"beni" <benik@elisra.com> wrote in message

Hi Beni,
lots of recent studies support the broad anti-cancer benefits of
hi-dose vitamin D.  It's been debated extensively here on
sle over the last couple of years with no concensus about
just how much is optimum, but I believe most of the downside
risks can be obviated with concurrent vitamin K.  Hence I take
a lot.
Magnesium has even broader benefits (cardio-, genoprotective,
anti-glycation) with virtually no downside (except its laxative action).
It also compliments selenium (which I regard as *very* important).
From my files:
************************
Vitamin D may confer some protection against vitamin A toxicity.  Vitamin D
(which should really be classified as a hormone) may offer considerable
protection against cancer143, but it too can be toxic (1,000 IU (25ug) can
lead to hypercalcaemia), although magnesium144d, selenium144a and vitamin
K144b, 144c may protect against the hypercalcemia.
[143a] Vitamin D in preventive medicine: are we ignoring the evidence?
Zittermann A in Br J Nutr. 2003 May;89(5):552-72.  PMID: 12720576
"Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin
D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone
calcitriol. Calcitriol receptors are present in more than thirty different
tissues. Apart from the kidney, several tissues also possess the enzyme
1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate.
Serum levels of 25(OH)D are the best indicator to assess vitamin D
deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European
children and young adults often have circulating 25(OH)D levels in the
insufficiency range during wintertime. Elderly subjects have mean 25(OH)D
levels in the insufficiency range throughout the year. In institutionalized
subjects 25(OH)D levels are often in the deficiency range. There is now
general agreement that a low vitamin D status is involved in the
pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to
a disturbed muscle function. Epidemiological data also indicate a low
vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis,
inflammatory bowel diseases, hypertension, and specific types of cancer.
Some intervention trials have demonstrated that supplementation with vitamin
D or its metabolites is able: (i) to reduce blood pressure in hypertensive
patients; (ii) to improve blood glucose levels in diabetics; (iii) to
improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral
dose necessary to achieve adequate serum 25(OH)D levels is probably much
higher than the current recommendations of 5-15 microg/d."

[143b] An estimate of premature cancer mortality in the U.S. due to
inadequate doses of solar ultraviolet-B radiation.  Grant WB in Cancer. 2002
Mar 15;94(6):1867-75.  PMID: 11920550
"BACKGROUND: There are large geographic gradients in mortality rates for a
number of cancers in the U.S. (e.g., rates are approximately twice as high
in the northeast compared with the southwest). [..] solar UV-B radiation is
associated with reduced risk of cancer of the breast, colon, ovary, and
prostate as well as non-Hodgkin lymphoma. Eight additional malignancies were
found to exhibit an inverse correlation between mortality rates and UV-B
radiation: bladder, esophageal, kidney, lung, pancreatic, rectal, stomach,
and corpus uteri. [.] CONCLUSIONS: The results of the current study
demonstrate that much of the geographic variation in cancer mortality rates
in the U.S. can be attributed to variations in solar UV-B radiation
exposure. Thus, many lives could be extended through increased careful
exposure to solar UV-B radiation and more safely, vitamin D3
supplementation, especially in nonsummer months."

[143c] Why the optimal requirement for Vitamin D(3) is probably much higher
than what is officially recommended for adults.
Vieth R in J Steroid Biochem Mol Biol. 2004 May;89-90:575-9.  PMID: 15225842
"The physiologic range for circulating 25-hydroxyvitamin D3 [25(OH)D; the
measure of Vitamin D nutrient status] concentration in humans and other
primates extends to beyond 200nmol/L (>80ng/mL). This biologic "normal"
value is greater than current population norms for 25(OH)D. Concentrations
of 25(OH)D that correlate with desirable effects extend to at least
70nmol/L, with no obvious threshold. Randomized clinical trials using 20mcg
(800IU) per day of Vitamin D show that this suppresses parathyroid hormone,
preserves bone mineral density, prevents fractures, lowers blood pressure
and improves balance. Calcium absorption from diet correlates with 25(OH)D
in the normal range. Health effects of Vitamin D beyond osteoporosis are
mostly supported by the circumstantial evidence of epidemiologic studies and
laboratory research. These include prevention of cancer and the autoimmune
diseases, insulin-dependent diabetes and multiple sclerosis. One mcg per day
of Vitamin D(3) (cholecalciferol) increases circulating 25(OH)D by about
1nmol/L (0.4ng/mL). A recommended dietary allowance (RDA) is the long-term
daily intake level that meets the total requirements for the nutrient by
nearly all healthy individuals (it would presume no sunshine). If 70nmol/L
is regarded as a minimum desirable target 25(OH)D concentration, then
current recommendations of 15mcg per day do not meet the criterion of an
RDA."

