypolipidemic effects by atheroma…. This study verified that aspirin could affect the course of
AS is acting as an anti-inflammatory
agent at medium doses. That may be another mechanism by which aspirin can
protect
against myocardial infarction and stroke”--also
similar results
with rabbits 2005. And in American Heart Association Journal (hereafter AHAJ)
1993 study: “Ultrasonic disappearance of lesions were observed only in the
900 mg daily but increased markedly in the 50
mg group… aspirin treatment slows carotid [artery] plaque growth in a
dose-dependent fashion….” In 2001 AHAJ in vitro
study found that at moderate dose (5 mmol/L) aspirin “slightly reduced
lymphocytes intercellular adhesion factor” and at 10 mmol/L “strong inhibition.” AHAJ 1995,
the transcription factor NF-kB [an immune regulatory factor] “provides an
additional mechanism for therapeutic effects of aspirin.” NF-kB[3]
and suppresses bacterial growth (Chlamydia pneumoniae), at, also summary. A study found
them in 20 of 36 who died of MI--more on COX-2 in AHAJ. AHAJ 1995: ”It is possible that
aspirin has previously unrecognized therapeutic effects in various clinical
situations, such as in viral infections (when used as an antipyretic agent) and
in AS (when used as an antiplatelet
agent).” AHAJ, 2009: [some pathogens were
shown] “to increase the uptake of oxidized LDL, expression of cytokines,
cellular adhesion molecules, and
reactive oxygen”. AHAJ on those
with CVD who underwent angioplasty showed
that aspirin at 900 mg[4]
(but not 50 mg) slowed the progression of plaque in the carotid artery[5].
In Summary: AS
is prevented at 900 mgs/day, not low dose. Chronic
and acute infections colonizing
the artery walls causes CVD.
Aspirin reduces the risk of infection through NF-kB and also through
COX-2 which attenuates the immune response to infections, thus in two ways
reduces atheroma. Infectious agents in
artery walls places everyone at risk for AS
and the formation of young unstable plaque
which causes over 85% of
MIs and strokes.
[2]
Other reactive chemical such as carbon monoxide and monosaccharides accelerate
the process and contribute to endothelial
dysfunction, as too does diabetes.
Carbon monoxide from cigarettes and diabetes each double the risk of
heart attack.
[4] Higher dose assures that there isn’t
aspirin
resistance (see below). Resistance is
complex topic with several methods of testing.
Articles failing to find these benefits use too low a dose—see position
paper.
[5]
The external carotid artery on the neck as it passes behind the mandible below
the ear is chosen for to measure the extent and progression of AS using ultra
sound. Ultrasound can be used for medical imaging
with a 2 megahertz and higher sound wave.
It allows resolution of small internal details of structure and
tissues.
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Aspirin is protective
in a third way. Near the end of paragraph 2, I listed the
second primary causes of CVD that of
glycation. Type-2 diabetes doubles the
risk of a heart attack (MI), one reason is glycation through elevated glucose. Aspirin
lowers insulin resistance and
improves serum glucose. What follows is
from the paper on Aspirin: “ treatment of type 2 (T2D)
with high dose aspirin or other salicylates has a positive effect upon obesity
and diet induced insulin resistance; thus by improving the
function of insulin it lowers serum glucose level through improved in glucose metabolism. Also the increased inflammation
diabetes is associated with morbidities for which aspirin is a treatment.
Given the positive effect upon insulin resistance and glucose management
for those with T2D a reasonable inference would be that aspirin reduces
the risk of developing T2D and the related fatty liver disease and
insulin resistance.” Given
the role of insulin and leptin as causes
of obesity, metabolic syndrome, and diabetes, those with these issues should
take a 325 mg aspirin with each meal and follow the low-carb dietary recommendations and if needed the weight loss program the dietary cure for T2D
Aspirin resistance
increases with time, but physicians prescribe the ineffective low-dose aspirin
for cardiac protection. A study
found
in stroke patients who took aspirin; 55% were resistant. “During
follow-up, aspirin resistance was associated
with an increased risk of death, MI, or CVD compared to patients who were
aspirin sensitive (24% vs. 10%). [When adjusted for age and heart failure] “HR
for aspirin resistance was 4.14” JACC,
a 4 fold risk increase. Low dose aspirin
is the norm in clinical trial of combo anticoagulants to lower risk of
thrombosis. E.g., in a BMJ
meta-study,
no benefit from aspirin as the 2nd anticoagulant. Cochrane
confirmed no advantage above 300 mg of aspirin for the use of Warfarin or
Plavix. Other studies
confirm
that anticoagulants aren’t worth their side effects--except for the small
highest risk group. A number of drug
cause aspirin resistance through affecting aspirin’s bio-pathways; this includes
statins. Also like with all drugs, used
daily resistance to its bio-activities will develop. There are over 100
research articles on aspirin resistance yet few physicians address this with
testing or prevent it with by using a higher dose.[1] More pharma framing the educational
information about aspirin.
