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Aspirin prevents MI, Cancer & Alzheimer's--a summary--jk

Aspirin (ASA, acetylsalicylic acid) (3/23/16), on aspirin, /nsaids

Reduces risk for cancer of Breast 39%, Colorectal 63%, Esophageal 73%, Hodgkin’s Lymphoma 60%, Ovarian 47%, Melanoma 55%, Prostate 39%, Stomach 62%, and other cancers including Bladder, Skin, Gastric & Leukemia.  Aspirin increases survival of stages I, II, & III cancers:  Breast 66%, Colon by 74%, and by extension all adenocarcinomas.  Aspirin reduces the risk of Alzheimer’s Disease 60%, and Heart Attacks 51%, and its anti-inflammatory action inhibits atherogenesis thus CVD; 350 mg or more, not low dose, see below.  Summaries of ASA on cancer protection, and on atherosclerosis protection

Why doesn’t everyone know of these benefits and doctors recommend a 325 mgs of aspirin daily?   The short answer is corporatization of medicine.  The perception in the press is the opposite of the truth, a truth which was succinctly stated by Harvard Prof. Marcia Angell, MD.:  “If we had set out to design the worst system that we could imagine, we couldn’t have imagined on as bad as we have” her video.  The list of benefits from taking aspirin (acetic salicylic acid) long-term is in the next section.  These benefits explain pharma’s multifaceted attack, which includes use of too low a dose (85 mg), coated aspirin which takes hours to dissolve, scare about ulcers & Reyes syndrome (bottom for rebuttals).   We have tobacco science generated by pharma.  However aspirin in its bioactive form of salicylic acid is found in plants as part for its immune function.  Given its wide distribution in plants mammals have evolved similar and other healthful uses, and they/us even biosynthesize the molecule—click on link.  Find out below why aspirin clearly should be your first choice.        

The recorded history of aspirin starts with the ancient Egyptians.  The Greeks used an extract of willow bark and leaves which contain the plant hormone salicylic acid.  Salicylic acid (SA) plays a key role in the establishment of resistance to microbial pathogens in many plants” at  (ASA is rapidly hydrolyzed in the stomach to salicylic acid, its active form.)  Hippocrates, the Greek physician, 420 BC wrote of its use to relieve pain & fever.  The Romans Pliny the Elder, and later Galen added its use as skin ulcer treatment.  The drug remained thereafter in the European pharmacopeia, and became widely used to treat malaria by the 1760s.  In 1853 a German chemist modified bitter salicylic acid (SA) to the less caustic ASA by adding an acetate group, and in 1899 the German dye and drug company Bayer marketed it as aspirin. 

“For almost 100 years the salicylates [aspirin family of drugs] have retained their preeminent position” Goodman and Gilman Pharmacology, 11th Ed, 2006, p. 692.  It is the standard against which all rheumatoid arthritis medication should be measured” supra 690.  3.5 gram is the recommended dose--Merck Manual 1987, p. 960, and same in earlier editions.  In 1958 production peaked at 20,000 tons (3 lb. per person).  In the late 50s aspirin’s share of sales fell to the heavily-marketed newer NSAIDs.  Following the 1973 discovery that aspirin reduces the incidence of heart attacks (MIs) by reducing blood clotting (thrombi) that completes occlusion of a coronary artery when plaque is leaked.  By the 1980s it regained its number 1 position, but too low a dose for prevent of cancer, CVD, etc.  Even at 1300 mg/d, [long-term] 8% of subjects were resistant” AHA to its anticoagulant action (MI protection).  Its biological half-life is dose dependent---2-3 hours for low dose and up to 15-30 hours for large doses. About 50 to 80% of aspirin is bound to albumin protein, while the rest remains in active, ionized state.   From 80 to 100% is excreted in the urine, sweat, saliva, and feces.   It has now slipped to 6th, and on my bottle are 15 lines of FDA warnings for stomach bleeding and in children Reyes syndrome.  Is the old wisdom and research false?  Or is it another example of tobacco science used to promote illnesses? 

