Aspirin's impact on female hearts

A recent study looks at why aspirin's effect on female hearts seems to be different than its effect on male hearts.

In both men and women, daily aspirin therapy is one of the mainstays of treatment in preventing heart attacks and strokes. Previous studies have shown as much as a 42-percent decrease in heart attacks among men who take aspirin compared to a placebo.

However, the recent Women's Health Study of almost 40,000 women showed that low-dose aspirin's effects on women did not reduce coronary artery disease, but did reduce the risk of stroke.

To investigate this and similar findings, researchers at The Johns Hopkins University School of Medicine conducted a study to determine if the protective effects of aspirin vary by gender. Aspirin is thought to be heart protective because of its ability to prevent platelets from clustering, or aggregating, thereby preventing blockages in the coronary arteries - blood clots.

Their results can be found in The Journal of American Medical Association (JAMA.)

They enrolled 571 men and 711 women over the age of 21. None took aspirin before the study began, and each had his or her platelet activity and function tested.

At this point, researchers observed that women displayed a greater degree of platelet activity than men, meaning there was a greater tendency for platelets to form clots.

After two weeks of low doses of aspirin therapy (81 milligrams), platelet function was again tested to determine if the aspirin had exerted the same degree of inhibition in women that it had in men.

While aspirin did inhibit platelet aggregation (clotting) somewhat, much of the same increased platelet activity seen in women before the study began persisted. A greater degree of suppression was noted among men.

The researchers then looked at the effect of aspirin on the direct COX-1 pathway of platelet aggregation. This is the pathway reputed to be the most susceptible to inhibition by aspirin. It is also the mechanism by which aspirin is said to exert its cardio-protective effect.

It was believed that aspirin would not inhibit the direct pathway of platelet aggregation in women as much as it did in men. Instead, the study showed that most women and men demonstrated complete suppression of the COX-1 pathway after two weeks of aspirin therapy.

In fact, the percent of aggregation in the direct COX-1 pathway decreased more in women than it did in men.

The Hopkins researchers discovered that low-dose aspirin therapy reduced platelet reactivity in women more than men, and women also retained more residual platelet reactivity than men. Consequently, additional research is called for to determine the benefits of aspirin therapy among women.

According to the American Heart Association (AHA,) heart disease is the No. 1 killer of both men and women in the U.S. Of the 157,804 stroke deaths in the U.S. in 2003, the AHA reports that 61 percent were women.

Ahhhh, the MIRACLE DRUG ASPIRIN SRIKES AGAIN! Snip> The researchers then looked at the effect of aspirin on the direct COX-1 pathway of platelet aggregation. This is the pathway reputed to be the most susceptible to inhibition by aspirin. It is also the mechanism by which aspirin is said to exert its cardio-protective effect. >Snip

NO THAT IS NOT THE ONLY WAY ASPIRIN WORKS! Aspirin = salicylate

SALICYLATE [salicylate] , any of a group of analgesics , or painkilling drugs, that are derivatives of salicylic acid. The best known is acetylsalicylic acid, or aspirin . Now often made synthetically, they were originally derived from salicin, the active ingredient in willow bark, used for centuries in the treatment of pain and fever. Salicylates also occur naturally in many plants used as foods (e.g., strawberries, almonds, tomatoes). LINK

NOW WE HAVE THIS ARTICLE;

1: Br J Pharmacol. 1982 May;76(1):211-3.

Mechanisms of elevation of rat brain tryptophan concentration by various doses of salicylate.

Badawy AA.

1 The roles of inhibition of liver tryptophan pyrrolase activity and of displacement of tryptophan from its binding sites on serum proteins have been investigated in relation to the increase in rat brain tryptophan concentration after administration of various doses of sodium salicylate. 2 The elevation of brain tryptophan concentration by sodium salicylate (0.5 mg/kg) was caused by inhibition of liver pyrrolase activity, whereas that by doses of the drug of 50 mg/kg and above was achieved mainly by tryptophan displacement. Both tryptophan displacement of pyrrolase inhibition caused the increase in brain tryptophan concentration by sodium salicylate at 10 mg/kg. 3 The smallest dose of salicylate capable of displacing serum-protein-bound tryptophan was 2.5 mg/kg.

PMID: 7082905 [PubMed - indexed for MEDLINE]

LINK

So aspirin works in TWO DIFFERENT WAYS NOT MENTIONED IN THE ABOVE ARTICLE BY 1. SLOWING TRYPTOPHAN PYRROLASE (OXYGENASE) ACTIVITY AND 2. DISPLACING BOUND TRYPTOPHAN FROM ALBUMIN MAKING THE TRYPTOPHAN FREE (THE EFFECTIVE FORM).

ANYONE TAKE VALIUM OR XANAX? READ BELOW;

1: Naunyn Schmiedebergs Arch Pharmacol. 1975 May 6;288(1):17-27.

Benzodiazepines: specific competitors for the binding of L-tryptophan to human serum albumin.

Muller WE, Wollert U.

By means of the gel filtration technique, the effect of nine benzodiazepine derivatives on the binding of L-tryptophan to human serum albumin was investigated. Using equimolar tryptophan and benzodiazepine concentrations, all benzodiazepines with binding constants higher than 10(4) (M(-1), displace L-tryptophan from its binding site to a high degree. The mechanism of the displacement was characterized as a competition for a common binding site. Some of the benzodiazepines displace L-tryptophan to a greater extent than salicylic acid. The benzostereospecific binding to human serum albumin. This study shows that there is only one binding site on the human serum albumin molecule, which binds tryptophan and the benzodiazepines in a highly stereospecific manner. Therefore it is concluded that the benzodiazepines and L-tryptophan must have similarities in their molecular structure, so that both can bind to the common binding site in such specific manner. These considerations are discussed in regard to the known influence of benzodiazepine derivatives on the L-tryptophan metabolism in brain. A direct involvement of the reported displacement in the pharmacological actions of the drugs seems not to be relevant because of their small therapeutical plasma levels.

PMID: 1161041 [PubMed - indexed for MEDLINE]LINK

SO VALIUM WORKS LIKE ASPIRIN IN THE DISPLACEMENT OF TRYPTOPHAN TURNING IT INTO THE EFFECTIVE FREE FORM.

TRYPTOPHAN WAS PULLED FROM THE MARKET IN 1989 MAKING IT AN ORPHAN DRUG. REBUTTAL?

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