Re: Potassium citrate?On Tue, 09 Jan 2007 03:02:10 -0600, Cyli <cylise@gmail . com > wrote:
>On Tue, 9 Jan 2007 08:17:03 +0200, "Juhana Harju"
><spamshantigiriorama.removespam@gmail . com > wrote:
>
>>Cyli wrote:
>
>>: I don't know of any particular reason potassium citrate would be all
>>: that superiour to potassium chloride or potassium tartrate.
>>
>>You are not well informed. The reason why potassium citrate works in
>>osteoporosis is the fact that it provides an alkaline source which
>>counteracts the highly prevalent low grade metabolic acidosis which in turn
>>leads to to slow leach of calcium and magnesium from the skeleton. Potassium
>>chloride does not provide an alkaline source of this mineral but potassium
>>citrate does. This is the reason to use potassium citrate.
>>
>>There is a recent study about this.
>>
>> * w w w .newswise . com /articles/view/524164/
>>
>> * tinyurl . com /zy7lg
>
>
>Interesting. First thing I've seen that goes into acid / alkaline
>balance that has any really observed results.
pH of the blood is tightly regulated. The normal pH of the human
arterial blood is 7.40, so it's slightly alkaline (7.0 is neutral). In
the venous blood it is just a bit lower because of the higher
concentration of the carbon dioxide in it. Intracellular pH values are
lower than those of the extracellular fluid and range from 6.8 to 7.3
depending on the tissue and its metabolic rate.
When arterial pH is below 7.40, the state is called
acidosis and when above it, it is called alkalosis.
Acidosis and alkalosis are both classified as either metabolic or
respiratory, depending on whether it is bicarbonate (HCO3-)
(metabolic) or carbon dioxide (pCO2) (respiratory) that primarily
deviates from the normal range in blood. In metabolic acidosis HCO3-
and thus plasma pH (hydrogen concentration) fall, in alkalosis they
rise. In respiratory alkalosis pCO2 value and thus the carbonic acid
concentration falls and pH rises and vice versa in respiratory
acidosis.
The most common imbalance in the acid-base balance in the
industrialized countries is a mild chronic metabolic acidosis caused
by the diet rich in acid producing foods. The typical American diet
produces after metabolism approximately 100 meq of acid every day.
This kind of a diet has been proved to cause aciduria and calciuria as
a consequence of acidosis and thus a loss of total calcium of the
body.
Normally the kidneys get rid of the extra acid, but the acid load may
be too large for kidneys to handle, especially, when we get older and
the performance of the kidneys is gradually reduced.
Over 23 years ago Bushinsky et al. showed in the study
Bushinsky DA, Krieger NS, Geisser DI, Grossman EB, Coe FL.
Effects of pH on bone calcium and proton fluxes in vitro.
Am J Physiol. 1983 Aug;245(2):F204-9.
PMID: 6881337
< * ajprenal.physiology.org/cgi/content/abstract/245/2/F204>
that in a laboratory test (in vitro) calcium flows out of bone (in
this test the cultured neonatal mouse's dome of the skull (calvaria)),
when the culture medium's ph wis < 7.40, and back to the bone when pH
is > 7.40. Below the abstract of the study
"Bone mineral is thought to decompose during acute and chronic
metabolic acidosis and thereby contribute to buffering of the acid
load. We cultured neonatal mouse calvariae for 3 h and found
calcium efflux from bone when the medium pH was below 7.40, calcium
influx into bone when the pH was above 7.40, and no net flux at pH
7.40. The calcium flux varied to the same extent when medium pH was
altered by a primary change in the medium bicarbonate concentration
or in the partial pressure of carbon dioxide. Calcium and proton
fluxes were inversely correlated (r = -0.713, P less than 0.001),
and the slope of the linear regression indicated that between 16
and 21 neq of proton entered the calvariae in exchange for each neq
of calcium that left. In 24-h cultures, acid medium also caused net
calcium efflux from bone, and alkaline medium caused net influx.
PTH increased calcium efflux at acid but not at alkaline medium pH.