In the ASA general article (http://healthfully.org/rc/id3.html) the 4 headings are
covered there with some different links
Antimicrobial: Given that pathogens play the
major role in cardiovascular disease, safe antimicrobial agents ought
to be widely researched. The lead starts
with plants: because of salicylic acid ability to inhibit many plant pathogens,
this
brother of aspirin is produced in many plants, and thus unlike other NSAIDS
animals have developed uses for this commonly supplied chemical, Plant Journal 1992, and book 2000. “Aspirin-triggered lipoxin enhances
macrophage [large immune cells] phagocytosis of bacteria [engulfing bacteria]
while inhibiting inflammatory cytokine production” 2011. Inhibits growth
of H. pylori, BMJ Gut,
2017, and clinical trial 2017. “The
aspirin N‐mustard agent expressed strong antibacterial activity against a
penicillin‐resistant bacteria and first‐order alkylation kinetics” biotechnology 2003.
Like so much of our profits first world, the trail is thin.
Antioxidant effects:
Salicylic acid’s [SA, active form of aspirin] immune action is
through “catalase
a
common enzyme found in nearly all living organisms exposed to oxygen…. It is a very important enzyme in protecting the
cell from oxidative
damage by reactive
oxygen species (ROS)… one catalase molecule can convert
approximately 5 million molecules of hydrogen peroxide to water and oxygen each
second… also catalyze various metabolites and toxins,” Wiki. “SA could also
protect plant
and mammalian catalases against inactivation by H2O2 in
vitro “, at. ROS are
the major cause of age related degenerative diseases. For example SA protect
fibrinogen. “In cultured
endothelial cells derived from human umbilical vein, aspirin (30–300 μM)
increased heme oxygenase-1 (HO-1) protein levels in a concentration-dependent
fashion up to fivefold over basal levels…. Pretreatment with aspirin or
bilirubin at low micromolar concentrations protected
endothelial cells [on endothelial
damage and Wiki]] from
hydrogen peroxide-mediated toxicity…./ a novel mechanism by which aspirin
prevents cellular injury under inflammatory conditions and in cardiovascular
disease.” at 2003. This effect was not demonstrated with other
NSAIDs. “The potent antioxidant property of gentisic acid [ASA
metabolite] may partly account for the anti-atherogenic effects of aspirin”, at 2005. Aterial endothelial dysfunction is strongly
linked to AS and thus CVD through failure to block pathogens &
formation of thrombosis through their reduced anticoagulant properties and
production of their adhesion molecules.
Anti-inflammatory effect is “not by
direct inhibition of COX like most other non-steroidal
anti-inflammatory drugs
(NSAIDs) but instead by suppression
of the expression of the enzyme (via a yet-unelucidated
mechanism)” Wiki,
thus unlike
the other NSAID which increase the risk of heart attack by 50% or more, aspirin
lowers the risk, “These findings provide direct in vivo evidence for an
anti-inflammatory action for both aspirin-triggered LXA4 and
LXA4 stable
analogues and their site of action in vivo, at 1987. Aspirin attenuates beta-caternin/TCF 4 signaling, at 2001.
Note, Peter Gotzsche expresses doubt of NSAIDs ability
to reduce inflammation, and this is supported by measure of finger
diameter.
Atherogenesis slowed:
“strong evidence that atherosclerosis is slowed down in a dose term” by 47%, and stopped.
