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Aspirin - Not Always a Harmless Pill


by Bruce Hagen,DC

Sioux Falls, South Dakota


Acetylsalicylic acid (ASA): Americans gobble it up in tablet form to the tune of $50 billion a year. Commonly known as aspirin, it is America's most widely used drug, both singularly and in combination with many prescription and patent medicines.

Unfortunately, most people think that aspirin is a harmless drug, though it is not. It may injure the stomach (sometimes severely), interfere with the absorption of several vitamins (especially C, K, and folic acid), and pose a special risk for pregnant women and patients with "bleeding" disorders (such as ulcers). It leads all over-the-counter drugs in causing adverse reactions requiring hospitalization. It is the major cause of childhood poisonings, as indicated by a National Safety Council report claiming that 400 children had died in one year from ASA ingestion (many from just one or two tablets).

In 1981, I authored an article warning that children suffering from influenza or chickenpox, if given aspirin, could develop Reye's syndrome (RS). This hazard was described in a publication released by the FDA as far back as 1978, and between that year and 1985, over 1,500 children died from RS. I personally believe that the aspirin manufacturers deliberately suppressed this vital information.

Aspirin given to pregnant women may interfere with the absorption and metabolism of folic acid in the fetus and result in such deformities as cleft palate or spina bifida in their offspring.

ASA has no effect on viruses or bacteria. It won't help a cold or the flu, nor will it shorten the duration of either. In fact, according to recent scientific evidence, it may prolong recovery. Aspirin used in combination with alcohol is even more damaging to stomach membranes. Not only can it cause heartburn, dyspepsia of the stomach, discomfort, nausea and vomiting, it is also responsible for ulcers with perforation and bleeding of the stomach mucosa and membranes, and gastrointestinal hemorrhage. Considering the fact that ulcers may lead to cancer of the stomach, this is certainly an ominous reaction.

Dr. Robert Schuller, pastor of California's Crystal Cathedral landmark, reported on his Sunday morning broadcast that he had struck his head on a car door during a visit to Holland years ago. He took four aspirin for the resultant headache from the injury; this thinned his blood and caused a stroke, requiring two brain surgeries to correct a hemorrhage in his brain. Those four aspirin nearly cost him his life!

Although commonly prescribed for heart attack prevention in the United States, a British Medical Journal report claimed that ASA was taken daily by 22,000 MDs, with no reduction in cardiac arrest, but with an increase in strokes. Patients with high blood pressure should not take aspirin because of the propensity of this latter occurrence.

It has been estimated that one aspirin causes a loss of one teaspoon of blood from the stomach membranes. Continued and prolonged use may elicit enough blood loss to cause iron deficiency anemia. Taken in combination with other drugs (such as anticoagulants) ASA may cause severe liver damage and possibly death. It may also depress kidney function in certain patients.

Aspirin blocks the enzyme cyclooxygenase, used in forming prostaglandins, which are "hormone-like" substances crucial in the alteration of blood vessel diameter. They also elevate body temperature when infection is present, play an important role in the clotting of blood, and protect the stomach membranes from excess acid formation. Interfering with prostaglandin production may alter our body's natural response to inflammation and delay the healing process.

ASA may cause or aggravate asthma. An allergic reaction to aspirin can also lead to other breathing problems. Large doses of the medication are also correlated with deafness and tinnitus (ringing in the ears).

One question is puzzling this author: Why are aspirin and other "over-the-counter" (OTC) drugs called "anti-inflammatory" drugs, when their most serious and common side effect is inflammation of the stomach? If these drugs are not safe to take when a woman is pregnant, why are they safe to ingest when she is not pregnant?

A number of OTC drugs interfere with the absorption and metabolism of vitamin C, which is necessary for the manufacture of collagen, present in cartilaginous material and necessary for joint repair. Therefore, when one takes OTC drugs for inflamed joints, they're actually causing damage to the tissues they're trying to repair.

Another result of aspirin ingestion may be hives. This is not limited to ASA, however. People who are allergic to aspirin can also be allergic to ibuprofen, ketoprofen, and naproxen.

In conclusion, I remind the reader to remember the adage that "there may not be a cure in a carload of medicine"that covers up pain and leaves its cause untreated. If ASA shares a common ingredient with corn salve, which burns the flesh off your corns and calluses, the only time aspirin should be taken is when one has a "corn" between their ears! (Note from Dr. Hurst: aspirin is included in a group of drugs known as Non Steroidal Anti Inflammatory Drugs or commonly known by the anacronym, NSAIDs.)


NSAIDs May Contribute to Congestive Heart Failure

Nonsteroidal anti-inflammatory drugs, among which are aspirin, ibuprofen, naproxen, celebrex, vioxx, etc. (NSAIDs) are commonly prescribed for migraines, sprains, strains, and countless other conditions in which pain and/or inflammation result. NSAIDs have come under fire in recent years, with mounting evidence suggesting possible dangerous side effects associated with their use.

