Calcium
and Phosphorus
References:
J Am Coll Nutr. 2002 Jun;21(3):239-44.
Calcium effects on phosphorus absorption: implications
for the prevention and co-therapy of osteoporosis.
Heaney RP, Nordin BE.
Creighton University, Omaha, Nebraska 68131, USA.
OBJECTIVE: To evaluate the effect of calcium intake on
absorption of dietary phosphorus, with special reference
to typical calcium intakes and to those likely to be encountered
in prevention and treatment of osteoporosis. SETTING: Two
academic health sciences centers; inpatient metabolic research
unit. METHODS: Evaluation of calcium and phosphorus balance
data obtained in two data sets, the first, 543 studies
of healthy women aged 35-65, and the second, 93 men and
women aged 19-78; development of multiple regression models
predicting fecal phosphorus (the complement of net absorbed
phosphorus); data from the two centers analyzed separately
as a check on the consistency of the findings. RESULTS:
Mean net absorption of phosphorus was 60.3% (+/- 18.1)
for data set 1 and 53.0% (+/-9.4) for data set 2. Just
two variables, fecal calcium and diet phosphorus, were
positively and independently associated with fecal phosphorus.
These variables explained 73% of the variance in fecal
phosphorus in data set 1 and 33% in data set 2. Fecal calcium
alone explained the lion's share of the relationship. The
coefficients of the fecal calcium term in the models fitted
to the data were 0.332+/-0.022 and 0.155+/-0.039, for data
sets I and 2, respectively. Adjusting for the relationship
between fecal calcium and calcium intake and using the
parameters of the larger data set, it follows that each
increase in calcium intake of 0.5 g (12.5 mmol) decreases
phosphorus absorption by 0.166 g (5.4 mmol). CONCLUSIONS: As
calcium intake increases without a corresponding increase
in phosphorus intake, phosphorus absorption falls and the
risk of phosphorus insufficiency rises. Intakes with high
Ca:P ratios can occur with use of supplements or food fortificants
consisting of non-phosphate calcium salts. Older patients
with osteoporosis treated with current generation bone
active agents should receive at least some of their calcium
co-therapy in the form of a calcium phosphate preparation. ↑ Back To Top
J Bone Miner Metab.
2000;18(6):321-7.
Effects of phosphorus-containing
calcium preparation (bone meal powder) and calcium carbonate
on serum calcium and phosphorus in young and old healthy
volunteers: a double-blinded crossover study.
Tsuboi M, Shiraki M, Hamada M, Shimodaira H.
New Medical Research System Clinic, Tokyo, Japan.
To
evaluate the effects of bone meal powder (BEC) on calcium
and phosphorus metabolism, a
calcium absorption test was conducted using a preparation
of calcium carbonate (CAC) as the control drug.
A total of 12 healthy volunteers, consisting of 6 younger
(aged 20-29 years, 3 men and 3 women) and 6 older (aged
60-69 years, 3 men and 3 women) persons, were subjected
to a double-blinded crossover study. Serum
calcium (s-Ca) level significantly increased to 105.3% +/-
1.9% (P < 0.01 vs the basal value; mean +/- SD) from
the basal value in the BEC group and to 104.4% +/- 2.7%
(P < 0.01) in the CAC group at 3h post load. Urinary
excretions of calcium (u-Ca/glomerular filtration rate,
u-Ca/GF) after BEC and CAC load rose to 226.6% +/- 154.5%
(P < 0.05) and 211.1% +/- 148.0% (P < 0.05), respectively. Serum
phosphorus (s-P) levels after BEC load increased to 110.0% +/-
15.1% (P < 0.05), whereas that after CAC load showed
no significant change (99.3% +/- 7.9%). On
the other hand, urinary excretion of phosphorus (u-P/GF)
after CAC load decreased to 60.0% +/- 32.4% (P < 0.01)
and that in the BEC group showed no significant change
(92.5% +/- 49.5%). The increase in s-Ca led to decrease
in serum intact parathyroid hormone (i-PTH) level [77.3%
+/- 33.4% (P < 0.05) for BEC and 69.5% +/- 20.3% (P < 0.01)
for CAC] although s-P was increased by the BEC load. The
responses to BEC and CAC administration were compared in
the younger and the older groups. The responses in the
younger and the older group showed fundamentally the same
trends and to the same extent. However, the changes in
serum ionized calcium (i-Ca) and i-PTH levels at 1.5 h
post load were significantly smaller in the older group
than in the younger group (P < 0.01; P < 0.05). The
increment in s-P level after BEC load in the older group
was larger than that in the younger group. In conclusion,
BEC can modulate not only calcium but also phosphorus metabolism
in both younger and older subjects. Further investigations
are required to evaluate the effects of BEC on bone density
and safety for renal function in long-term observations ↑ Back To Top
Biofactors. 2004;21(1-4):39-42.
