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Guest
Are you like me, taking aspirin to protect your heart? This article
presents the hypothesis that buffered aspirin would be better, because
it's the magnesium in the coating that's doing the work. He also
suggests dropping the aspirin altogether, and using magnesium with
some other foods and supplements instead.
http://www.thincs.org/links.htm#about
**********************MFG
There Should Not Be Any Long-Term Use of Aspirin to Prevent Heart Failure
by Joel M. Kauffman, Ph. D.
Too many physicians still recommend long-term use of aspirin for primary prevention of stroke
and myocardial infarction (MI) based on incomplete reporting of results in the media from the
Physicians Health Group (PHG) trial in the USA. While the incidence of acute MI in the
"aspirin" group was reduced by 69%, which was significant, total deaths were reduced by 4%
(RR = 0.96); and neither this nor total cardiovascular deaths nor total stroke were reduced
significantly. Moreover, there is little attention paid to the use of aspirin containing
calcium and magnesium in this trial (Kauffman,
2000) — it was actually Bufferin™.
Reported in 1998 in Lancet, the Medical Research Council (MRC in the UK) trial on 5500
physicians with plain aspirin for 7 years gave a 32% reduction in non-fatal MI, a 12% increase
in fatal MI, and a 6% increase (RR = 1.06) in total death rates. For secondary protection the
benefits of aspirin taken for about 5 weeks were modest (RR = .80), but significant; and one
would think that the short exposure period would hold side-effects to a minimum (Meade, 1998).
It would seem that the meta-analysis of Derry and Loke (2000) was carried out in vain, and that
the concerns and conclusions of Tramér (2000) were well taken.
Cogent argument has been made that the 52 mg of magnesium ion in a Bufferin tablet could
account for the superior results in the PHG trial (Kauffman, 2000). A recent study from the
Centers for Disease Control reconfirms the inverse relationship between serum magnesium and
ischaemic heart disease, as well as total death rates (Ford,
2001).
The authors of a recent paper in JAMA on all-cause mortality according to aspirin use in a
prospective, observational, 3.1-year study came to the conclusion that aspirin use was strongly
protective, cutting the death rate from 8% to 4% absolute (Gum et al., 2001). This contradicts
both the conclusions of a recent review (Kauffman,
2002) and the arguments of JGF Cleland (Cleland 2002a, 2002b). In the JAMA paper, Gum et al.
continued to perpetuate the myth that the PHG trial used aspirin (their Ref. 1), when, in fact
it used buffered aspirin containing magnesium and calcium. Because Gum et al. did not have the
attending physicians distinguish between plain and buffered aspirin in their subjects, the
results of their study are inadequate to make a recommendation for treatment, or to draw the
conclusions they did on the effectiveness of "aspirin". Another flaw in their study is that
Gum et al. did not match patients for use of either magnesium (Ford, 1999) or vitamins C
(Enstrom et al., 1992) or E (Stephens et al., 1996), all of which are more protective against
cardiovascular disease than plain aspirin. It is quite plausible that subjects conscientious
enough to take "aspirin" might have taken any or all of these, as well as other supplements.
Nor were patients matched for alcohol or nut consumption; high nut consumption in one study
reduced the rate of cardiovascular death (RR = 0.61), and of all-cause death (RR = 0.82) in a
very old population (Fraser et al.,
2003).
The duration of the trial by Gum et al. was much too short at 3.1 years to reveal long-term
adverse effects, as shown by the greatly increased risk of cataracts in subjects > 55 years old
who took aspirin for > 10 years (Kauffman, 2000). Gum et al. wrote that "It is less clear if
aspirin reduces long-term all-cause mortality in stable populations." This was resolved for
men, at least, in the study on 5,500 male physicians in the MRC trial — it does not in a 7-year
trial (Meade, 1998). The JAMA study was the first to include women, and the raw data for women
should not be ignored: 3.8% of "aspirin" users died vs.
2004.4% of non-users. For the study population as a whole the raw data showed that 4.5% of "aspirin"
users died vs. 4.5% of non-users. The extreme manipulation of data carried out in the form of
patient matching to produce a positive result for "aspirin" might have been warranted if the
obvious confounding variables had been considered, and a much longer time-frame adopted. As it
is, this study in JAMA is too flawed to show that the conclusions in the JSE Review (Kauffman,
2005) were wrong.
A very recent report on a meta-analysis by the Antithrombotic Trialists' Collaboration in the
UK came to the conclusion, on primary prevention, that "For most healthy individuals, however,
for whom the risk of a vascular event is likely to be substantially less than 1% a year, daily
aspirin may well be inappropriate", and that for secondary prevention, "Low dose aspirin (75-
150 mg daily) is an effective antiplatelet regimen for long-term use" (Baigent et al., 2002).