One of the most severe potential side effects may be congestive heart failure (CHF) in susceptible patients, according to a study in the March 27, 2000 issue of the Archives of Internal Medicine. Patients admitted to hospitals with a primary diagnosis of CHF (365 cases) were compared with patients without CHF (658 cases) admitted to the same hospitals for other conditions. Patients were interviewed to gather data on recent use of aspirin and other NSAIDs.

Results: Use of NSAIDs in previous week doubled the risk of hospital admission for CHF. Additionally, patients who reported taking higher levels of NSAIDs in the previous week were more likely to be admitted for CHF than patients taking lower levels. Why this relationship exists is unknown, although the authors speculate that possible drug interactions (NSAIDs and other drugs used by heart patients) may contribute to the problem. They emphasize that �NSAIDs should be used with caution in patients with a history of cardiovascular disease.� Talk to your doctor about the potential dangers of NSAIDs and other commonly prescribed drugs.



Page J, Henry D. Consumption of NSAIDs and the development of congestive heart failure in elderly patients. Archives of Internal Medicine, March 27, 2000:160, pp777-84.


NSAIDs for Soft Tissue Lesions


by Warren Hammer,MS,DC,DABCO

It seems to have become standard procedure for nonsteroidal anti-inflammatory drugs (NSAIDs) to be used for acute injuries. Their main action is to inhibit prostaglandins, pro-inflammatory mediators responsible for the production of painful stimuli. There is no question that they often reduce pain and swelling, and therefore help a patient perform motion earlier during recovery, but what is the effect on the soft tissue? Elder, et al.,1 asked the question and performed experiments on the medial ligaments (right knee) of 50 rats through surgical transection. Half of the ligaments were given Celecoxib, a COX-2 inhibitor similar to Celebrex, for the first six days of recovery, while the other half were not. (The injured animals were sacrificed 14 days after the operation.) The ligaments given the anti-inflammatory had a 32-percent lower load to failure than the untreated injured (control) ligaments.

Elder, et al., state that to their knowledge, there were no previous reported studies regarding the effect of COX-2 inhibitors on any soft tissue disorders. This article tells us that these drugs, which have been widely advertised, were never tested for their effects on soft tissue. I suppose that patients with osteoarthritis or rheumatoid arthritis have been relieved of pain, but they are in a precarious situation if they experience an injury to their soft tissue.

Whatever happened to the acceptance of nature and its innate healing ability? There's an old adage: "Hurry to give a new drug while it's still working." I always thought that inflammation was the body's first line of defense against acute injury. Why inhibit a normal bodily reaction? It makes no sense to immediately give an anti-inflammatory drug to a recent injury. An inflammatory response is beneficial by removing cellular debris from sites of injury to allow quicker healing.2 This type of intervention is similar to the old theory of prescribing aspirin as soon as a slight fever arises.

The COX-2 inhibitors were developed to minimize the gastrointestinal symptoms caused by the earlier NSAIDs, such as Advil and Motrin. NSAID use has been linked to disorders ranging from dyspepsia to gastric ulceration with bleeding. Contraindications to use are patients over 60 years of age, arthritis, a history of gastrointestinal disease, anticoagulant or corticosteroid.1 The study determined, "Complications related to NSAID use among arthritis patients are responsible for 16,500 deaths per year in the United States.3

NSAIDs may delay muscle healing in minor stretch injuries.4 In a trial that treated acute hamstring injuries with NSAIDs versus a placebo group with the same physiotherapy regimen, reduction of pain and swelling, and return to normal strength, were no better with or without NSAIDs. It noted, "Surprisingly, in the group with severe strains, reduction of pain was better in the placebo group." As a result, this study did not advocate the use of NSAIDs in acute hamstring strains.4

Recently, Mariano Rivera, the great Yankees relief pitcher, was diagnosed with a shoulder strain. The strain was confirmed by MRI, and he received an injection of cortisone. Several weeks later, he was pitching again, and re-aggravated the shoulder. He was sent back to rehabilitation, with the hope that he would be available to pitch in the postseason. It seems logical that any inflammatory ability of his body to create healing was immediately repressed, and his "strain" was not given a chance to completely heal.




1.       Elder CL, Dahners LE, Weinhold PS. A cyclooxygenase-2 inhibitor impairs ligament healing in the rat. Amer J Sports Med 2001;29(6):801-805.

2.       Almekinders LC. Anti-inflammatory treatment of muscular injuries in sports. Sports Med 1993;15:139-145.

3.       Singh G. Recent considerations in nonsteroidal anti-inflammatory drug gastropathy. Am J Med 1998;105(1B):31S-38S.