Sodium azide resulted in net influx of calcium into bone at all
values of medium pH. Calcium release by cultured calvariae in
response to low medium pH is associated with proton buffering; over
3 h the stoichiometry indicates that little buffering is due to the
dissolution of calcium-containing crystals. Effects of medium pH on
calcium release are amplified by PTH, and calcium efflux can be
prevented by the metabolic inhibitor sodium azide."
Potassium citrate and potassium bicarbonate are alkaline supplements,
which have been shown to eliminate or reduce the acid overload caused
by the typical western diet, reduce urinary calcium, increase bone
mass and improve skeletal metabolism. Below references and links to
some studies related to these supplements:
Jehle S, Zanetti A, Muser J, Hulter HN, Krapf R.
Partial Neutralization of the Acidogenic Western Diet with Potassium
Citrate Increases Bone Mass in Postmenopausal Women with Osteopenia.
J Am Soc Nephrol. 2006 Oct 11; [Epub ahead of print]
PMID: 17035614 [PubMed - as supplied by publisher]
< * jasn.asnjournals.org/cgi/content/abstract/ASN.2006030233v1>
Sakhaee K, Maalouf NM, Abrams SA, Pak CY.
Effects of potassium alkali and calcium supplementation on bone
turnover in postmenopausal women.
J Clin Endocrinol Metab. 2005 Jun;90(6):3528-33. Epub 2005 Mar 8.
PMID: 15755853 [PubMed - indexed for MEDLINE]
< * jcem.endojournals.org/cgi/content/full/90/6/3528>
Marangella M, Di Stefano M, Casalis S, Berutti S, D'Amelio P, Isaia
GC.
Effects of potassium citrate supplementation on bone metabolism.
Calcif Tissue Int. 2004 Apr;74(4):330-5.
PMID: 15255069 [PubMed - indexed for MEDLINE]
< * w w w .springerlink . com /content/3cvubepxe4nckdpd/>
Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr.
Improved mineral balance and skeletal metabolism in postmenopausal
women treated with potassium bicarbonate.
N Engl J Med. 1994 Jun 23;330(25):1776-81.
PMID: 8190153 [PubMed - indexed for MEDLINE]
< * content.nejm.org/cgi/content/full/330/25/1776>
Frassetto L, Morris RC Jr, Sebastian A.
Long-term persistence of the urine calcium-lowering effect of
potassium bicarbonate in postmenopausal women.
J Clin Endocrinol Metab. 2005 Feb;90(2):831-4. Epub 2004 Nov 30.
PMID: 15572425 [PubMed - indexed for MEDLINE]
< * jcem.endojournals.org/cgi/content/full/90/2/831>
You cannot get too much potassium from the diet, but from supplements
you can, if you are careless and overdose. And potassium overdose can
be dangerous. Therefore IMHO you should always use these supplements
under a physician's supervision.
There is another way to improve your acid-base balance: improve your
diet! Select more base producing foods than acid producing foods.
Almost all green and bright colored vegetables are base producing. So
are most fruit.
Below some studies about the effwtcs of fruit and vegetable intake on
the bone mineral status and in the prevention of osteoporosis:
Prynne CJ, Mishra GD, O'Connell MA, Muniz G, Laskey MA, Yan L,
Prentice A, Ginty F.
Fruit and vegetable intakes and bone mineral status: a cross sectional
study in 5 age and sex cohorts.
Am J Clin Nutr. 2006 Jun;83(6):1420-8.
PMID: 16789345 [PubMed - indexed for MEDLINE]
< * w w w .ajcn.org/cgi/content/abstract/83/6/1420>
Lanham-New SA.
Fruit and vegetables: the unexpected natural answer to the question of
osteoporosis prevention?
Am J Clin Nutr. 2006 Jun;83(6):1254-5.
PMID: 16762933 [PubMed - indexed for MEDLINE]
< * w w w .ajcn.org/cgi/content/full/83/6/1254>
Vatanparast H, Baxter-Jones A, Faulkner RA, Bailey DA, Whiting SJ.
Positive effects of vegetable and fruit consumption and calcium intake
on bone mineral accrual in boys during growth from childhood to
adolescence: the University of Saskatchewan Pediatric Bone Mineral
Accrual Study.
Am J Clin Nutr. 2005 Sep;82(3):700-6.
