Calcium, Osteoporosis & Arteriosclerotic Plaque

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Calcium & Arteriosclerotic Plaque

 

In order to absorb calcium, the body needs comparable amounts

of another *mineral* element, magnesium. Milk and dairy products

contain only small amounts of magnesium.Without the presence of *magnesium*, the

body only absorbs 25 percent of the available calcium content.

The remainder of the calcium spells trouble. Without the accompanying

magnesium, excess calcium is utilized by the body in *injurious* ways.

 

The body uses calcium to build the mortar on arterial walls which becomes

atherosclerotic plaques. Excess calcium is converted by the kidneys into painful

stones which grow in size like pearls in oysters, blocking our urinary tracts.

Excess calcium contributes to arthritis; painful calcium buildup

often is manifested as arthritis or gout.

 

The USDA has formulated a chart of recommended daily intakes of

vitamins and minerals.

The term that FDA uses is Recommended Daily Allowance (RDA).

The RDA for calcium is 1000 mg.

The RDA for magnesium is 750 mg.

 

Society stresses the importance of calcium, but rarely magnesium.

Yet, *magnesium* is vital to " enzymatic " activity.

 

In addition to insuring proper absorption of calcium, magnesium is

critical to proper neural and muscular function and to maintaining

proper *pH* balance* in the body.

 

Magnesium, along with vitamin B6 (pyridoxine), helps to dissolve

calcium phosphate stones which often accumulate from supplemental calcium

and 'excesses' of dairy foods.

 

Good sources of magnesium include green beans and other beans, green

leafy vegetables like kale and collards, organic whole grains

and fresh squeezed orange juice and other fresh squeezed fruit juices.

 

Non-dairy sources of calcium include green leafy vegetables,

almonds, asparagus, broccoli,cabbage, oats and oat bran, beans,

parsley, sesame seeds and organic tofu.

 

Osteoporosis is NOT a problem that should be associated with

lack of calcium *intake*. Osteoporosis results from calcium *loss*.

 

The massive amounts of protein, phosphoric acid, methionine,

and 'arachidonic' acids which are found in milk result

in a *50 percent* *loss* of calcium in the *urine*. In other words, by doubling

your milk intake there will be a *loss* of 1-1.5 percent in *skeletal* *mass*

per year in menopausal women.

 

The calcium contained in leafy green vegetables is more *easily*

*absorbed* than the calcium in milk.

 

If a postmenopausal woman loses 1-1.5 percent bone mass per year,

what will be the effect after 20 years? When osteoporosis occurs levels of

calcium *excreted* from the bones into the blood are high.

 

Milk only adds to these high levels of calcium which is *excreted*

or used by the body to add to damaging atherosclerosis, gout, kidney

stones, etc.

 

WHO GETS BONE DISEASE?

 

Why do nations with the highest rates of bone disease also have the

highest milk consumption rates?

 

The highest rates of osteoporosis are to be found in Denmark,

Holland,Norway, and Sweden.

 

We are told to consume 1000 milligrams per day of calcium. Inuit

Eskimos consume 3500 milligrams of calcium each day, and by age 40

are crippled.

 

THE KEY TO OSTEOPOROSIS

It's not how much calcium you eat. It's how much calcium you prevent

from leaving your bones.

 

WHY DOES CALCIUM LEAVE BONES?

 

There are 28 amino acids in nature. The human body can manufacture

19 of them. The other nine are called " essential. " We must get them

from the foods we eat.

 

One of those " essential " aminos is methionine--

 

One needs methionine for many human metabolic functions including

digestion, detoxification of heavy metals, and muscle metabolism.

However, an excess of methionine can be toxic.

 

Methionine = C-5, H-11, NO, S

 

Methionine is a good source for sulfur.

That's the problem. Eat foods containing too much methionine, and

your blood will become acidic. The sulfur converts to sulfates and

weak forms of sulphuric acid.