Effect of dietary calcium:
Phosphorus ratio on bone mineralization and intestinal
calcium absorption in ovariectomized rats.
Koshihara M, Masuyama R, Uehara M, Suzuki K.
Department of Nutritional Science, Faculty of Applied Bioscience,
Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku,
Tokyo 156-8502, Japan.
We investigated the effect of dietary calcium:phosphorus
(Ca:P) ratio on bone mineralization and intestinal Ca absorption
in ovariectomized (OVX) rat models of osteoporosis and
sham-operated rats. Thirty 12-wk-old female Wistar rats
were divided into three groups of OVX rats and three groups
of sham rats. Thirty days after the adaptation period,
OVX rats and sham rats were fed a diet formulated Ca:P,
1:0.5, 1:1 or 1:2 (each diet containing 0.5% Ca), respectively
for 42 d. In both sham and OVX rats, serum osteocalcin,
a marker of bone turnover, was increased by decreasing
Ca:P ratio (1:2). In contrast, rats fed the Ca:P = 1:0.5
diet (dietary P restriction) suppressed the increased serum
parathyroid hormone, osteocalcin and urinary deoxypyridinoline,
and increased Ca absorption in both sham and OVX rats compared
to the Ca:P = 1:1 and 1:2 diets. Especially, in OVX rats,
the decreased bone mineral density of the fifth lumbar
was also suppressed when rats were fed the Ca:P = 1:0.5
diet. These
results indicated that the elevation of dietary Ca:P ratio
may inhibit bone loss and increase intestinal Ca absorption
in OVX rats. ↑ Back To Top
Bone Miner. 1987 Jul;2(4):333-6.
Hypercalcemia of sarcoidosis treated with cellulose
sodium phosphate.
Dwarakanathan A, Ryan WG.
Department of Medicine, Rush-Presbyterian-St Luke's Medical
Center, Chicago, IL 60612.
A patient with pulmonary sarcoidosis and symptomatic hypercalcemia
had elevated serum 1,25-dihydroxyvitamin D and angiotensin-converting
enzyme levels, with evidence of deterioration of renal
function. Pulmonary function tests were normal and there
were no other findings to warrant immediate steroid use. She
was treated with cellulose sodium phosphate, in
an effort to control the hypercalcemia. Serum
calcium declined to normal values within 4 weeks and was
associated with symptomatic improvement and normalization
of BUN and creatinine, indicating perhaps a direct relationship
between serum calcium and renal function in this setting. These
observations suggest that the hypercalcemia of sarcoidosis
may be successfully treated with cellulose sodium phosphate
presumably by reducing intestinal calcium absorption, but
further clinical trials will be necessary to establish
its effectiveness in the long term. ↑ Back To Top
Kidney Int. 1991 May;39(5):973-83.
Potassium administration reduces and potassium
deprivation increases urinary calcium excretion in healthy
adults [corrected]
Lemann J Jr, Pleuss JA, Gray
RW, Hoffmann RG.
Department of Medicine, Medical College of Wisconsin, Milwaukee.