Pharma had by late 1980s gained control of research and production of information.  Aspirin the drug of choice by your parents and grandparents was “shown” to be unsafe in published tobacco studies.  Pharma drummed into the publics and physicians’ heads that aspirin is ineffective & frequently causes stomach bleeds, ulcers, and Reyes Syndrome in children.  However, as Goodman and Gilman supra 690, “many clinicians favor the use of other NSAIDs perceived to have better gastrointestinal tolerability, even though this perception remains unproven by convincing clinical trials”—ASA's low rate.  As for Reyes syndrome, diagnosis was based on symptoms.  “Between 1980 and 1997, the number of reported cases of Reye’s syndrome decreased from 555 cases in 1980 to about 2 cases per year since 1994… when genetic testing for inborn errors of metabolism…” Moreover a mechanism of cause is lacking:  “in 93% of the cases a viral infection had occurred in the preceding three-week period… and no animal model of Reye’s syndrome has been developed with aspirin” Wiki 2008.  And only 55% salicylate detected, 73% viral infection, yet the FDA’s warning remains on bottles of aspirin against its usage for those under 19, plus gastro-intestinal irritation and bleeding, thus getting parents and their children onto other NSAIDs, all of which increase the risk of MIs and lack protections listed below.  The rise in heart attacks, arthritis, Alzheimer’s disease, ALS, Parkinson’s, and cancer in part results from the reduction in the use of aspirin (other cause high carb diet).  Nearly everyone dies earlier thanks to pharma’s corporate tobacco ethics.   


The first reference to aspirin was by a 5th century BC Greek physician who rote of a bitter powder that came from the bark of the willow tree, and it eased pains and reduced fever.  The medicinal part of the plant is the inner bark of the tree. The active extract of the bark is called salicin after the Latin name for the white willow tree. It was isolated in crystalline form in 1828 by Henri Leroux, a French pharmacist. Raffaele Piria, an Italian chemist was able to convert it to salicylic acid. Salicylic acid was isolated from the herb called meadowsweet by German researchers in 1839. While it was somewhat effective, it also caused digestive problems when consumed in high doses.

A French chemist, Charles Frederic Gerhardt, first prepared acetylsalicylic acid in 1899 and was the first to name it aspirin. This preparation of aspirin was one of many reactions Gerhardt conducted for his paper on anhydrides and he did nothing further with it. Six years later in 1859, von Gilm created the substance again.  In 1897, a chemist at Friedrich Bayer and Co. obtained acetylsalicylic acid and claimed to discover aspirin. Bayer gave it the trade name “aspirin” and launched a marketing campaign. 


Aspirin, an NSAID, (Non Steroidal Anti-Inflammatory Drug) has 5 medicinal uses:  antipyretic (reduce fever), analgesic (pain), anti-inflammatory (swelling), anti-platelet (reduce blood clotting), inhibit the synthesis of prothrombin, and promote apoptosis (cell death).  The two common side effects are gastrointestinal distress (stomach bleeding and ulcers) and tinnitus (high frequency hum) at higher doses.


Fever is part of the immune response to pathogens.  Aspirin reduces the immune response, and thus moderately reduces fever. 


Inflammation is sufficient cause pain.  Thus aspirin can produce a modest reduction in pain.  Since in most instances pain becomes less over time, this results in a belief by many of aspirin being an effective analgesic.  Aspirin and other NSAIDs do not interact with neural pain receptors.    


Aspirin and all other COX-1 inhibitors reduce clotting, and thereby promote increased bleeding when injured.  Blood clot, a thrombus, is the final product of the blood coagulation step in homeostasis.  It is achieved via the aggregation of platelets and other clotting factors to form a platelet plug.   Thrombin is a coagulation protein that is part of the platelet formation.  It works by converting the soluble fibrinogen into strands of insoluble fibrin, as well as catalyzing many other coagulation-related reactions.  Aspirin inhibits prothrombin synthesis

A thrombosis is a clot in an intact blood vessel, and is thus pathological.   A thrombus in a large blood vessel will decrease blood flow through that vessel. In a small blood vessel, blood flow may be completely cut-off resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is an emolus.  Some conditions elevate the risk of thrombi developing including atrial fibrillation, atherosclorsis, myocardial infraction (heart attack caused by a blood clot), physical trauma, and extended periods of inactivity.  Women are at an increased risk of a thrombi in a vein (usual in her leg), and this risk increases moderately with the taking of estrogen.  Aspirin signficantly reduces the risk of thrombus.[i]  Thrombus in a coronary vessel results in over 60% of all heart attacks.  Since aspirin very significantly lower the risk for a thrombus, it thus significant reduces the risk for an MI, stroke, and pulmonary embolism.    

