The full reference for the above article is

Montero-Odasso M, Duque G.
Vitamin D in the aging musculoskeletal system: an authentic strength
preserving hormone.
Mol Aspects Med. 2005 Jun;26(3):203-19. Review.
PMID: 15811435 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15811435>

Other articles about this topic:

Shionoiri A.
[Fall preventing effect of vitamin D]
Clin Calcium. 2006 Jul;16(7):111-6. Japanese.
PMID: 16816481 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=16816481>

Nakagawa K.
[Effect of vitamin D on the nervous system and the skeletal muscle]
Clin Calcium. 2006 Jul;16(7):98-103. Japanese.
PMID: 16816479 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=1681647>

Boonen S, Bischoff-Ferrari HA, Cooper C, Lips P, Ljunggren O, Meunier
PJ, Reginster JY.
Addressing the musculoskeletal components of fracture risk with
calcium and vitamin D: a review of the evidence.
Calcif Tissue Int. 2006 May;78(5):257-70. Epub 2006 Apr 21. Review.
PMID: 16622587 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=R
etrieve&dopt=abstractplus&list_uids=16622587>

Venning G.
Recent developments in vitamin D deficiency and muscle weakness among
elderly people.
BMJ. 2005 Mar 5;330(7490):524-6. Review.
PMID: 15746134 [PubMed - indexed for MEDLINE]
<http://bmj.bmjjournals.com/cgi/content/full/330/7490/524>

Bischoff-Ferrari HA, Conzelmann M, Dick W, Theiler R, Stahelin HB.
[Effect of vitamin D on muscle strength and relevance in regard to
osteoporosis prevention]
Z Rheumatol. 2003 Dec;62(6):518-21. German.
PMID: 14685712 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=R
etrieve&dopt=abstractplus&list_uids=14685712>

Visser M, Deeg DJ, Lips P; Longitudinal Aging Study Amsterdam.    
Low vitamin D and high parathyroid hormone levels as determinants of
loss of muscle strength and muscle mass (sarcopenia): the Longitudinal
Aging Study Amsterdam.
J Clin Endocrinol Metab. 2003 Dec;88(12):5766-72.
PMID: 14671166 [PubMed - indexed for MEDLINE]
<http://jcem.endojournals.org/cgi/content/full/88/12/5766>

Janssen HC, Samson MM, Verhaar HJ.
Vitamin D deficiency, muscle function, and falls in elderly people.
Am J Clin Nutr. 2002 Apr;75(4):611-5. Review.
PMID: 11916748 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/75/4/611>

McCarty MF.
Vitamin D status and muscle strength.
Am J Clin Nutr. 2002 Dec;76(6):1454-5; author reply 1455-6.
PMID: 12450916 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/76/6/1454>

Other potential contributing factor to sarcopenia may be diet related
mild chronic metabolic acidosis, which is common in western countries
and worsens with age due to age-related renal functional decline.
Chronic metabolic acidosis is known to cause muscle protein breakdown.
Supplements like  potassium bicarbonate (KHCO3) neutralize metabolic
acidosis and may prevent continuing age-related loss of muscle mass
and restore previously accrued deficits. Similar effect may be
achieved by including a large amount of alkaline producing vegetables,
fruit and berries into the diet or/and supplementing with alkaline
minerals calcium, potassium and magnesium.

Related references:

Frassetto L, Morris RC Jr, Sebastian A.
Potassium bicarbonate reduces urinary nitrogen excretion in
postmenopausal women.
J Clin Endocrinol Metab. 1997 Jan;82(1):254-9.
PMID: 8989270 [PubMed - indexed for MEDLINE]
<http://jcem.endojournals.org/cgi/content/full/82/1/254>

