Re: the business of carbs or is it the conspiracy or carbs?
- From: GMCarter <fiar@xxxxxxxxxxx>
- Date: Fri, 16 Jun 2006 10:24:31 GMT
On Fri, 16 Jun 2006 01:12:48 GMT, Jim Chinnis <jchinnis@xxxxxxxxxxxx>
wrote:
snip
But studies on the whole seem to show that reducing homocysteine worsens
rather than improves risk of heart disease and stroke.
What studies? I understood the situation was to the contrary. Elevated
homocysteine is associated with CHD, albeit weakly.
What data are you referring to?
George M. Carter
****
Am Heart J. 2006 Feb;151(2):282-7. Related Articles, Links
Click here to read
Homocysteine-lowering trials for prevention of cardiovascular
events: a review of the design and power of the large randomized
trials.
B-Vitamin Treatment Trialists' Collaboration.
BACKGROUND: Dietary supplementation with folic acid and vitamin
B12 lowers blood homocysteine concentrations by about 25% to 30% in
populations without routine folic acid fortification of food and by
about 10% to 15% in populations with such fortification. In
observational studies, 25% lower homocysteine has been associated with
about 10% less coronary heart disease (CHD) and about 20% less stroke.
METHODS: We reviewed the design and statistical power of 12 randomized
trials assessing the effects of lowering homocysteine with B-vitamin
supplements on risk of cardiovascular disease. RESULTS: Seven of these
trials are being conducted in populations without fortification (5
involving participants with prior CHD and 2 with prior stroke) and 5
in populations with fortification (2 with prior CHD, 2 with renal
disease, and 1 with prior stroke). These trials may not involve
sufficient number of vascular events or last long enough to have a
good chance on their own to detect reliably plausible effects of
homocysteine lowering on cardiovascular risk. But, taken together,
these 12 trials involve about 52,000 participants: 32,000 with prior
vascular disease in unfortified populations and 14,000 with vascular
disease and 6000 with renal disease in fortified populations. Hence, a
combined analysis of these trials should have adequate power to
determine whether lowering homocysteine reduces the risk of
cardiovascular events within just a few years. CONCLUSION: The
strength of association of homocysteine with risk of cardiovascular
disease may be weaker than had previously been believed. Extending the
duration of treatment in these trials would allow any effects
associated with prolonged differences in homocysteine concentrations
to emerge. Establishing a prospective meta-analysis of the ongoing
trials of homocysteine lowering should ensure that reliable
information emerges about the effects of such interventions on
cardiovascular disease outcomes.
****
Mayo Clin Proc. 2006 Feb;81(2):177-82. Related Articles,
Links
Association of plasma homocysteine with coronary artery
calcification in different categories of coronary heart disease risk.
Kullo IJ, Li G, Bielak LF, Bailey KR, Sheedy PF 2nd, Peyser PA,
Turner ST, Kardia SL.
Division of Cardiovascular Diseases, Mayo Clinic College of
Medicine, 200 First St SW, Rochester, MN 55905, USA.
kullo.iftikhar@xxxxxxxx
OBJECTIVE: To Investigate the association of plasma homocystelne
with coronary artery calcification (CAC) in strata based on 10-year
risk of coronary heart disease (CHD) in a cohort enriched in persons
with hypertension. PARTICIPANTS AND METHODS: Fasting plasma
homocystelne was measured by liquid chromatography electrospray tandem
mass spectrometry. Coronary artery calcification was measured
noninvasively by electron beam computed tomography and CAC score
calculated using the method of Agatston et al. The 10-year CHD risk
was calculated based on the Framingham risk score. The association of
homocysteine with log-transformed CAC score was assessed in the pooled
sample and within each risk stratum by linear regression after
adjustment for conventional risk factors. RESULTS: In the 1071
participants studied, homocysteine was associated with CAC quantity (P
= .01) after adjustment for CHD risk factors (age, male sex, total and
high-density lipoproteln cholesterol, diabetes, history of smoking,
body mass Index, and systolic blood pressure), serum creatinine, and
statin and hypertension medication use. When the association was
assessed in strata based on 10-year CHD risk, homocysteine was
significantly (P = .003) associated with CAC quantity in participants
at Intermediate 10-year risk of CHD (6%-20%) independent of other risk
factors but not in those at lower risk or higher risk. CONCLUSION:
Plasma homocysteine is associated with quantity of CAC Independent of
CHD risk factors. When studied in categories of 10-year CHD risk, the
association was significant in participants at intermediate risk but
not in those at low or high risk. Plasma homocysteine levels may have
clinical utility as a marker of CHD risk in such individuals.
****
Atherosclerosis. 2006 Jun 13; [Epub ahead of print] Links
Homocysteine and coronary heart disease risk in the PRIME study.
Troughton JA, Woodside JV, Young IS, Arveiler D, Amouyel P,
Ferrieres J, Ducimetiere P, Patterson CC, Kee F, Yarnell JW, Evans A;
on behalf of the PRIME Study Group.
Faculty of Medicine, Queen's University Belfast, Belfast, Northern
Ireland, UK.
INTRODUCTION: Despite recent meta-analyses suggesting that
homocysteine is an independent predictor of coronary heart disease
(CHD), there is debate regarding whether elevated homocysteine may be
deleterious only in the presence of other risk factors, with which it
acts synergistically to exert a multiplicative effect on CHD risk,
emerging only as a CHD predictor in patients with pre-existing risk
factors. The Prospective Epidemiological Study of Myocardial
Infarction (PRIME) Study is a multicentre prospective study of 10593
men from France and Northern Ireland, investigating cardiovascular
risk factors. We investigated: (1) whether higher homocysteine is
associated with increased CHD risk in the PRIME case-control cohort;
(2) whether homocysteine interacts synergistically with pre-existing
CHD risk factors. METHODS: Homocysteine was measured in 323
participants who had developed CHD at 5-year follow-up and in 638
matched controls. RESULTS: There was no significant difference in
homocysteine between cases and controls (p=0.18). Homocysteine was
significantly higher in current smokers (geometric mean mumol/l
(interquartile range mumol/l) 9.45 (7.43, 11.75)) compared with
non-smokers (8.90 (7.32, 10.70); p=0.007). There was a significant
interaction between homocysteine, smoking and CHD risk (chi(2)=10.29,
d.f.=2, p=0.006). CONCLUSIONS: These findings suggest that elevated
homocysteine is significantly associated with CHD risk in current
smokers.
PMID: 16774755 [PubMed - as supplied by publisher]
.
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