Mechanisms: By NO endothelial cells oxidative damage,
inhibits leukocyte
attacks, cytokinies, CD36,
FFA & diabetes,
benefits long-term (more than 8 years, degree increases with duration) usage by
those with arthritis
patients. For journal and for position paper on cancer, and limited value of chemotherapy.
Autophagy
and age related conditions (AGES): Autophagy is the general natural healing
process including replacement of defective cells and their parts. With age the
mitochondrial functions decline the rates of mitochondrial production of ATP
declines. The high fructose (reactive
sugar) diet is what makes humans the sickest of mammals, mainly through damage
to the mitochondria. Aspirin increases
rate of glucose metabolism, thereby lowering the rate of fructation
glycation. This is protective for the endothelial
cell .
AVOID
OTHER NSAIDs: All NSAIDs (Advil, Aleve, others) with long-term
usage greatly increases risk of MI & CVD--American Heart association warning also in journal sources by causing CVD through inhibition of COX-2, which causes plaque formation through increasing the inflammation response.
Aspirin however blocks this inflammatory
affect.[2] The NSAIDs that are selective COX-2 inhibitors are the worse. Celebrex, Bextra, &
Vioxx killed
over 100,000
Americans. Celebrex is still marked
& heavily advertised—though band in Europe and Canada after exposure of
coronary risk.
Heart attack deaths lowered 51% for higher dose; it prevents aspirin resistance, and.
For unstable
angina, a 236% reduction in death, cardiac event 152% meta-study; previous MI 2 studies by 44%. Method by artery
infection. “Reduction of stroke & death of 25% to 42% using
900 to 1300 mg aspirin daily” AHA.
Statins block aspirin. ASA stops
atherosclerosis summary. And Acetaminophen (Tylenol, APAP) is worse than
the other NSAIDs
Aspirin is safe:
the active form aspirin (salicylic
acid) has evolved salubrious
biological functions. Salicylic acid is
made by a large number of plants to fight invasive pathogens infects. Being
widely available, mammals have evolved
uses for it. In fact humans synthesize a
small amount of salicylic acid—see. It is thus both safe and beneficial once
circulating in the blood. And the risk
of ulcer, which doubles to 4% lifetime, this occurs because of pathogens that
compromise the protective mucus membrane that lines the stomach and duodenum. Those
without colonies of the Helicobacter
pylori bacteria
are essential protected from the corrosive effect of an
aspirin pill.
Recommended
healthful: the non-technical explanation on diet
and CVD should
be
followed. The switch to a low fat thus
high carb diet in the 70s has caused the obesity, CVD, and diabetes epidemics
(sugar consumption has doubled). Pharma’s drugs for cholesterol and
hypertension are not worth the side effect; for hypertension and high cholesterol
are symptoms, not the
problem/cause. For prevention and cure
change your diet, exercise,
and take aspirin, CoQ10 and post-menopause estradiol. Starting in the teens take Q10, vitamin
C 1,000 mg
(both as antioxidants) and fish oil, and around the age of 30, take a 325 mg or
more of aspirin
and don’t take the other NSAIDs
because they cause CVD—AHA. For mild to moderate pain including head
ache, take uncoated aspirin (coated take too long to dissolve) at the standard
dose on the 1960s and before, 100 mg to start (three of the 325 mg) and then
take one or two as needed. Aspirin once
came in the standard effective dose of 500 mgs.
Read the other two papers on aspirin one lists its many
benefits which has
a response to pharma’s assault upon the usage of aspirin. The other article
goes into to how aspirin prevents
cancer and
increases survival. The financial
reasons behind pharma’s assault
upon aspirin also apply to their assault upon hormone replacement therapy. Take
Testosterone from a
compounding pharmacy at dose recommended when level drops below 450 ng/dL. Women
going through and post menopause take natural
estradiol with progesterone at the
recommended dose from a compounding pharmacy.
Like with aspirin pharma has marketed hormone replacement therapies that
are inferior to the natural hormones, and for testosterone estrogen at too low
a dose. For those with CVD or hypertension
(a sign of AS) take 325 mgs with meals.
If you still believe in the role of
cholesterol then take fish oil and at bed time Inositol
hexanicotinate or Niacin slow release
250 mg. And read Junk treatments to understand
why and how doctors have been
become tools of pharma. You ought to
take better care of your body than your car.