            CELL APOPTOSIS

Aspirin alone has been found to lower the risk of at least 9 common cancers over 20%, and as high as 70%.  A dose-dependent reduction in cell viability was observed in colorectal cancer cells treated with aspirin.   The reduction in cell viability was accompanied by an increase in cell death due to apoptosis through an active process induced by aspirin.  It operates through NF-kB (nuclear factor-kappa B).  It is found in all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.  NF-kB plays a key role in regulating the immune response to infection[ii].    It was found that prolonged treatment with aspirin induced a dose-dependent reduction in cytoplasmic I B levels that correlated with the reduction in the number of viable cells.  This and related results suggest that the degradation is associated with aspirin-induced cell death.  This effect is limited to certain tissues:  it had no effect in embryonic kidney or lung adenocarcinoma cells.  This effect upon apoptosis varies with cell line[iii].



The most serious is gastrointestinal bleeding, which is not a result of the NSAID’s effect upon clotting (a deceptive way COX-2 inhibitors were marketed), but rather as an irritant effecting the mucous membrane which protects the stomach.  That only a small percentage have this problem suggests that presence of Helicobacter pylori, the bacterial cause of ulcers, plays a role.  Given this it is prudent to take a coated NSAID.[iv]  Long term usage approximately doubles the risk of ulcer, from 2% to 4% risk.   

Tinnitus sound is associated with high doses of NSAIDs for prolonged periods of time.  Its severity and duration vary, though usually it ends once the medication is removed.  Tinnitus is associated with other NSAIDS besides aspirin, and is common without a drug vector.[v] 


All NSAIDs, but for aspirin, accelerate the formation of atherosclerosis by blocking the process which reduces the rate of plaque formation.  Simply put, most plaque formation is the result of a white-cell initiated response primarily to pathogen within the artery wall (see Cholesterol Myth and Infection in Artery Walls Causes Atherosclerosis) and certain reactive chemical involved in metabolism in the artery walls where the plaque forms.  The termination of this response is affected by COX-2 inhibitors, with the exception of aspirin increases the rate of plaque formation.[vi]


NSAIDs chief mechanism is through the reduction of the cyclooxygenase (COX-1 & COX-2 and structural variants thereof) enzymes which are responsible for the formation of prostanoids, including prostaglandins, prostacyclin, and thromboxane.  This inhibition of COX-1 & COX­-2 can provide relief from inflammation and pain.  The COX enzymes convert arachidonic acid to prostaglandin H2, the precursor of the series-2 prostanoids.  COX-1 is a constitutive enzyme, being found in most mammalian cells; and COX-2 is an induced enzyme, becoming abundant in activated macrophages and other cells at sites of inflammation.  Selective inhibitions by NSAIDs of the COX family of enzymes produce moderate variation upon the effects of this family of drugs. 

                        Thromboxane is a member of the family of lipids knows as eicosanoids.  Thromboxane is named for its role in clot formation (thrombosis).  It is produced in platelets from endoperoxides by the COX enzyme from arachidonic acid.  Its action is by binding to thromboxane receptors.  Thromboxane is a vasoconstrictor and a potent hypertensive agent that facilitates platelet aggregation (blood clotting) by both stimulating activation of new platelets as well as increasing platelet aggregation.  Vasoconstriction at the site of a wound also reduces bleeding. 

            Inflammation is a complex biological response to vascular tissues to harmful stimuli such as pathogens, damaged cells, or irritants.  It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue.  This healing response when prolonged and uncheck can lead to a host of conditions including hay fever, atherosclerosis, and rheumatoid arthritis.  It is the reason why chronic infections are statistically associated with atherosclerosis and myocardial infraction (MI).  