[143d] Calcium and vitamin D. Diagnostics and therapeutics.  Holick MF in
Clin Lab Med. 2000 Sep;20(3):569-90.  PMID: 10986622
"Vitamin D is neither a vitamin nor a nutrient if adequate exposure to
sunlight is available to produce adequate quantities of vitamin D3 in the
skin. It is well known that an adequate supply of vitamin D, either from the
diet or from the skin, is important for maximum bone health throughout life.
The new revelation that 25(OH)D can be metabolized to 1,25(OH)2D in the
colon, prostate, and skin opens a new chapter in the vitamin D story. It is
quite possible that there are two levels of vitamin D sufficiency. One level
requires that the serum 25(OH)D levels be at least 20 ng/mL to satisfy the
body's requirement for the renal production of 1,25(OH)2D that regulates
calcium absorption, and bone calcium mobilization and bone mineralization.
The second level may need higher circulating levels of 25(OH)D for maximum
cellular health because of the conversion of 25(OH)D to 1,25(OH)2D in
extrarenal tissues, such as the prostate, colon, and skin."

[143e] Calcium and vitamin D. Their potential roles in colon and breast
cancer prevention.  Garland CF, Garland FC, Gorham ED in Ann N Y Acad Sci.
1999;889:107-19.  PMID: 10668487
"The geographic distribution of colon cancer is similar to the historical
geographic distribution of rickets. The highest death rates from colon
cancer occur in areas that had high prevalence rates of rickets--regions
with winter ultraviolet radiation deficiency, generally due to a combination
of high or moderately high latitude, high-sulfur content air pollution (acid
haze), higher than average stratospheric ozone thickness, and persistently
thick winter cloud cover. The geographic distribution of colon cancer
mortality rates reveals significantly low death rates at low latitudes in
the United States and significantly high rates in the industrialized
Northeast. The Northeast has a combination of latitude, climate, and air
pollution that prevents any synthesis of vitamin D during a five-month
vitamin D winter. Breast cancer death rates in white women also rise with
distance from the equator and are highest in areas with long vitamin D
winters. Colon cancer incidence rates also have been shown to be inversely
proportional to intake of calcium. These findings, which are consistent with
laboratory results, indicate that most cases of colon cancer may be
prevented with regular intake of calcium in the range of 1,800 mg per day,
in a dietary context that includes 800 IU per day (20 micrograms) of vitamin
D3. (In women, an intake of approximately 1,000 mg of calcium per 1,000 kcal
of energy with 800 IU of vitamin D would be sufficient.) In observational
studies, the source of approximately 90% of the calcium intake was vitamin
D-fortified milk. Vitamin D may also be obtained from fatty fish. In
addition to reduction of incidence and mortality rates from colon cancer,
epidemiological data suggest that intake of 800 IU/day of vitamin D may be
associated with enhanced survival rates among breast cancer cases."

[143f]  A protective role of dietary vitamin D3 in rat colon carcinogenesis.
Mokady E, Schwartz B, Shany S, Lamprecht SA in Nutr Cancer.
2000;38(1):65-73.   PMID: 11341047
"The aim of the present work was to gain insight into a putative anticancer
effect of dietary vitamin D3 (cholecalciferol) in a rat model of colon
carcinogenesis. Male rats were assigned to three different dietary groups.
The dietary regimens were based on a standard murine-defined diet (AIN-76A)
or a stress diet containing 20% fat, reduced Ca2+ concentration, a high
phosphorus-to-Ca2+ ratio, and either low or high vitamin D3 content.
Colorectal cancer was induced by administration of the procarcinogen
1,2-dimethylhydrazine (DMH). Blood Ca2+, 1,25-dihydroxyvitamin D3
[1,25(OH)2D3], and 25-hydroxyvitamin D3 [25(OH)D3] levels were measured in
DMH-treated rats and in respective weight- and age-matched dietary control
groups. Colonic epithelial proliferation was assessed by determining
thymidine kinase (TK) activity, bromodeoxyuridine (BrdUrd) incorporation
into crypt cell DNA, and the mean labeling index along the colonic crypt
continuum. Maintenance of rats on the stress diet either unmodified or
supplemented with vitamin D3 in the absence of carcinogen treatment provoked
a time-dependent rise in colonic TK activity and hyperproliferation of
colonic epithelium. DMH treatment of rats maintained on the standard diet
caused a marked increase in the proliferative indexes of colonic epithelium
and in expansion of the crypt proliferative compartment. TK activity and the
crypt mitotic zone were significantly augmented in the animal group fed the
stress diet. Supplementary vitamin D3 abrogated the stress diet-enhanced
colonic responses to the carcinogenic insult. Colon tumor multiplicity was
fourfold higher in animals fed the stress diet than in animals maintained on
a standard diet. The marked rise in colonic tumor multiplicity and
adenocarcinoma incidence in rats fed the stress diet was obliterated by
supplemental dietary vitamin D3. Cumulatively, the present results indicate
that dietary vitamin D3 impedes the neoplastic process in murine large
intestine and strengthen the view that inappropriate changes in dietary
components and micronutrients are contributory determinants of colorectal
cancer."