PMID: 16155286 [PubMed - indexed for MEDLINE]
< * w w w .ajcn.org/cgi/content/full/82/3/700>
Muhlbauer RC, Lozano A, Reinli A, Wetli H.
Various selected vegetables, fruits, mushrooms and red wine residue
inhibit bone resorption in rats.
J Nutr. 2003 Nov;133(11):3592-7.
PMID: 14608079 [PubMed - indexed for MEDLINE]
< * jn.nutrition.org/cgi/content/full/133/11/3592>
New SA, Millward DJ.
Calcium, protein, and fruit and vegetables as dietary determinants of
bone health.
Am J Clin Nutr. 2003 May;77(5):1340-1; author reply 1341.
PMID: 12716695 [PubMed - indexed for MEDLINE]
< * w w w .ajcn.org/cgi/content/full/77/5/1340>
New SA.
Intake of fruit and vegetables: implications for bone health.
Proc Nutr Soc. 2003 Nov;62(4):889-99. Review. Erratum in: Proc Nutr
Soc. 2004 Feb;63(1):187.
PMID: 15018489 [PubMed - indexed for MEDLINE]
< * w w w .ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15018489>
Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP.
Potassium, magnesium, and fruit and vegetable intakes are associated
with greater bone mineral density in elderly men and women.
Am J Clin Nutr. 1999 Apr;69(4):727-36.
PMID: 10197575 [PubMed - indexed for MEDLINE]
< * w w w .ajcn.org/cgi/content/full/69/4/727>
It has been shown that metabolic acidosis induces bone calcium efflux
initially by physicochemical dissolution and subsequently by
cell-mediated mechanisms involving inhibition of osteoblasts and
stimulation of osteoclasts. It has also been shown that the
cell-mediated bone resorption is regulated by prostaglandins, mainly
by the inflammatory prostaglandin PGE2. The production of PGE2 is
catalyzed by the enzyme COX-2, and it has been shown in vitro that
COX-2 inhibitors such as indomethacin, inhibit PGE2 synthesis and net
calcium efflux.
I don't suggest that anyone would take indomethacin or other synthetic
NSAIDs to prevent or treat osteoporosis, but there are a number of
foods and herbs, which inhibit COX-2 enxyme and reduce inflammation.
The following links have information about them:
Reducing Inflammation with Diet and Supplements: The Story of
Eicosanoid Inhibition
general review by Subhuti Dharmananda, Ph.D., Director, Institute for
Traditional Medicine, Portland, Oregon
< * w w w . it monline.org/arts/lox.htm>
List of Anti-inflammatory Food - MetabolismAdvice . com
< * w w w .metabolismadvice . com /anti_inflammatory_food/>
Herbal anti-inflammatories | G. Douglas Andersen
< * w w w .chiroweb . com /archives/17/13/06.html>
Finally, some references about the acid-induced cell-mediated, PGE2
regulated bone resorption I mentioned above:
Krieger NS, Parker WR, Alexander KM, Bushinsky DA.
Prostaglandins regulate acid-induced bone resorption.
Am J Physiol Renal Physiol. 2000 Dec;279(6):F1077-82. Erratum in: Am J
Physiol Renal Physiol 2001 Sep;281(3):section F following table of
contents.
PMID: 11097626 [PubMed - indexed for MEDLINE]
< * ajprenal.physiology.org/cgi/content/full/279/6/F1077>
Bushinsky DA, Parker WR, Alexander KM, Krieger NS.
Metabolic, but not respiratory, acidosis increases bone PGE(2) levels
and calcium release.
Am J Physiol Renal Physiol. 2001 Dec;281(6):F1058-66.
PMID: 11704556 [PubMed - indexed for MEDLINE]
< * ajprenal.physiology.org/cgi/content/full/281/6/F1058>
Bushinsky DA, Smith SB, Gavrilov KL, Gavrilov LF, Li J, Levi-Setti R.
Chronic acidosis-induced alteration in bone bicarbonate and phosphate.
Am J Physiol Renal Physiol. 2003 Sep;285(3):F532-9. Epub 2003 May 20.
PMID: 12759230 [PubMed - indexed for MEDLINE]
< * ajprenal.physiology.org/cgi/content/full/285/3/F532>
--
Matti Narkia