   "Previously we demonstrated that low grade chronic metabolic
   acidosis exists normally in humans eating ordinary diets
   that yield normal net rates of endogenous acid production
   (EAP), and that the degree of acidosis increases with age.
   We hypothesize that such diet-dependent and age-amplifying
   low grade metabolic acidosis contributes to the decline in
   skeletal muscle mass that occurs normally with aging. This
   hypothesis is based on the reported finding that chronic
   metabolic acidosis induces muscle protein breakdown, and
   that correction of acidosis reverses the effect.
   Accordingly, in 14 healthy postmenopausal women residing in
   a General Clinical Research Center and eating a constant
   diet yielding a normal EAP rate, we tested whether
   correcting their "physiological" acidosis with orally
   administered potassium bicarbonate (KHCO3; 60–120 mmol/day
   for 18 days) reduces their urinary nitrogen loss. KHCO3
   reduced EAP to nearly zero, significantly reduced the blood
   hydrogen ion concentration (P < 0.001), and increased the
   plasma bicarbonate concentration (P < 0.001), indicating
   that pre-KHCO3, diet-dependent EAP was significantly
   perturbing systemic acid-base equilibrium, causing a low
   grade metabolic acidosis. Urinary ammonia nitrogen, urea
   nitrogen, and total nitrogen levels significantly decreased.
   The cumulative reduction in nitrogen excretion was 14.1 ±
   12.3 g (P < 0.001). Renal creatinine clearance and urine
   volume remained unchanged. We conclude that in
   postmenopausal women, neutralization of diet-induced EAP
   with KHCO3 corrects their preexisting diet-dependent low
   grade metabolic acidosis and significantly reduces their
   urinary nitrogen wasting. The magnitude of the KHCO3-induced
   nitrogen-sparing effect is potentially sufficient to both
   prevent continuing age-related loss of muscle mass and
   restore previously accrued deficits."

Frassetto LA, Morris RC, Sebastian A.
Effect of age on blood acid-base composition in adult humans: role of
age-related renal functional decline.
Am J Physiol. 1996 Dec;271(6 Pt 2):F1114-22.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8
997384&dopt=Abstract>

   "... Otherwise healthy adults manifest a low-grade diet-
   dependent metabolic acidosis, the severity of which
   increases with age at constant EAP, apparently due in part
   to the normal age-related decline of renal function."

Frassetto L, Sebastian A.
Age and systemic acid-base equilibrium: analysis of published data.
J Gerontol A Biol Sci Med Sci. 1996 Jan;51(1):B91-9.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8
548506&dopt=Abstract>

   "To investigate whether systemic acid-base equilibrium
   changes with aging in normal adult humans, we reviewed
   published articles reporting the acid-base composition of
   arterial, arterialized venous, or capillary blood in age-
   identified healthy subjects. We extracted or calculated
   blood hydrogen ion concentration ([H+]), plasma bicarbonate
   concentration ([HCO3(-)]), blood PCO2, and age, and computed
   a total of 61 age-group means, distributed among eight 10-
   year intervals from age 20 to 100 years. Using linear
   regression analysis, we found that with increasing age,
   there is a significant increase in the steady-state blood
   [H+] (p < .001), and reduction in steady-state plasma
   [HCO3(-)] (p < .001), indicative of a progressively
   worsening low-level metabolic acidosis. Blood PCO2 decreased
   with age (p < .05), in keeping with the expected respiratory
   adaptation to metabolic acidosis. Such age-related
   increasing metabolic acidosis may reflect in part the normal
   decline of renal function with increasing age. The role of
   age-related metabolic acidosis in the pathogenesis of the
   degenerative diseases of aging warrants consideration."

Mitch WE, Medina R, Grieber S, May RC, England BK, Price SR, Bailey
JL, Goldberg AL.
Metabolic acidosis stimulates muscle protein degradation by activating
the adenosine triphosphate-dependent pathway involving ubiquitin and
proteasomes.
J Clin Invest. 1994 May;93(5):2127-33.
PMID: 8182144 [PubMed - indexed for MEDLINE]
<http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=8182144>

   "Metabolic acidosis often leads to loss of body protein due mainly
   to accelerated protein breakdown in muscle.
   
   [...]
   
   These results are consistent with, but do not prove that
   acidosis stimulates muscle proteolysis by activating the
   ATP-ubiquitin-proteasome-dependent, proteolytic pathway."

May RC, Masud T, Logue B, Bailey J, England BK.
Metabolic acidosis accelerates whole body protein degradation and
leucine oxidation by a glucocorticoid-dependent mechanism.
Miner Electrolyte Metab. 1992;18(2-5):245-9.
PMID: 1465068 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1
465068&dopt=Abstract>

   "... We conclude that chronic metabolic acidosis accelerates
   whole body protein turnover and reduces the efficiency of
   protein utilization by accelerating amino acid oxidation.
   These changes may require an intact glucocorticoid axis."

May RC, Masud T, Logue B, Bailey J, England B.
Chronic metabolic acidosis accelerates whole body proteolysis and
oxidation in awake rats.
Kidney Int. 1992 Jun;41(6):1535-42.
PMID: 1501410 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1
501410&dopt=Abstract>

   "... We conclude that chronic metabolic acidosis accelerates
   whole body protein turnover and affects the reincorporation
   of amino acid into body proteins by accelerating amino acid
   oxidation."