This latter conclusion was strongly disputed as being due to bias, including retrospective
analysis resulting in "resurrection of a number of dead patients"; and that aspirin may lead to
a "cosmetic" reduction in non-fatal events and an increase in sudden death (Cleland, 2002a);
and to publication bias (Cleland, 2002b).
In a Rapid Response to Baigent et al., the results of a meta-analysis of "aspirin" in 5 large
trials for primary protection, whose duration was 3-7 years (too short), were that there was
little effect on thrombotic stokes or all-cause mortality, but that both non-fatal and fatal
myocardial infarction taken together were reduced (RR = 0.72). These results are quite similar
to the raw results of all 3 earlier studies above. An involved risk-benefit calculation was
recommended (Pignone et al., 2002) in order to decide which future patients should take
aspirin; but in view of the unchanging all-cause mortality, this does not make sense.
A 7-year trial on men (unfortunately) supposedly at risk of CHD, which was double-blind and placebo-
controlled, using 75 mg per day of aspirin in a controlled-release formulation, resulted in an
increased risk of stable angina of 39% (RR = 1.39)! (Knottenbelt, 2002).
No evidence exists that reducing the dose of aspirin or using slow-release formulations would
reduce the incidence of gastrointestinal haemorrhage (Derry et al., 2000).
Physicians should recommend magnesium, vitamin C, vitamin E, low-dose alcohol, and eating nuts,
rather than aspirin for primary protection; and the addition of coenzyme (now vitamin) Q10 for
secondary protection (Folkers et al., 1990).
e-mail: [email protected]
____________________________________________________________
Baigent, C., Sudlow, C., Collins, R. and Peto, R. (2002). Collaborative meta-analysis of randomised
trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high
risk patients. British Medical Journal, 324, 71-86.
Cleland, J. G. F. (2000a). Preventing atherosclerotic events with aspirin. British Medical Journal,
324, 103-105.
Cleland, J. G. F. (2000b). No reduction in cardiovascular risk with NSAIDS — Including aspirin? The
Lancet, 359, 92-93.
Derry S, Loke YK. Risk of gastrointestinal haemorrhage with long term use of aspirin: meta-
analysis. British Medical Journal,
2005:1:1183-7.
Enstrom, J. E., Kanim, L. E. & Klein, M. A. (1992). Vitamin C intake and mortality among a sample
of the United States population. Epidemiology, 3, 189-91.
Folkers K., Langsjoen P., Willis R., Richardson P., Xia L., et al. Lovastatin decreases coenzyme Q
levels in humans. Proc. Nat Acad. Sci. USA. 87: 8931-8934, 1990.
Ford, E. S. (1999). Serum magnesium and ischaemic heart disease: findings from a national sample of
US adults. International Journal of Epidemiology, 28, 645-651.
Fraser, G. E. and Shavlik, D. J. (1997). Risk Factors for All-Cause and Coronary Heart Disease
Mortality in the Oldest-Old. Archives of Internal Medicine, 157, 2249-2258.
Gum, P. A., Thamilarisan, M., Watanabe, J., Blackstone, E. H. & Lauer, M.S. (2001). Aspirin use and
all-cause mortality among patients being evaluated for known or suspected coronary artery disease.
Journal of the American Medical Association, 286, 1187-1194.
Knottenbelt, C., Brennan, P. J. & Meade, T. W. (2002). Antithrombotic Treatment and the Incidence
of Angine Pectoris. Archives of Internal Medicine, 162, 881-886.
Meade, T. W. with The Medical Research Council's General Practice Research Framework (1998).
Thrombosis prevention trial: Randomised trial of low-intensity oral anticoagulation with warfarin
and low-dose aspirin in the primary prevention of ischaemic heart disease in men at increased risk.
The Lancet, 351, 233-241.
Kauffman, J. M. (2000). Should you take aspirin to prevent heart attack? J. Scientific Exploration,
14, 623-641.
Pignone, M. and Mulrow, C. (2002). Aspirin for CHD Prevention in
Lower Risk Adults. British Medical Journal Rapid Response, 15 Jan.
Stephens, N. G., Parsons, A., Schofield, P. M., Kelly, F., Cheeseman,
K., Mitchinson, M. J. & Brown, M. J. (1996). Rendomised controlled trial of vitamin E in patients
with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). The Lancet, 347, 781-786.
