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) 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. 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
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
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 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 (but not 50 mg) slowed the progression of plaque in the carotid artery. 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. The role of LDL
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.
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. More pharma framing the educational information
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. For papers on developing the use of aspirin for atherosclerosis and for 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. 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.
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
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
pylori bacteria are
essential protected from the corrosive effect of an aspirin pill.
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.