[143g]  Vitamin D3 is a potent inhibitor of tumor cell-induced angiogenesis.
Majewski S, Skopinska M, Marczak M, Szmurlo A, Bollag W, Jablonska S in J
Investig Dermatol Symp Proc. 1996 Apr;1(1):97-101.  PMID: 9627702
"Vitamin D3 derivative 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) exerts various
biological effects in cells that possess vitamin D3 receptor (VDR),
including enhancement of cell differentiation and inhibition of cell
proliferation. These activities of 1,25(OH)2D3 might be responsible for its
anti-neoplastic effects, as shown in various experimental systems. The aim
of this study was to compare the anti-angiogenic activity of 1,25(OH)2D3,
retinoids, and interleukin-12 (IL-12) in an experimental tumor cell-induced
angiogenesis assay in mice. Tumor cell-induced angiogenesis assay was
performed in x-ray immunosuppressed BALB/c mice by intradermal injections of
human tumor cell lines of different origin. The injections resulted within 3
d in a local formation of new blood vessels, and the intensity of
angiogenesis correlated with the number of injected cells. Systemic
treatment of the mouse recipients with 1,25(OH)2D3 significantly decreased
angiogenesis, comparable to the effect of retinoids (all-trans retinoic acid
[RA], 9-cis RA and 13-cis RA) and of IL-12. In vitro preincubation of the
cells with all compounds (except IL-12) led to the inhibition of their
angiogenic capability in vivo. Moreover, combination of 1,25(OH)2D3 and
retinoids resulted in a synergistic inhibition of angiogenesis. The results
strongly suggest that anti-angiogenic compounds with relatively low toxicity
(e.g., 1,25(OH)2D3, retinoids, and IL-12) and their combinations could be
beneficial in the treatment of some angiogenesis-associated malignancies."

[144a] [The protective effect of sodium selenite and vitamin E in
hypervitaminosis D]  Sokolova SV, Spirichev VB, Kudrin AN in Farmakol
Toksikol. 1977 Jan-Feb;40(1):67-9.  PMID: 300690
"Vitamin D2 (160 000-240 000 IU/kg) produced during 5 days pronounced
hypercalciemia and metastatic calcification of internal organs. Subcutaneous
injection of sodium selenite (10 mg/kg) brought down the level of calcium in
the blood plasma and decreased calcification of internal organs. Conjoint
introduction of sodium selenite (30 gamma/kg) and of vitamin "E" (50 mg/kg)
lowered the aortal calcinosis by 54 per cent, of the lung--by 93, of the
heart--by 86 and of the kidney--by 96 per cent."

[144b] Effect of continuous combined therapy with vitamin K(2) and vitamin
D(3) on bone mineral density and coagulofibrinolysis function in
postmenopausal women.  Ushiroyama T, Ikeda A, Ueki M in Maturitas 2002 Mar
25;41(3):211-21   PMID: 11886767