4.       Stanley KL, Weaver JE. Pharmacologic management of pain and inflammation in athletes. Clin Sports Med 1998;17 (2): 1998:375-392.

Warren Hammer,MS,DC,DABCO



NSAIDs -- The Unintended Consequences


by Alan Cook, DC

We have forgotten. Prior to 1938, the year penicillin was synthesized, there was a very small pharmacy industry. Contrast this with 1997, where the pharmacy companies' stocks are almost universally a good investment, and their advertisements appear in all forms of the media. We have also forgotten the many examples of the pharmacy industry's wares causing unintended consequences. Remember the stories of diethylstilbestrol (DES) and cancer and reproductive tract defects, swine flu vaccine and Guillain-Barre syndrome, or aspirin and Reyes syndrome?

Another story of unintended consequences associated with drugs is unfolding currently. The class of drugs is familiar to all of us -- non-steroidal anti-inflammatory drugs (NSAIDs). Much has been written with regards to NSAIDs and their caustic effects on the gastrointestinal tract.1-7 Toxicity and the extent of damage caused tends to vary widely when comparing the many NSAIDs; they are not all equal. The unintended consequences of NSAIDs are not limited to the GI tract: this is just the most widely written about and experienced side effect.

Researchers estimate that 8-10% of the overall incidence of end-stage renal disease (ESRD) is attributable to acetaminophen. The risk was dose dependent with measurable increases of risk beginning at 105-365 pills per year or greater than 1000 pills per lifetime. Aspirin did not increase the risk of ESRD; however, other NSAIDs (non-aspirin, non-acetaminophen) sharply increased ESRD risk in persons who consumed 5000 or more pills during their lifetime.8 These are doses easily achieved with over-the-counter products. Only recently have negative side effects on the central nervous system been appreciated. Cases of aseptic meningitis, psychosis, and cognitive dysfunction have been reported.9 These side effects are more commonly seen in the elderly.

A mechanism of action of NSAIDs is to inhibit prostaglandin synthesis. Prostaglandins are involved in pain and inflammation mechanisms, but this is not their only function. Prostaglandins are also involved in thermo-regulation and melatonin synthesis.10 This directly impacts body temperature, sleep, and may affect circadian rhythm.

A recent double blind study found that normal circadian decrease in body temperature during the nighttime hours was attenuated by the administration of aspirin or ibuprofen.11 Daytime body temperature was not affected by these same NSAIDs. In addition, melatonin was suppressed by the administration of these NSAIDs during the nighttime hours. This confirmed earlier reports of suppression of melatonin synthesis10 and alteration of normal sleep patterns in healthy individuals.12,13 These effects were not found in all study subjects; there were wide variations. Gastrointestinal damage, kidney damage, cognitive disturbances, alteration of sleep and circadian rhythms -- all are unintended consequences directly attributable to NSAIDs. But wait ... there's more.

The first-line treatment for osteoarthritis, from the medical perspective, is NSAIDs. These drugs are recommended for chronic use either as an over-the-counter or prescription item. Here is the sad irony. Human articular cartilage is continually remodelled during growth and development and during adult life. The remodelling involves, in part, the synthesis of glycosaminoglycans (GAG) -- the principal macromolecule of the extracellular matrix. Normal synthesis and breakdown of these molecules is mediated by chondrocytes.14-16 Changes in the metabolic activity of these cells has been postulated to be a factor in the development of cartilage lesions characteristic of osteoarthritis.17-19 If the synthesis of GAG is reduced, this may eventually lead to deterioration, which is part of the osteoarthritic process. Conversely, the ability to accelerate the synthesis of GAG should aid in repair and regeneration.

A study of the effect on GAG synthesis in human articular cartilage using NSAIDs was undertaken (this was an in vitro experiment).20 The following table rates the various NSAIDs as to those that stimulate GAG synthesis, have no significant effect, and those that have significant inhibitory effects.

NSAID (generic name)

NSAID (trade name)

effect on GAG synthesis


(European drug)














tiaprofenic acid

(European drug)



* * *



Naprosyn, Aleve



Advil, Motrin





These distinct categories discount the individual variabilities that were present. For example:

When considering aceclofenac, 35 cartilage samples showed stimulation of GAG synthesis, none showed inhibition;

When considering diclofenac, 2 samples showed increased GAG synthesis, 27 showed some degree of inhibition;

When considering naproxen, 27 samples showed significant inhibition, none showed stimulation of GAG synthesis.