May RC, Kelly RA, Mitch WE.
Metabolic acidosis stimulates protein degradation in rat muscle by a
glucocorticoid-dependent mechanism.
J Clin Invest. 1986 Feb;77(2):614-21.
PMID: 3511100 [PubMed - indexed for MEDLINE]
<http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3511100>

   "... We conclude that chronic metabolic acidosis depresses
   nitrogen utilization and increases glucocorticoid
   production. The combination of increased glucocorticoids and
   acidosis stimulates muscle proteolysis but does not affect
   protein synthesis. These changes in muscle protein
   metabolism may play a role in the defense against acidosis
   by providing amino acid nitrogen to support the glutamine
   production necessary for renal ammoniagenesis."

Williams B, Layward E, Walls J.
Skeletal muscle degradation and nitrogen wasting in rats with chronic
metabolic acidosis.
Clin Sci (Lond). 1991 May;80(5):457-62.
PMID: 1851685 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1
851685&dopt=Abstract>

   "1. Chronic metabolic acidosis is associated with impaired
   growth and negative nitrogen balance, suggesting that it
   promotes endogenous protein catabolism. 2. Skeletal muscle
   is the major repository of body protein and is a potential
   target for stimuli of protein catabolism. 3. This study in
   vivo examines the effects of chronic metabolic acidosis on
   the relationship between growth, nitrogen disposal and
   skeletal muscle catabolism in the rat. 4. Growth, nitrogen
   utilization and acquisition of body mass were significantly
   impaired in acidotic animals compared with pair-fed
   controls. 5. Total nitrogen excretion was significantly
   increased in acidotic rats despite decreased urea
   production. The time course of this response to acidosis was
   synchronous with that of accelerated protein catabolism in
   skeletal muscle. 6. It is proposed that metabolic acidosis
   impairs growth by stimulating skeletal muscle protein
   catabolism. It is suggested that this forms part of a co-
   ordinated multi-organ homoeostatic response to acidosis,
   skeletal muscle and down-regulated urea production supplying
   the nitrogen required for renal ammoniagenesis."

Morris RC, Schmidlin O, Tanaka M, Forman A, Frassetto L, Sebastian A.
Differing effects of supplemental KCl and KHCO3: pathophysiological
and clinical implications.
Semin Nephrol. 1999 Sep;19(5):487-93. Review.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
0511388&dopt=Abstract>

Kurtz I, Maher T, Hulter HN, Schambelan M, Sebastian A.
Effect of diet on plasma acid-base composition in normal humans.
Kidney Int. 1983 Nov;24(5):670-80.
PMID: 6663989 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=6
663989&dopt=Abstract>

Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr.
Estimation of the net acid load of the diet of ancestral
preagricultural Homo sapiens and their hominid ancestors.
Am J Clin Nutr. 2002 Dec;76(6):1308-16.
PMID: 12450898 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/76/6/1308>

   "... Results: The mean (± SD) NEAP for 159 retrojected
   preagricultural diets was -88 ± 82 mEq/d; 87% were net base-
   producing. The computational model predicted NEAP for the
   average American diet (as recorded in the third National
   Health and Nutrition Examination Survey) as 48 mEq/d, within
   a few percentage points of published measured values for
   free-living Americans; the model, therefore, was not biased
   toward generating negative NEAP values. The historical shift
   from negative to positive NEAP was accounted for by the
   displacement of high-bicarbonate-yielding plant foods in the
   ancestral diet by cereal grains and energy-dense, nutrient-
   poor foods in the contemporary diet—neither of which are net
   base-producing.

   Conclusions: The findings suggest that diet-induced
   metabolic acidosis and its sequelae in humans eating
   contemporary diets reflect a mismatch between the nutrient
   composition of the diet and genetically determined
   nutritional requirements for optimal systemic acid-base
   status."

What significance is the fact iron destroys vitamin D or more precisely

in those with iron overload .. vitamin D is decreased .. in those with
supplemental iron induced iron overload .. vitamin D is decreased.

Bleeding / venesection / bloodletting / phlebotomy .. RESTORES ..
vitamin D .

<<snip>>
The results reveal that the low serum 25-OHD concentration in patients
with hemochromatosis is directly related to the extent of iron loading
and it is improved by venesection therapy.
<<snip>>

Iron induced decreased vitamin D.