[1] Warfarin once the leading prescription
anticoagulant has guidelines
requiring regular blood testing to measure for to adjust it dosage. This inconvenience
and expense has made
Plavix (clopidogrel) a mega-blockbuster with 48 million American taking it
daily in 2006. Aspirin is an effective,
safer drug, at “anticoagulant.”
Everywhere I look I find corporate influence affecting guidelines.
[2] “Furthermore,
work from Serhan’s group shows that acetylation of COX-2 by low dose aspirin leads
to its biosynthesis of 15R-hydroxyelcosatetraenoic acid. This intermediate is
then converted by
transcellular metabolism to the anti-inflammatory lipoxin 15-epi-lipoxin A4 in
leukocytes’--AHA, and. This
distinguish aspirin from other NSAIDs by the production of lipoxin
In the ASA general article (http://healthfully.org/rc/id3.html)
the 4
headings are covered there with some different links
Antimicrobial: Given that pathogens play the
major role in cardiovascular
disease, safe antimicrobial agents ought to be widely researched. The lead
starts with plants: because of salicylic acid ability to inhibit
many
plant pathogens, this brother of aspirin is produced in many plants, and thus
unlike other NSAIDS animals have developed uses for this commonly supplied
chemical, Plant
Journal 1992, and book 2000. “Aspirin-triggered
lipoxin enhances macrophage [large immune cells] phagocytosis of bacteria [engulfing
bacteria] while inhibiting inflammatory cytokine production” 2011. Inhibits
growth of H. pylori, BMJ Gut, 2017, and clinical
trial 2017. “The aspirin N‐mustard agent expressed strong
antibacterial
activity against a penicillin‐resistant bacteria and first‐order alkylation
kinetics” biotechnology
2003. Like so much of our
profits first world, the trail is thin.
Antioxidant effects:
Salicylic acid’s [SA, active form of aspirin] immune action is
through “catalase
a
common enzyme found in nearly all living organisms exposed to oxygen…. It is a very important enzyme in protecting the
cell from oxidative
damage by reactive
oxygen species (ROS)… one catalase molecule can convert
approximately 5 million molecules of hydrogen peroxide to water and oxygen each
second… also catalyze various metabolites and toxins,” Wiki. “SA could also
protect plant
and mammalian catalases against inactivation by H2O2 in
vitro “, at. ROS are
the major cause of age related degenerative diseases. For example SA protect
fibrinogen. “In cultured
endothelial cells derived from human umbilical vein, aspirin (30–300 μM)
increased heme oxygenase-1 (HO-1) protein levels in a concentration-dependent
fashion up to fivefold over basal levels…. Pretreatment with aspirin or
bilirubin at low micromolar concentrations protected
endothelial cells [on endothelial
damage and Wiki]] from
hydrogen peroxide-mediated toxicity…./ a novel mechanism by which aspirin
prevents cellular injury under inflammatory conditions and in cardiovascular
disease.” at 2003. This effect was not demonstrated with other
NSAIDs. “The potent antioxidant property of gentisic acid [ASA
metabolite] may partly account for the anti-atherogenic effects of aspirin”, at 2005. Aterial endothelial dysfunction is strongly
linked to AS and thus CVD through failure to block pathogens &
formation of thrombosis through their reduced anticoagulant properties and
production of their adhesion molecules.
Anti-inflammatory effect is “not by
direct inhibition of COX like most other non-steroidal
anti-inflammatory drugs
(NSAIDs) but instead by suppression
of the expression of the enzyme (via a yet-unelucidated
mechanism)” Wiki,
thus unlike
the other NSAID which increase the risk of heart attack by 50% or more, aspirin
lowers the risk, “These findings provide direct in vivo evidence for an
anti-inflammatory action for both aspirin-triggered LXA4 and
LXA4 stable
analogues and their site of action in vivo, at 1987. Aspirin attenuates beta-caternin/TCF 4 signaling, at 2001.
Note, Peter
Gotzsche expresses doubt of NSAIDs ability
to reduce inflammation, and this is supported by measure of finger
diameter.
Atherogenesis slowed:
“strong evidence that atherosclerosis is slowed down in a dose term” by 47%, and stopped.