OBJECTIVES: To investigate the therapeutic effect of combined use of vitamin
K(2) and D(3) on vertebral bone mineral density in postmenopausal women with
osteopenia and osteoporosis. SUBJECTS AND METHODS: We enrolled 172 women
with vertebral bone mineral density <0.98 g/cm(2) (osteopenia and
osteoporosis) as measured by dual-energy X-ray absorptiometry. In this
study, we employed the criteria for diagnosis of osteopenia and osteoporosis
using dual energy X-ray absorptiometry proposed by the Japan Society of Bone
Metabolism in 1996. Subjects were randomized into four groups (each having
43 subjects in vitamin K(2) therapy group, vitamin D(3) therapy group,
vitamin K(2) and D(3) combined therapy group, or a control group receiving
dietary therapy alone) and treated with respective agents for 2 years, with
bone mineral density was measured prior to therapy and after 6, 12, 18, and
24 months of treatment. The bone metabolism markers analyzed were serum type
1 collagen carboxyterminal propeptide (P1CP), serum intact osteocalcin, and
urinary pyridinoline. Tests of blood coagulation function consisted of
measurement of activated partial thromboplastin time (APTT) and analysis of
concentrations of antithrombin III (AT III), fibrinogen, and plasminogen.
RESULTS: Combined therapy with vitamin K(2) and D(3) for 24 months markedly
increased bone mineral density (4.92 +/- 7.89%), while vitamin K(2) alone
increased it only 0.135 +/- 5.44%. The bone markers measured, revealed
stimulation of both bone formation and resorption activity. We observed an
increase in coagulation and fibrinolytic activity that was within the normal
range, suggesting that balance was maintained in the
fibrinolysis-coagulation system. CONCLUSIONS: Continuous combination therapy
with vitamin K(2) and D(3) may be useful for increasing vertebral bone mass
in postmenopausal women. Furthermore, the increase in coagulation function
observed during this therapy was within the physiological range, and no
adverse reactions were observed.

[144c] Effect of vitamin K2 on experimental calcinosis induced by vitamin D2
in rat soft tissue.  Seyama Y, Horiuch M, Hayashi M, Kanke Y in Int J Vitam
Nutr Res 1996;66(1):36-8  PMID: 8698544
"The effect of vitamin K2 on calcium (Ca) and inorganic phosphorus (P)
levels in the aorta and kidney obtained from experimental calcinosis induced
by vitamin D2(2.5 x 10(5) I.U./ kg b.w.) of male rats was investigated. A
high dose of vitamin K2 (100 mg/kg b.w.) inhibited the increase in the
aortic Ca and P or in the renal Ca and P induced by vitamin D2, and a low
dose of vitamin K2 (10 mg/kg b.w.) showed the same tendency, but the degree
of the efficacy was small. It may be suggested that a high dose of vitamin
K2 suppressed experimental calcification of soft tissues induced by vitamin
D2. Therefore, a pharmacological dose of vitamin K2 might have a usefulness
for the prevention and treatment of arteriosclerosis with calcification."
[Dosed over a period of 6 weeks: human equivalent (after adjusting for
metabolic differences) = 1.2 gm/d of K2]

[144d] Effects of a dietary magnesium deficiency and excess vitamin D3 on
swine coronary arteries.  J Am Coll Nutr. 1990 Apr;9(2):155-63 by Ito M, Cho
BH, Kummerow FA.  PMID: 2159962

The effect of a moderate magnesium (Mg) deficiency on coronary arteries of
61 swine, fed various levels of vitamin D3, was studied by light and
electron microscopy. The effect of subnormal Mg intake on vitamin D3-induced
intimal lesions of the arteries showed a trend towards increased damage. The
degree of cell degeneration and intimal thickening, which was induced by
high vitamin D intakes, was as great in swine whose diet was low in Mg and
moderately high in vitamin D as it was in those on twice as much vitamin D.
Also, the degree of arterial calcification was intensified by inadequate Mg
intake at the two higher vitamin D intakes. Present findings indicate that
suboptimal dietary Mg, in combination with an excess of vitamin D, has an
additive effect in the initiation of ultrastructural changes in the coronary
arteries. Extension of the study is indicated to ascertain the extent to
which further reduction of Mg intake can potentiate vitamin-D-induced
coronary lesions.

**************************
Magnesium ions are essential for the operation of kinases, enzymes that use
a magnesium-ATP complex as a phosphoryl-group donating substrate, and are
critical in maintaining genomic stability38d,f.  Magnesium deficient animals
show signs of premature aging38b-d.  In humans magnesium has been
successfully used to treat kidney stones, high blood pressure, migraine,
coronary artery spasm, irregular heart rhythms and diabetes.  Levels of
magnesium in drinking water correlate with longevity via decreased
cardiovascular disease38a.  Most people are magnesium deficient; their diets
don't even supply the RDA of magnesium; it seems sensible to supplement with
magnesium to stave off premature aging.  Magnesium synergises well with
vitamin B6 (pyridoxine).86

Selenium's ability to reduce cancer incidence suggests the selenoenzymes may
also provide some genomic protection.15, 16, 54, 71

Summary: Vitamins B3 (niacin) and B9 (folate) can provide considerable
protection against DNA damage and errors.  Since almost all adult cancers
are the result of DNA damage and errors then these vitamins may prevent many
cancers.  Magnesium and selenium are also important for genomic stability.
If DNA damage is implicated in aging then selenium, magnesium and vitamin B3
(niacin) and B9 (folate) may be essential to help ward off premature aging.