 

In order to neutralize the acid, in its wisdom, the body leeches

calcium from bones.

 

" Dietary protein increases production of acid in the blood which can

be neutralized by calcium mobilized from the skeleton. "

American Journal of Clinical Nutrition, 1995; 61 (4)

 

Animal proteins (dairy,red meat) contain more methionine than plant

proteins. Let's compare cow's milk to non-gmo soymilk:

Methionine in 100 grams of soymilk: .040 grams

Methionine in 100 grams of whole milk: .083 grams

Methionine in 100 grams of skim milk: .099 grams

 

Now, let's compare 100 gram portions of non-gmo tofu to meat: (All

ofthe meat products are lean and without skin)

 

Silken soft tofu: .074 grams

Hamburger: .282 grams

Roast ham: .535 grams

Swiss cheese .784 grams

Roast chicken: .801 grams

 

 

In 1988, N.A. Breslau and colleagues identified the relationship

betweenprotein-rich diets and calcium metabolism, noting that protein

causedcalcium loss. His work was published in the Journal of Clinical

Endocrinology (1988;66:140-6).

 

A 1994 study published in the American Journal of Clinical Nutrition

(Remer T, Am J Clin Nutr 1994;59:1356-61)

found that animal protein causes calcium to be 'leached' from the

bonesand excreted in the urine.

 

MORE SUPORTING EVIDENCE:

 

" Osteoporosis is caused by a number of things, one of the most

important being too much protein. "

Science 1986;233(4763)

---

- " Even when eating 1,400 mg of calcium daily, one can lose up to 4%

of his or her bone mass each year while consuming a high-protein

diet. "

 

American Journal of Clinical Nutrition 1979;32(4)

 

----------------------------

" Increasing one's protein intake by 100% may cause calcium *loss* to

double. " Journal of Nutrition, 1981; 111 (3)

 

---

 

" The average man in the US eats 175% more protein than the

recommended daily allowance and the average woman eats 144% more. "

 

Surgeon General's Report on Nutrition and Health, 1988

 

---

" Consumption of dairy products, particularly at age 20 years, were

associated with an increased risk of hip fractures... metabolism of

dietary protein causes increased urinary excretion of calcium. "

American Journal of Epidemiology 1994;139

 

 

---

The Framingham Heart Study is the largest and most exciting heart

study in the history of mankind. Some of the highlights of this exhaustive

50year study:

 

In 1960, Cigarette smoking was found to increase the risk of heart

disease.

 

In 1970, high blood pressure was found to increase the risk of

stroke. During the 1980's, high levels of HDL cholesterol were found

to reduce risk of death from heart disease.

 

In the 1990's, homocysteines were identified as key factors in heart

attack deaths.

 

*Homocysteines* are normal breakdown products of " methionine " and

are believed to exert a number of toxic effects in the body.

 

I recently spoke with the senior investigator of the Framinham heart study,

WilliamCastelli, M.D. (E-mail: willi-)

 

Dr. Castelli has suggested that an elevated homocysteine level is a risk factor

for

heart disease. The first evidence of this was published in the

AmercianJournal of Cardiology (Glueck, 1995;75:132 & shy;6).

 

Two recent publications resulting from Framingham data indicate a

positive correlation between cardiovascular disease mortality and blood

serum levels of *homocysteine*.

 

Bostom AG, et. al, Nonfasting plasma total homocysteine levels and

all-cause and cardiovascular disease mortality in elderly Framingham

menand women. Arch Intern Med 1999; 159:1077-1080. Bostom A.G., et. al,

Nonfasting plasma total homocysteine levels and

stroke incidence in elderly persons: the Framingham Study. Ann

InternMed 131[5], 352-355, 1999.

---

Post subject: Physiochemical principles of cardiovascular calcification.

 

--

 

Physiochemical principles of cardiovascular calcification.

 

Tomazic BB.