            Unfortunately, the COX inhibitors (but for aspirin) also inhibit the mechanism that limits plaque formation.  In a long-term study terminated in December of 2004, Celebrex (a Cox-2 inhibitor) was compared to naproxen as to their ability to reduce the risk of Alzheimer’s disease, the VIGOR study.  Two years into the study it was found that those taking Celebrex had twice the risk of MI, and those on naproxen had a 50% greater risk.  These findings can be extended to most, if not all of the NSAIDs but for Aspirin.  A 2005 article published by the American Heart Association ( describes the mechanism for the accelerated plaque formation and who aspirin because of the production of 6-Los does not:


Inhibition of COX-2 also has as a theoretical side effect an increase in the flux of arachidonate through the LO pathways, which may be especially important in the setting of inflammation in the atheromatous plaque. The 12-,15-, and 5-LOs all have key roles in inflammation, and the role of each in atherosclerosis has been examined. Although 12-LO and 15-LO appear to contribute to LDL oxidation, the data supporting the proatherogenic role of these enzymes are inconsistent.  Data suggest that 15-LO products may be anti-inflammatory.  Furthermore, work from Serhan’s group shows that acetylation of COX-2 by low-dose aspirin leads to its biosynthesis of 15R-hydroxyeicosatetraenoic acid.  This intermediate is then converted by transcellular metabolism to the antiinflammatory lipoxin 15-epi-lipoxin A4 in leukocytes.

      Mehrabian and colleagues have demonstrated convincingly that 5-LO is a critical determinant of atherogenesis in mouse models of the disease, even in the setting of profound hypercholesterolemia. The inflammatory eicosanoids derived from increased 5-LO expression in plaque–leukotriene B4 and the cysteinyl-leukotrienes–are active in the atherothrombotic vasculature, having been shown to promote inflammatory cell activation, cell proliferation, and vasoconstriction. In human subjects, Dwyer and colleagues showed that a promoter haplotype comprising 4 linked polymorphisms in the 5-LO activating peptide (an accessory protein that facilitates presentation of substrate arachidonate to 5-LO) confers an approximately 2-fold increased risk of myocardial infarction (MI) and stroke in an Icelandic population. Thus, the potential importance of shifting the flux of arachidonate through the LO pathway by inhibiting COX activity bears consideration as we attempt to dissect the vascular consequences of coxib use.  


Whatever, the exact pathway, a large body of evidence shows that the long-term taking of aspirin does not accelerate atherosclerosis.

[i]   The drug industry promotes the use of heparin and warfarin which are more expensive, have more serious side effects, and are less effective than aspirin. 

[ii] NF-κB is widely used by eukaryotic cells as a regulator of genes that control cell proliferation and cell survival. As such, many different types of human tumors have misregulated NF-κB: that is, NF-κB is constitutively active. Active NF-κB turns on the expression of genes that keep the cell proliferating and protect the cell from conditions that would otherwise cause it to die. In tumor cells, NF-κB is active either due to mutations in genes encoding the NF-κB transcription factors themselves or in genes that control NF-κB activity (such as IκB genes); in addition, some tumor cells secrete factors that cause NF-κB to become active. Blocking NF-κB can cause tumor cells to stop proliferating, to die, or to become more sensitive to the action of anti-tumor agents. Thus, NF-κB is the subject of much active research among pharmaceutical companies as a target for anti-cancer therapy

[iii] This is because mutations leading to cancer effect various pathways and to varying degrees.  No two cancers have the same set of mutated genes, and their mutations on any gene will also vary.  

[iv] Perspective studies of coated and uncoated aspirin are flawed because those with gastrointestinal distress are more likely to take a coated aspirin.  The drug industry has, for financial reasons, has used deceptively clinical research to show the superiority of products.  The result thereof has been in the last century over a million premature deaths.  All NSAIDs, but for aspirin, accelerate atherosclerosis.      


[v] Tinnitus is very widespread in industrialized countries.  It is frequently associated with prolonged exposure to unnatural levels of noise.  In a 1953 study of 80 tinnitus-free university students who were placed in an anechoic chamber, 93% reported hearing a buzzing, pulsing, or whistling sound.

[vi] At  COX-2 inhibitors promote the inflammation response and thereby accelerate atheromatous plaque deposits.  The 12-,15-, and 6-Los all have key roles in inflammation and atherosclerosis by contributing to LDL and VLDL oxidation.  It appears that 15-LO is anti-inflammatory, and aspirin leads to its synthesis.  Thus unlike others NSAIDs aspirin reduces rather than increases the product of athreomatous plaque.    

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for any medical advice, diagnosis, and treatment.