[38a] Chemical qualities of water that contribute to human health in a
positive way.  Hopps HC, Feder GL in Sci Total Environ. 1986 Oct;54:207-16.
PMID: 3810127

[38b] Magnesium status and ageing: an update.  Durlach J, Bac P, Durlach V,
Rayssiguier Y, Bara M, Guiet-Bara A in Magnes Res 1998 Mar;11(1):25-42
PMID: 9595547

[38c] Magnesium and ageing. II. Clinical data: aetiological mechanisms and
pathophysiological consequences of magnesium deficit in the elderly.
Durlach J, Durlach V, Bac P, Rayssiguier Y, Bara M, Guiet-Bara A in Magnes
Res 1993 Dec;6(4):379-94  PMID: 8155490

[38d] Role of magnesium in genomic stability.  Hartwig A. in Mutat Res 2001
Apr 18;475(1-2):113-21  PMID: 11295157

[38e] Oral Mg(2+) supplementation reverses age-related neuroendocrine and
sleep EEG changes in humans.  Held K, Antonijevic IA, Kunzel H, Uhr M,
Wetter TC, Golly IC, Steiger A, Murck H in Pharmacopsychiatry 2002
Jul;35(4):135-43   PMID: 12163983
"Our results suggest that [720mg/d] Mg(2+) partially reverses sleep EEG and
nocturnal neuroendocrine changes occurring during aging."

[38f]  Magnesium intake in relation to risk of colorectal cancer in women.
Larsson SC, Bergkvist L, Wolk A in JAMA. 2005 Jan 5;293(1):86-9.  PMID:
15632340
"This population-based prospective study suggests that a high magnesium
intake may reduce the occurrence of colorectal cancer in women."

[128a] Magnesium supplementation reduces development of diabetes in a rat
model of spontaneous NIDDM.  Balon TW, Gu JL, Tokuyama Y, Jasman AP, Nadler
JL in Am J Physiol 1995 Oct;269(4 Pt 1):E745-52   PMID: 7485490
"We examined the effects of a magnesium-supplemented (Mg-S) diet in the male
obese Zucker diabetic fatty rat, a model of non-insulin-dependent diabetes
mellitus (NIDDM). Obese rats were maintained on either a control (0.20% Mg)
or magnesium-supplemented (Mg-S; 1% Mg) diet for 6 wk beginning at 6 wk of
age. The rats maintained on the Mg-S diet had markedly lower fasting and
fed-state blood glucose concentrations and an improved glucose disposal. By
12 wk of age, all of the eight animals on the control diet became diabetic,
whereas diabetes developed in only one of eight animals on the Mg-S diet.
Insulin and C-peptide concentrations, in addition to pancreatic GLUT-2 and
insulin mRNA expression, were higher in the male obese Mg-S rats than in
their control-fed counterparts. A subgroup of rats on the control diet with
established diabetes was switched to a Mg-S diet for an additional 4 wk. The
Mg-S diet did not reverse diabetes once already established. These data
indicate that an increased dietary Mg intake in male obese rats prevents
deterioration of glucose tolerance, thus delaying the development of
spontaneous NIDDM."

[128b] Synergistic interaction of magnesium and vanadate on glucose
metabolism in diabetic rats.  Matsuda M, Mandarino L, DeFronzo RA in
Metabolism 1999 Jun;48(6):725-31  PMID: 10381146
"Based on these results, MgV is superior to either V alone or Mg alone in
improving insulin sensitivity and glycogen synthesis in diabetic rats."