<<snip>>
when transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia.
<<snip>>

Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro
inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D
production in renal tubules.
Sato K, Nohtomi K, Demura H, Takeuchi A, Kobayashi T, Kazama J, Ozawa H

Bone. 1997 Jul ; 21(1): 57-64

A 60-year-old man with portal hypertensive gastropathy due to type C
liver cirrhosis developed severe bone pains, marked hypophosphatemia
with inappropriately increased urinary excretion of phosphate (%TRP;
9.6%), and hyperalkaline phosphatasia, after intravenous administration

of saccharated ferric oxide (SFO) at a dose of 80-240 mg/week over a
period of more than 5 years. The total iron infused was estimated to be

more than 25 g. On a diagnosis of SFO-induced osteomalacia, the
infusion of iron was immediately discontinued, and phosphate and
vitamin D2 (1000 IU/day) were administered. Serum levels of 25-OHD2
increased after 1 week, whereas levels of 1,25-(OH)2D2 did not increase

until 3 months later, accompanied by improvement of renal tubular
reabsorption of phosphate and gradual improvement of the bone pains.
The patient has been doing well for the last 2 years, with normal serum

levels of phosphate, calcium, and alkaline phosphatase, without any
supplementation of phosphate, vitamin D, or iron-containing agents. In
primary culture of neonatal mouse renal tubules, in which 1,25-(OH)2D3
was produced from 25-OHD3 in response to PTH, SFO significantly
inhibited PTH-induced production of 1,25-(OH)2D3 at 30 mumol/L, which
is attainable in the urine of patients receiving a therapeutic
intravenous dose of SFO. Furthermore, SFO decreased the calcium content

and inhibited 45Ca incorporation in cultured fetal mouse parietal bones

at 3 mumol/L. Such SFO concentration may be transiently observed in the

plasma of patients receiving excessive intravenous doses of SFO for a
prolonged period. These in vitro findings together with the clinical
observations suggest that SFO, after filtration through the glomerulus
and reabsorption in the proximal renal tubules, impaired proximal renal

tubular function, such as tubular reabsorption of phosphate and 1
alpha-hydroxylase activity, leading to hypophosphatemic osteomalacia.
Furthermore, it is highly likely that SFO in the peripheral blood, when

transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia. Although SFO-induced osteomalacia is reversible

simply by discontinuation of the agent, excessive and prolonged
administration of SFO should be avoided.

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

1: Gastroenterology. 1985 Apr;88(4):865-9. Related Articles, Links

Low serum 25-hydroxyvitamin D in hereditary hemochromatosis: relation
to iron status.

Chow LH, Frei JV, Hodsman AB, Valberg LS.

Under normal conditions, vitamin D absorbed from the diet or
synthesized in the skin is transported to the liver where it undergoes
hydroxylation. The purpose of this study was to determine whether
excess hepatic iron affects this process and the subsequent production
of 1,25-dihydroxyvitamin D (1,25-[OH]2D) in the kidney. Mean serum
25-hydroxyvitamin D (25-OHD) concentrations in untreated hereditary
hemochromatosis were 13 +/- 6 (SD) in 9 patients with cirrhosis, 13 +/-

6 in 5 patients with hepatic fibrosis, and 22 +/- 6 in 10 patients with

normal hepatic architecture aside from siderosis and were significantly

lower than the levels found in 24 controls matched for age, sex, and
season, p less than 0.05. The mean serum 25-OHD levels in the two
groups with hemochromatosis and hepatic damage were significantly lower

than the value in the group with normal hepatic architecture, p less
than 0.05. Serum 25-OHD levels in individual patients were inversely
related to the size of body iron stores as measured by exchangeable
body iron, r = -0.64, or serum ferritin, r = -0.47, p less than 0.05.
In 15 patients removal of excess body iron by venesection therapy
produced a significant increase in the mean serum 25-OHD from 20 ng/ml
to 30 ng/ml, p less than 0.05. In contrast, mean serum 1,25-[OH]2D
levels were similar in iron-loaded and control subjects, indicating
that the regulation of this metabolite was intact in patients with
hemochromatosis. The results reveal that the low serum 25-OHD
concentration in patients with hemochromatosis is directly related to
the extent of iron loading and it is improved by venesection therapy.

PMID: 3838288 [PubMed - indexed for MEDLINE]

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DEAD PEOPLE WALKING
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Interesting, but other variables are far more important to sarcopenia,
such as lack of exercise (in particular resistance exercise), adequate
protein intakes (elderly people are a population who often lack protein
in their diet), adequate buffering agents (eg,mag, cal, etc) to avoid
low level acidosis, low levels of anabolic hormones: testosterone, GH,
etc, and other issues. Adequate vitamin intakes (including D) are also
essential, but alone, without addressing the above issues, will have
little effect.