Part I.
While I don't pretend to be a magnesium scientist and cannot hope, in one post, to point readers to the whole of magnesium research (much of which assumes a basic understanding of biochemistry), I can point to a few review papers and studies for further edification on the various points I've made.
(I use sequential numbers below to separate the studies. They do not correlate to my points in the previous post.)
I offer these studies simply as a courtesy. I do not consider it my job, as a layperson, to educate physicians about the importance of understanding magnesium or to cite chapter and verse as to the basics.
It is my firm understanding, based on reading through the science and being familiar with how pharmaceutical studies are conducted -- not to mention the narrow, disconnected focus that scientific researchers can bring to any given subject -- that we must approach these wholesale supplementations with calcium extremely cautiously. The risks are profound and surely outweigh any need to be "right."
We cannot extrapolate widely from narrow-focus studies that examine, for example, only bone density. We must look at the long-range and systemic effect of the over-abundance or deficiency of these minerals, which affect every cell in the body. And we also must be aware of the various lifestyle issues (alcohol consumption, diet, even the "hardness" of the water in a patient's geographic area) that affect these variables.
1.
(I can't find the link for this paper but will be happy to send the PDF to you if you can't find it in a literature search.)
Review paper by USC's Robert K. Rude, MD:
"Clinical Review Magnesium Deficiency: A Cause of Heterogenous Disease in Humans"
JOURNAL OF BONE AND MINERAL RESEARCH
Volume 13, Number 4, 1998
2.
Skeletal and hormonal effects of magnesium deficiency.
Rude RK, Singer FR, Gruber HE.
USC Keck School of Medicine, Los Angeles, CA, USA
J Am Coll Nutr. 2009 Apr;28(2):131-41.
http://tinyurl.com/y8bezen
Excerpt:
Magnesium (Mg) is the second most abundant intracellular cation where it plays an important role in enzyme function and trans-membrane ion transport. Mg deficiency has been associated with a number of clinical disorders including osteoporosis. Osteoporosis is common problem accounting for 2 million fractures per year in the United States at a cost of over $17 billion dollars.
The average dietary Mg intake in women is 68% of the RDA, indicating that a large proportion of our population has substantial dietary Mg deficits. The objective of this paper is to review
the evidence for Mg deficiency-induced osteoporosis and potential reasons why this occurs, including a cumulative review of work in our laboratories and well as a review of other published studies linking Mg deficiency to osteoporosis.
Epidemiological studies have linked dietary Mg deficiency to osteoporosis. As diets deficient in Mg are also deficient in other nutrients that may affect bone, studies have been carried out with select dietary Mg depletion in animal models. Severe Mg deficiency in the rat (Mg at 0.0002% of total diet; normal 0.05%) causes impaired bone growth, osteopenia and skeletal fragility. This degree of Mg deficiency probably does not commonly exist in the human population. We have therefore induced dietary Mg deprivation in the rat at 10%, 25% and 50% of recommended nutrient requirement. We observed bone loss, decrease in osteoblasts, and an increase in osteoclasts by histomorphometry. Such reduced Mg intake levels are present in our population. We also investigated potential mechanisms for bone loss in Mg deficiency. Studies in humans and and our rat model demonstrated low serum parathyroid hormone (PTH) and 1,25(OH)2-vitamin D levels, which may contribute to reduced bone formation. It is known that cytokines can increase osteoclastic bone resorption. Mg deficiency in the rat and/or mouse results in increased skeletal substance P, which in turn stimulates production of cytokines.
With the use of immunohistocytochemistry, we found that Mg deficiency resulted in an increase in substance P, TNF and IL1 . Additional studies assessing the relative presence of receptor activator of nuclear factor kB ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), found a decrease in OPG and an increase in RANKL favoring an increase in bone resorption.
These data support the notion at dietary Mg intake at levels not uncommon in humans may perturb bone and mineral metabolism and be a risk factor for osteoporosis.
CONTINUED
I'm starting to wonder if modern guidelines on calcium supplementation, especially in pregnant women, are contributing to higher rates of autism, not to mention other neurocognitive issues.