Mechanisms: By NO endothelial cells oxidative damage,
inhibits leukocyte
attacks, cytokinies, CD36,
FFA & diabetes,
benefits long-term (more than 8 years, degree increases with duration) usage by
those with arthritis
patients. For journal and for position paper on cancer, and limited value of chemotherapy.
AVOID
OTHER NSAIDs: All NSAIDs (Advil, Aleve, others) with long-term
usage greatly increases risk of MI & CVD--American Heart association warning also in journal sources by causing CVD through inhibition of COX-2, which causes plaque formation through increasing the inflammation response.
Aspirin however blocks this inflammatory
affect.[1] The NSAIDs that are selective COX-2 inhibitors are the worse. Celebrex, Bextra, &
Vioxx killed
over 100,000
Americans. Celebrex is still marked
& heavily advertised—though band in Europe and Canada after exposure of
coronary risk.
Heart attack deaths lowered 51% for higher dose; it prevents aspirin resistance, and.
For unstable
angina, a 236% reduction in death, cardiac event 152% meta-study; previous MI 2 studies by 44%. Method by artery
infection. “Reduction of stroke & death of 25% to 42% using
900 to 1300 mg aspirin daily” AHA.
Statins block aspirin. ASA stops
atherosclerosis summary. And Acetaminophen (Tylenol, APAP) is worse than
the other NSAIDs
Aspirin is safe: the active form aspirin (salicylic acid)
has evolved salubrious biological functions.
Salicylic acid is made by a large number of plants to fight invasive
pathogens infects. Being widely
available, mammals have evolved uses for it.
In fact humans synthesize a small amount of salicylic acid—see. It is thus both safe and beneficial once
circulating in the blood. And the risk
of ulcer, which doubles to 4% lifetime, this occurs because of pathogens that
compromise the protective mucus membrane that lines the stomach and duodenum. Those
without colonies of the Helicobacter
pylori bacteria
are essential protected from the corrosive effect of an
aspirin pill.
Recommended
healthful: the non-technical explanation on diet
and CVD should
be
followed. The switch to a low fat thus
high carb diet in the 70s has caused the obesity, CVD, and diabetes epidemics
(sugar consumption has doubled). Pharma’s drugs for cholesterol and
hypertension are not worth the side effect; for hypertension and high cholesterol
are symptoms, not the
problem/cause. For prevention and cure
change your diet, exercise,
and take aspirin, CoQ10 and post-menopause estradiol. Starting in the teens take Q10, vitamin
C 1,000 mg
(both as antioxidants) and fish oil, and around the age of 30, take a 325 mg or
more of aspirin
and don’t take the other NSAIDs
because they cause CVD—AHA. For mild to moderate pain including head
ache, take uncoated aspirin (coated take too long to dissolve) at the standard
dose on the 1960s and before, 100 mg to start (three of the 325 mg) and then
take one or two as needed. Aspirin once
came in the standard effective dose of 500 mgs.
Read the other two papers on aspirin one lists its many
benefits which has
a response to pharma’s assault upon the usage of aspirin. The other article
goes into to how aspirin prevents
cancer and
increases survival. The financial
reasons behind pharma’s assault
upon aspirin also apply to their assault upon hormone replacement therapy. Take
Testosterone from a
compounding pharmacy at dose recommended when level drops below 450 ng/dL. Women
going through and post menopause take natural
estradiol with progesterone at the
recommended dose from a compounding pharmacy.
Like with aspirin pharma has marketed hormone replacement therapies that
are inferior to the natural hormones, and for testosterone estrogen at too low
a dose. For those with CVD or hypertension
(a sign of AS) take 325 mgs with meals.
If you still believe in the role of
cholesterol then take fish oil and at bed time Inositol
hexanicotinate or Niacin slow release
250 mg. And read Junk treatments to understand
why and how doctors have been
become tools of pharma. You ought to
take better care of your body than your car.
[1] “Furthermore, work from Serhan’s group shows
that acetylation of COX-2 by low dose aspirin leads to its biosynthesis of
15R-hydroxyelcosatetraenoic acid. This
intermediate is then converted by transcellular metabolism to the
anti-inflammatory lipoxin 15-epi-lipoxin A4 in leukocytes’--AHA, and. This distinguish aspirin from other NSAIDs by
the production of lipoxin
|