 

OBJECTIVES: The objectives of this review article are to provide detailed

physicochemical information on the nature of pathological cardiovascular

deposits, PCD, isolated from different sites of the human cardiovascular system.

 

In order to help to understand the complex mechanism of the formation of PCD,

special emphasis is focused on the attempt to recognize early precursor(s) of

PCD by utilizing combined in vivo and in vitro studies.

 

BACKGROUND: The common idea is that PCD is hydroxyapatite (HAP), Ca5(PO4)3OH;

however, this is questionable and deserves critical evaluation.

 

METHODS: After isolation of PCD, deproteination followed, producing pure

inorganic fraction of deposits that were subject to chemical analyses, x-ray

diffraction (XRD), FT-IR spectroscopy, optical, scanning electron microscopy

(SEM), polarizing microscopy, energy dispersive x-ray micro-analyses (EDS) and

thermodynamic solubility measurements. The same methods were used to

characterize the in vitro and in vivo formed calcific deposits.

 

RESULTS: The results of chemical analyses provided essential information that

PCD contained significant organic fraction; inorganic fraction appears to be

bioapatite, corresponding to defect HAP with substantial macro incorporation of

sodium, magnesium, carbonate and fluoride. Structural XRD data show apatitic

pattern; however, variable crystallinity of PCD suggests that crystallization is

a time and flow dynamics-dependent process. Critical thermodynamic solubility

measurements unequivocally prove that PCD are significantly more soluble than

HAP.

 

CONCLUSIONS: The PCDs are morphologically and chemically heterogeneous products

which may be a consequence of time-dependent hydrolytic transformation of

precursors that may include amorphous calcium phosphate and octacalcium

phosphate (OCP) Ca4H(PO4)3.

 

Publication Types:

Review

Review, Tutorial

 

PMID: 11374037 [PubMed - indexed for MEDLINE]

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

1374037 & dopt=Abstract-------

 

--\

-----Post subject: Lipid oxidation products have opposite effects

on calcifying vascular cell and bone cell differentiation

 

-

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=9\

108780 & dopt=Abstract

 

A possible explanation for the paradox of arterial calcification in osteoporotic

patients.

 

Parhami F, Morrow AD, Balucan J, Leitinger N, Watson AD, Tintut Y, Berliner JA,

Demer LL.

 

Department of Medicine, University of California, Los Angeles School of

Medicine, USA. fparhami

 

Atherosclerotic calcification and osteoporosis often coexist in patients,

yielding formation of bone mineral in vascular walls and its simultaneous loss

from bone.

 

To assess the potential role of lipoproteins in both processes, we examined the

effects of minimally oxidized low-density lipoprotein (MM-LDL) and several other

lipid oxidation products on calcifying vascular cells (CVCs) and bone-derived

preosteoblasts MC3T3-E1. In CVCs, MM-LDL but not native LDL inhibited

proliferation, caused a dose-dependent increase in alkaline phosphatase

activity, which is a marker of osteoblastic differentiation, and induced the

formation of extensive areas of calcification.

 

 

Similar to MM-LDL, oxidized

1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC) and the

isoprostane 8-iso prostaglandin E2 but not PAPC or isoprostane 8-iso

prostaglandin F2 alpha induced alkaline phosphatase activity and differentiation

of CVCs.

 

In contrast, MM-LDL and the above oxidized lipids inhibited differentiation of

the MC3T3-E1 bone cells, as evidenced by their stimulatory effect on

proliferation and their inhibitory effect on the induction of alkaline

phosphatase and calcium uptake.

 

These results suggest that specific oxidized lipids may be the common factors

underlying the pathogenesis of both atherosclerotic calcification and

osteoporosis.

 

PMID: 9108780 [PubMed - indexed for MEDLINE]

_________________

 

JoAnn Guest

mrsjoguest

DietaryTipsForHBP

http://www.geocities.com/mrsjoguest

 

 

 

 

 

 

 

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