[128c] The effect of magnesium supplementation in increasing doses on the
control of type 2 diabetes.  Lima Mde L, Cruz T, Pousada JC, Rodrigues LE,
Barbosa K, Cangucu V in Diabetes Care 1998 May;21(5):682-6   PMID: 9589224
"In the placebo and in the 20.7 mmol [0.5g] Mg groups, neither a change in
plasma and intracellular levels nor an improvement in glycemic control were
observed. Replacement with 41.4 mmol [1g] Mg tended to increase plasma,
cellular, and urine Mg and caused a significant fall (4.1 +/- 0.8 to 3.8 +/-
0.7 mmol/l) in fructosamine (normal, 1.87-2.87 mmol/l). CONCLUSIONS: Mg
depletion is common in poorly controlled patients with type 2 diabetes,
especially in those with neuropathy or coronary disease. More prolonged use
of Mg in doses that are higher than usual is needed to establish its routine
or selective administration in patients with type 2 diabetes to improve
control or prevent chronic complications."

[128d] Improved insulin response and action by chronic magnesium
administration in aged NIDDM subjects.  Paolisso G, Sgambato S, Pizza G,
Passariello N, Varricchio M, D'Onofrio F in Diabetes Care 1989
Apr;12(4):265-9   PMID: 2651054
"In eight aged non-insulin-dependent diabetes mellitus (NIDDM) subjects,
insulin response and action were studied before and after chronic magnesium
supplementation (2 g/day) to diet. [.] In conclusion, our data suggest that
NIDDM subjects may benefit from therapeutic chronic administration of
magnesium salts."

[128e] Daily magnesium supplements improve glucose handling in elderly
subjects.  Paolisso G, Sgambato S, Gambardella A, Pizza G, Tesauro P,
Varricchio M, D'Onofrio F in Am J Clin Nutr 1992 Jun;55(6):1161-7   PMID:
1595589
"aged subjects were enrolled in a double-blind, randomized, crossover study
in which placebo (for 4 wk) and chronic magnesium administration (CMA) (4.5
g/d for 4 wk) were provided. [.] CMA vs placebo significantly increased
erythrocyte magnesium concentration and improved insulin response and
action. Net increase in erythrocyte magnesium significantly and positively
correlated with the decrease in erythrocyte membrane microviscosity and with
the net increase in both insulin secretion and action. In aged patients,
correction of a low erythrocyte magnesium concentration may allow an
improvement of glucose handling."

[128f] Magnesium Intake and Risk of Type 2 Diabetes in Men and Women.
Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, Manson JE, Hu FB
in Diabetes Care. 2004 Jan;27(1):134-140.  PMID: 14693979
"Our findings suggest a significant inverse association between magnesium
intake and diabetes risk."

[128g]  Role of magnesium in insulin action, diabetes and cardio-metabolic
syndrome X.  Barbagallo M, Dominguez LJ, Galioto A, Ferlisi A, Cani C, Malfa
L, Pineo A, Busardo' A, Paolisso G. in Mol Aspects Med. 2003
Feb-Jun;24(1-3):39-52.  PMID: 12537988
"By contrast, in NIDDM patients daily Mg administration, restoring a more
appropriate intracellular Mg concentration, contributes to improve
insulin-mediated glucose uptake. The benefits deriving- from daily Mg
supplementation in NIDDM patients are further supported by epidemiological
studies showing that high daily Mg intake are predictive of a lower
incidence of NIDDM. In conclusion, a growing body of studies suggest that
intracellular Mg may play a key role in modulating insulin-mediated glucose
uptake and vascular tone. We further suggest that a reduced intracellular Mg
concentration might be the missing link helping to explain the
epidemiological association between NIDDM and hypertension."

****************************
Selenium is toxic in the milligram range, with claims for the toxic starting
level between 900ug/d73 to 6000ug/d72a.  The organically-bound forms
(especially selenomethionine72c,d) are safer and perhaps more bioactive than
the inorganic forms of selenium (e.g. selenite or selenate72a).  Concurrent
magnesium supplementation is advisable since magnesium may provide some
protection against selenium toxicity45a.
[45a] Effect of dietary selenium and magnesium on human mammary tumor growth
in athymic nude mice.  Yan L, Boylan LM, Spallholz JE in Nutr Cancer
1991;16(3-4):239-48  PMID: 1775386
"Low dietary Mg also resulted in an apparent increase in Se toxicity in
these animals."

***************************
Cheers,
Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm

Michael,

Thanks for all the good info, I appreciate you taking the time to
provide it.

I'm curious how you buy your supplements, and who you buy them from?
I'm looking for the most economical way to do this.  Obviously, I get
the LE Mix and the booster from LEF.  Some of the others are NOW brand,
from a local health food store ... but, that is *not* cheap.  Some I
buy from Vitamin World, and one or two from GNC.  So yeah, I'm buying
mostly retail.  :)

Are many of the things you take in powder form?

Thanks again!

James