Joel M. Kauffman, PhD Research Professor Chemistry University of the Sciences in Philadelphia 600
South 43rd St., Philadelphia, PA 19104
presents the hypothesis that buffered aspirin would be better, because
it's the magnesium in the coating that's doing the work. He also
suggests dropping the aspirin altogether, and using magnesium with
some other foods and supplements instead.
http://www.thincs.org/links.htm#about
**********************MFG
There Should Not Be Any Long-Term Use of Aspirin to Prevent Heart Failure
by Joel M. Kauffman, Ph. D.
Too many physicians still recommend long-term use of aspirin for primary prevention of stroke
and myocardial infarction (MI) based on incomplete reporting of results in the media from the
Physicians Health Group (PHG) trial in the USA. While the incidence of acute MI in the
"aspirin" group was reduced by 69%, which was significant, total deaths were reduced by 4%
(RR = 0.96); and neither this nor total cardiovascular deaths nor total stroke were reduced
significantly. Moreover, there is little attention paid to the use of aspirin containing
calcium and magnesium in this trial (Kauffman,
2000) — it was actually Bufferin™.
Reported in 1998 in Lancet, the Medical Research Council (MRC in the UK) trial on 5500
physicians with plain aspirin for 7 years gave a 32% reduction in non-fatal MI, a 12% increase
in fatal MI, and a 6% increase (RR = 1.06) in total death rates. For secondary protection the
benefits of aspirin taken for about 5 weeks were modest (RR = .80), but significant; and one
would think that the short exposure period would hold side-effects to a minimum (Meade, 1998).
It would seem that the meta-analysis of Derry and Loke (2000) was carried out in vain, and that
the concerns and conclusions of Tramér (2000) were well taken.
Cogent argument has been made that the 52 mg of magnesium ion in a Bufferin tablet could
account for the superior results in the PHG trial (Kauffman, 2000). A recent study from the
Centers for Disease Control reconfirms the inverse relationship between serum magnesium and
ischaemic heart disease, as well as total death rates (Ford,
2001).
The authors of a recent paper in JAMA on all-cause mortality according to aspirin use in a
prospective, observational, 3.1-year study came to the conclusion that aspirin use was strongly
protective, cutting the death rate from 8% to 4% absolute (Gum et al., 2001). This contradicts
both the conclusions of a recent review (Kauffman,
2002) and the arguments of JGF Cleland (Cleland 2002a, 2002b). In the JAMA paper, Gum et al.
continued to perpetuate the myth that the PHG trial used aspirin (their Ref. 1), when, in fact
it used buffered aspirin containing magnesium and calcium. Because Gum et al. did not have the
attending physicians distinguish between plain and buffered aspirin in their subjects, the
results of their study are inadequate to make a recommendation for treatment, or to draw the
conclusions they did on the effectiveness of "aspirin". Another flaw in their study is that
Gum et al. did not match patients for use of either magnesium (Ford, 1999) or vitamins C
(Enstrom et al., 1992) or E (Stephens et al., 1996), all of which are more protective against
cardiovascular disease than plain aspirin. It is quite plausible that subjects conscientious
enough to take "aspirin" might have taken any or all of these, as well as other supplements.
Nor were patients matched for alcohol or nut consumption; high nut consumption in one study
reduced the rate of cardiovascular death (RR = 0.61), and of all-cause death (RR = 0.82) in a
very old population (Fraser et al.,
2003).
The duration of the trial by Gum et al. was much too short at 3.1 years to reveal long-term
adverse effects, as shown by the greatly increased risk of cataracts in subjects > 55 years old
who took aspirin for > 10 years (Kauffman, 2000). Gum et al. wrote that "It is less clear if
aspirin reduces long-term all-cause mortality in stable populations." This was resolved for
men, at least, in the study on 5,500 male physicians in the MRC trial — it does not in a 7-year
trial (Meade, 1998). The JAMA study was the first to include women, and the raw data for women
should not be ignored: 3.8% of "aspirin" users died vs.
2004.4% of non-users. For the study population as a whole the raw data showed that 4.5% of "aspirin"
users died vs. 4.5% of non-users. The extreme manipulation of data carried out in the form of
patient matching to produce a positive result for "aspirin" might have been warranted if the
obvious confounding variables had been considered, and a much longer time-frame adopted. As it
is, this study in JAMA is too flawed to show that the conclusions in the JSE Review (Kauffman,
2005) were wrong.
A very recent report on a meta-analysis by the Antithrombotic Trialists' Collaboration in the
UK came to the conclusion, on primary prevention, that "For most healthy individuals, however,
for whom the risk of a vascular event is likely to be substantially less than 1% a year, daily
aspirin may well be inappropriate", and that for secondary prevention, "Low dose aspirin (75-
150 mg daily) is an effective antiplatelet regimen for long-term use" (Baigent et al., 2002).