The weaknesses to the above study include the fact that it was done in vitro (it is too invasive to contemplate measuring GAG synthesis in vivo with current testing techniques) and the measurements were taken over only seven days. To the researchers' credit, this was the best study to date looking at this crucial issue. How ironic that use of several of the above listed NSAIDs, if prescribed for an osteoarthritic patient, would inhibit GAG synthesis, thereby hastening the decline of the articular cartilage -- an iatrogenic worsening of the degenerative process.

Given the damage wrought by the class of non-steroidal anti-inflammatory drugs, it is astounding how large an audience they have captured. Documented side effects to the gastrointestinal tract, liver, kidneys, central nervous system, endocrine system, and articular cartilage should strike a note of warning to all. Yet, NSAIDs are the most frequently prescribed medications worldwide.21 Remarkably, some chiropractors recommend these drugs, even for chronic use. Perhaps, in addition to your favorite NSAID, the use of alcohol and cigarettes should be considered.


1.       Langman MJS, et al. Risk of bleeding peptic ulcer associated with individual nonsteroidal anti-inflammatory drugs. Lancet 1994;343:1075-8.

2.       Melo Gomes JA, et al. Double-blind comparison of efficacy and gastroduodenal safety of diclofenac/misoprostol, piroxicam, and naproxen in the treatment of osteoarthritis. Ann Rheum Dis 1993;52:881-5.

3.       Gabriel SE, Jaakkimainen L, Bombardier C. Risk for serious gastrointestinal complications related to use of nonsteroidal anti-inflammatory drugs. Ann Int Med 1991;115:787-96.

4.       Griffin MR, Piper JM, Daugherty JR, et al. Nonsteroidal anti-inflammatory drug use and increased risk for peptic ulcer disease in elderly persons. Ann Intern Med 1991;114:257-63.

5.       Ballinger AB, Kumar PJ, Scott DL. Misoprostol in the prevention of gastroduodenal damage in rheumatology. Ann Rheum Dis 1192;51:1089-93.

6.       Ehsanullah RS, Page MC, Tildesley G, et al. Prevention of gastroduodenal damage induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine. BMJ 1988;297:1017-21.

7.       Cryer B, Feldman M. Effects of nonsteroidal anti-inflammatory drugs on endogenous gastrointestinal prostaglandins and therapeutic strategies for prevention and treatment of nonsteroidal anti-inflammatory drug-induced damage. Arch Intern Med 1992;152:1145-55.

8.       Perneger TV, Whelton PK, Klag MJ. Risk of kidney failure with the use of acetaminophen, aspirin, and nonsteroidal anti-inflammatory drugs. NEJM 1994;331:1675-9.

9.       Hoppmann RA, et. al. Central nervous system side effects of nonsteroidal anti-inflammatory drugs. Arch Int Med 1991;151:1309-13.

10.    Surrall K et al. Effect of ibuprofen and indomethacin on human plasma melatonin. J Pharm Pharmacol 1987;39:840-3.

11.    Murphy PJ, Myers BL, Badia P. Nonsteroidal anti-inflammatory drugs alter body temperature and suppress melatonin in humans. Physiology and Behavior 1996;59:133-9.

12.    Murphy P, et al. Effects of some nonsteroidal anti-inflammatory drugs on sleep in humans. Sleep Res 1992;22:165.

13.    Murphy P, et al. Nonsteroidal anti-inflammatory drugs affect normal sleep patterns in humans. Physiol Behav 1994;55:1063-6.

14.    Muir H, Hardingham TE. Cartilage matrix biochemistry. In: Scott JT (ed.) Copeman's Textbook of the Rheumatic Diseases 1. Edinburgh: Churchill-Livingstone, 1986: 177-98.

15.    Kempson G. The mechanical properties of articular cartilage. In: Sokoloff L (ed.) The Joints in Synovial Fluid 2. New York: Academic Press, 1980: 177-238.

16.    Dingle JT. A possible role for catabolin in tissue remodelling and repair. In: Elliot K. (ed.) The Fetus and Independent Life. Pitmans, 1981: 203-14.

17.    Hammerman D. The biology of osteoarthritis. N Engl J Med 1989;320:1322-30.

18.    Dingle JT, et al. The sensitivity of synthesis of human cartilage matrix to inhibition by IL1 suggests a mechanism for the development of osteoarthritis. Cell Biochem Function 1991;9:99-102.

19.    Dingle JT. Cartilage damage and repair: the roles of IL1, NSAIDs and prostaglandins in osteoarthritis. In: New Frontiers in Prostaglandin Therapeutics. Excerpta Medica. Princetown, USA. 1990:1-5.

20.    Dingle JT. The effect of NSAIDs on human articular cartilage glycosaminoglycan synthesis. Eur J Rheum Inflam 1996;16:47-52.

21.    Saag KG, Cowdery JS. Nonsteroidal anti-inflammatory drugs. Spine 1994;19:1530-4.

Alan Cook, DC
Eureka, California



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