Posted by JLx on October 4, 2005, at 18:25:19
In reply to Re: AT MY WITS END -- Cholesterol Homocysteine » JLx, posted by vitaqueen on October 4, 2005, at 15:47:28
> You mean testing for lipoprotein(a) is different than testing for cholesterol? I've never heard of this before. Of course, no "doctor" ever told me to have my homocysteine checked before either.
I hadn't heard of it before that page either. Here's somebody from The Cleveland Clinic, for a more traditional view, stating that he doesn't recommend it for routine screening, but then he says,
"However, one should be aware of the Lp(a) level in special populations, ie, patients with premature coronary heart disease, those with a strong family history of cardiovascular disease, those who have undergone angioplasty or coronary artery bypass grafting, and those with documented cardiovascular disease in the absence of traditional risk factors. In addition to aggressive lowering of elevated levels of LDL-C, attempts to lower Lp(a) in these groups may be warranted on the basis of the epidemiological associations discussed above, especially in light of the efficacy and tolerability of the newer forms of niacin and of fenofibrate." http://www.clevelandclinicmeded.com/ccjm/sept1999/ccjmoneminutesep99.htm
> Calcium and magnesium are two I do not take with any regularity. I'm probably naive about this, but for some reason -- since cholesterol has been referred to as a calcium build-up, I'm hesitant to take calcium -- the magnesium is in the same "liquid calcium" I have, so I'm not getting that either.
I wouldn't worry about calcium, as you probably get enough from food but magnesium is another story.
Magnesium helps regulate blood sugar, it's part of the relaxation phase of muscle, it's a vasodilator.
"According to Mildred S Seelig, MD, author of The Magnesium Factor, "Most modern heart disease is caused by magnesium deficiency. A vast and convincing body of research, largely ignored, has convinced us and many of our colleagues of this fact. The diet of the industrial world is short on magnesium, and this is causing an epidemic of heart disease in the modern world." http://www.medicalnewstoday.com/medicalnews.php?newsid=21087
I read her book, "The Magnesium Factor" and it's VERY convincing. Over 75 pages of medical studies as references, some of them her own research as that's been her focus for many years apparently. (Most are "abstract unavailable" on PudMed unfortuntately.)
Carolyn Dean, who is an M.D. and a naturopath, in "The Miracle of Magnesium" seems to stop just short of accusing cardiologists of malpractice in not routinely advising their patients about magnesium.
Magnesium is depleted by stress, by high fat/sugar/carb/protein diets, decreases with age.
Some studies re heart:
Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15466951&query_hl=13Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker. More recent work shows that Mg also acts as a statin.
Interactions of magnesium and potassium in the pathogenesis of cardiovascular disease.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6536839&query_hl=13The interactions of Mg and K in cardiovascular disease are diverse and complex. However, Mg deficiency and loss from the heart and arteries, caused e.g. by dietary deficiency or imbalance, or by diseases and their treatment, can contribute to cardiovascular damage, and to functional abnormalities. ... The heart, with its high metabolic activity, is particularly vulnerable to Mg deficiency or loss because of the importance of Mg in mitochondrial structure and enzymatic function. ... A high Ca/Mg ratio also predisposes to arterial spasms, and increases catecholamine release. Thus the arrhythmogenic potential of Mg deficiency can be related to imbalances between Mg and K or between Mg and Ca, or both. Electrical or K-induced catecholamine release is increased by a low Mg/Ca ratio, as are increased fatty acids and lipids and intravascular hypercoagulability.
Protective role of magnesium in cardiovascular diseases: a review.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12349904&query_hl=16
A considerable number of experimental, epidemiological and clinical studies are now available which point to an important role of Mg2+ in the etiology of cardiovascular pathology. In human subjects, hypomagnesemia is often associated with an imbalance of electrolytes such as Na+, K+ and Ca2+. Abnormal dietary deficiency of Mg2+ as well as abnormalities in Mg2+ metabolism play important roles in different types of heart diseases such as ischemic heart disease, congestive heart failure, sudden cardiac death, atheroscelerosis, a number of cardiac arrhythmias and ventricular complications in diabetes mellitus. Mg2+ deficiency results in progressive vasoconstriction of the coronary vessels leading to a marked reduction in oxygen and nutrient delivery to the cardiac myocytes. Numerous experimental and clinical data have suggested that Mg2+ deficiency can induce elevation of intracellular Ca2+ concentrations, formation of oxygen radicals, proinflammatory agents and growth factors and changes in membrane perrmeability and transport processes in cardiac cells.Role of magnesium and potassium in the pathogenesis of arteriosclerosis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6399344&query_hl=16Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid.
Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8867781&query_hl=30
The data indicate that Mg deficiency caused either by poor diet and/or errors in Mg metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Data from our laboratories and others indicate that reduction in extracellular and intracellular free Mg ions (Mg2+) can induce an entire array of pathophysiological phenomena known to be important in atherogenesis, that is, vasospasm, increased vascular reactivity, elevation in [Ca2+]i, formation of proinflammatory agents, oxygen radicals, platelet aggegation, reduction in cardiac bioenergetics, cardiac failure, oxidation of lipoproteins, gender-related modulation of endothelial-derived relaxing factor/NO, changes in membrane fatty acid saturation, changes in membrane plasmalogens and N-phospholipids (suggesting changes in intracellular phospholipid signals), and probably transcription factors.You can read what Dr. Atkins, who was a cardiologist, has to say about magnesium on this page: http://www.coldcure.com/html/dep.html#atkins
I know you're not really looking to add another supplement, but I think magnesium, especially magnesium orotate, would be well advised.
JL
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URL: http://www.dr-bob.org/babble/alter/20050924/msgs/562853.html