This study was undertaken to evaluate the effects of dietary
K intake, independent of whether the accompanying anion
is Cl- or HCO3-, on urinary Ca excretion in healthy adults.
The effects of KCl, KHCO3, NaCl and NaHCO3 supplements,
90 mmol/day for four days, were compared in ten subjects
fed normal constant diets. Using synthetic diets, the effects
of dietary KCl-deprivation for five days followed by recovery
were assessed in four subjects and of KHCO3-deprivation
for five days followed by recovery were assessed in four
subjects. On
the fourth day of salt administration, daily urinary Ca
excretion and fasting UCa V/GFR were lower during the administration
of KCl than during NaCl supplements (delta = -1.11
+/- 0.28 SEM mmol/day; P less than 0.005 and -0.0077 +/-
0.0022 mmol/liter GFR; P less than 0.01), and
lower during KHCO3 than during control (-1.26 +/-
0.29 mmol/day; P less than 0.005 and -0.0069 +/- 0.0019
mmol/liter GFR; P = 0.005). Both
dietary KCl and KHCO3 deprivation (mean reduction in dietary
K intake -67 +/- 8 mmol/day) were accompanied by an increase
in daily urinary Ca excretion and fasting UCaV/GFR
that averaged on the fifth day +1.31 +/- 0.25 mmol/day
(P less than 0.005) and +0.0069 +/- 0.0012 mmol/liter GFR
(P less than 0.005) above control. Both daily urinary Ca
excretion and fasting UCaV/GFR returned toward or to control
at the end of recovery. These observations indicate that:
1) KHCO3 decreases fasting and 24-hour urinary Ca excretion;
2) KCl nor NaHCO3, unlike NaCl, do not increase fasting
or 24-hour Ca excretion and 3) K deprivation increases
both fasting and 24-hour urinary Ca excretion whether the
accompanying anion is Cl- or HCO3-. The mechanisms for
this effect of K may be mediated by: 1) alterations in
ECF volume, since transient increases in urinary Na and
Cl excretion and weight loss accompanied KCl or KHCO3 administration,
while persistent reductions in urinary Na and Cl excretion
and a trend for weight gain accompanied K deprivation;
2) K mediated alterations in renal tubular phosphate transport
and renal synthesis of 1.25-(OH)2-vitamin D, since KCl
or KHCO3 administration tended to be accompanied by a rise
in fasting serum PO4 and TmPO4 and a fall in fasting
UPO4 V/GFR, a fall in serum 1,25-(OH)2-D and a decrease
in fasting UCa V/GFR, while dietary KCl or KHCO3 deprivation
were accompanied by a reverse sequence. ↑ Back To Top
Clin Calcium. 2005 Sep;15(9):1501-6.
[Phosphorus intake and bone mineral density (BMD)]
Kawaura A, Nishida Y, Takeda
E. [Article in Japanese]
Department of Clinical Nutrition, Institute of Health Biosciences,
University of Tokushima Graduate School.
Phosphorus regulates the bone formation and inhibits the
bone resorption. It is still expected as one of anti-osteoporosis
nutrients. The amounts of phosphorus intake with calcium
are increasing from 1960 to 1995. Because
phosphorus affects the regulation of calcium metabolism,
the balance of these nutrients is important. Tuero
suggested that more than 1,000 mg/day of calcium intake
and more than 0.74 of Ca/P were associated with better
bone mineral density (BMD) values in young women. However,
there are few reports of correlations between appropriate
phosphorus intake, Ca/P rate and BMD. ↑ Back To Top
Best Pract Res Clin Endocrinol Metab. 2003 Dec;17(4):623-51
Diagnosis and management of electrolyte emergencies.
Weiss-et EM, Takala J, Jakob
SM.
Department of Intensive Care
Medicine, Inselpital, University Hospital Bern, CH-3010
Bern, Switzerland.