This latter conclusion was strongly disputed as being due to bias, including retrospective
analysis resulting in "resurrection of a number of dead patients"; and that aspirin may lead to
a "cosmetic" reduction in non-fatal events and an increase in sudden death (Cleland, 2002a);
and to publication bias (Cleland, 2002b).
In a Rapid Response to Baigent et al., the results of a meta-analysis of "aspirin" in 5 large
trials for primary protection, whose duration was 3-7 years (too short), were that there was
little effect on thrombotic stokes or all-cause mortality, but that both non-fatal and fatal
myocardial infarction taken together were reduced (RR = 0.72). These results are quite similar
to the raw results of all 3 earlier studies above. An involved risk-benefit calculation was
recommended (Pignone et al., 2002) in order to decide which future patients should take
aspirin; but in view of the unchanging all-cause mortality, this does not make sense.
A 7-year trial on men (unfortunately) supposedly at risk of CHD, which was double-blind and placebo-
controlled, using 75 mg per day of aspirin in a controlled-release formulation, resulted in an
increased risk of stable angina of 39% (RR = 1.39)! (Knottenbelt, 2002).
No evidence exists that reducing the dose of aspirin or using slow-release formulations would
reduce the incidence of gastrointestinal haemorrhage (Derry et al., 2000).
Physicians should recommend magnesium, vitamin C, vitamin E, low-dose alcohol, and eating nuts,
rather than aspirin for primary protection; and the addition of coenzyme (now vitamin) Q10 for
secondary protection (Folkers et al., 1990).
e-mail: [email protected]
____________________________________________________________
Baigent, C., Sudlow, C., Collins, R. and Peto, R. (2002). Collaborative meta-analysis of randomised
trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high
risk patients. British Medical Journal, 324, 71-86.
Cleland, J. G. F. (2000a). Preventing atherosclerotic events with aspirin. British Medical Journal,
324, 103-105.
Cleland, J. G. F. (2000b). No reduction in cardiovascular risk with NSAIDS — Including aspirin? The
Lancet, 359, 92-93.
Derry S, Loke YK. Risk of gastrointestinal haemorrhage with long term use of aspirin: meta-
analysis. British Medical Journal,
2005:1:1183-7.
Enstrom, J. E., Kanim, L. E. & Klein, M. A. (1992). Vitamin C intake and mortality among a sample
of the United States population. Epidemiology, 3, 189-91.
Folkers K., Langsjoen P., Willis R., Richardson P., Xia L., et al. Lovastatin decreases coenzyme Q
levels in humans. Proc. Nat Acad. Sci. USA. 87: 8931-8934, 1990.
Ford, E. S. (1999). Serum magnesium and ischaemic heart disease: findings from a national sample of
US adults. International Journal of Epidemiology, 28, 645-651.
Fraser, G. E. and Shavlik, D. J. (1997). Risk Factors for All-Cause and Coronary Heart Disease
Mortality in the Oldest-Old. Archives of Internal Medicine, 157, 2249-2258.
Gum, P. A., Thamilarisan, M., Watanabe, J., Blackstone, E. H. & Lauer, M.S. (2001). Aspirin use and
all-cause mortality among patients being evaluated for known or suspected coronary artery disease.
Journal of the American Medical Association, 286, 1187-1194.
Knottenbelt, C., Brennan, P. J. & Meade, T. W. (2002). Antithrombotic Treatment and the Incidence
of Angine Pectoris. Archives of Internal Medicine, 162, 881-886.
Meade, T. W. with The Medical Research Council's General Practice Research Framework (1998).
Thrombosis prevention trial: Randomised trial of low-intensity oral anticoagulation with warfarin
and low-dose aspirin in the primary prevention of ischaemic heart disease in men at increased risk.
The Lancet, 351, 233-241.
Kauffman, J. M. (2000). Should you take aspirin to prevent heart attack? J. Scientific Exploration,
14, 623-641.
Pignone, M. and Mulrow, C. (2002). Aspirin for CHD Prevention in
Lower Risk Adults. British Medical Journal Rapid Response, 15 Jan.
Stephens, N. G., Parsons, A., Schofield, P. M., Kelly, F., Cheeseman,
K., Mitchinson, M. J. & Brown, M. J. (1996). Rendomised controlled trial of vitamin E in patients
with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). The Lancet, 347, 781-786.
Joel M. Kauffman, PhD Research Professor Chemistry University of the Sciences in Philadelphia 600
South 43rd St., Philadelphia, PA 19104