Electrolyte
and fluid imbalances are disorders frequently observed
in critical care patients. In many instances patients are
asymptomatic, but they may
also present with neurological alterations, severe muscle
weakness, nausea and vomiting or cardiovascular emergencies.
Therefore, a pathophysiological understanding of these
disorders is necessary for initiating an appropriate therapy.
After a precise history-including drug prescriptions-has
been obtained from the patient or his/her relatives, determination
of the hydration status of the patient and measurement
of acid-base status, plasma and urine osmolality and electrolytes
are the first steps in the assessment of the disease. Once
a diagnosis has been established, great attention has to
be paid to the rate at which the disorder is corrected
because this-if inappropriate-may cause more severe damage
to the patient than the disease itself. This chapter addresses
the initial diagnostic and therapeutic steps of the most
common electrolyte emergencies. ↑ Back To Top
Eur J Nutr. 2001 Oct;40(5):200-13.
Diet,
evolution and aging--the pathophysiologic effects of the
post-agricultural inversion of the potassium-to-sodium
and base-to-chloride ratios in the human diet.
Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian
A.
University of California, San Francisco 94143, USA.
Theoretically, we humans should be better adapted physiologically
to the diet our ancestors were exposed to during millions
of years of hominid evolution than to the diet we have
been eating since the agricultural revolution a mere 10,000
years ago, and since industrialization only 200 years ago.
Among the many health problems resulting from this mismatch
between our genetically determined nutritional requirements
and our current diet, some might be a consequence in part
of the deficiency of potassium alkali salts (K-base), which
are amply present in the plant foods that our ancestors
ate in abundance, and the exchange of those salts for sodium
chloride (NaCl), which has been incorporated copiously
into the contemporary diet, which at the same time is meager
in K-base-rich plant foods. Deficiency of K-base in the
diet increases the net systemic acid load imposed by the
diet. We know that clinically-recognized chronic metabolic
acidosis has deleterious effects on the body, including
growth retardation in children, decreased muscle and bone
mass in adults, and kidney stone formation, and that correction
of acidosis can ameliorate those conditions. Is it possible
that a lifetime of eating diets that deliver evolutionarily
superphysiologic loads of acid to the body contribute to
the decrease in bone and muscle mass, and growth hormone
secretion, which occur normally with age? That is, are
contemporary humans suffering from the consequences of
chronic, diet-induced low-grade systemic metabolic acidosis?
Our group has shown that contemporary net acid-producing
diets do indeed characteristically produce a low-grade
systemic metabolic acidosis in otherwise healthy adult
subjects, and that the degree of acidosis increases with
age, in relation to the normally occurring age-related
decline in renal functional capacity. We also found that neutralization
of the diet net acid load with dietary supplements of potassium
bicarbonate (KHCO3) improved calcium and phosphorus balances,
reduced bone resorption rates, improved nitrogen balance,
and mitigated the normally occurring age-related decline
in growth hormone secretion--all without restricting dietary
NaCl. Moreover, we found that co-administration
of an alkalinizing salt of potassium (potassium citrate)
with NaCl prevented NaCl from increasing urinary calcium
excretion and bone resorption, as occurred with NaCl administration
alone. Earlier studies estimated dietary acid load from
the amount of animal protein in the diet, inasmuch as protein
metabolism yields sulfuric acid as an end-product. In cross-cultural
epidemiologic studies, Abelow found that hip fracture incidence
in older women correlated with animal protein intake, and
they suggested a causal relation to the acid load from
protein. Those studies did not consider the effect of potential
sources of base in the diet. We considered that estimating
the net acid load of the diet (i. e., acid minus base)
would require considering also the intake of plant foods,
many of which are rich sources of K-base, or more precisely
base precursors, substances like organic anions that the
body metabolizes to bicarbonate. In following up the findings
of Abelow et al., we found that plant food intake tended
to be protective against hip fracture, and that hip fracture
incidence among countries correlated inversely with the
ratio of plant-to-animal food intake. These findings were
confirmed in a more homogeneous population of white elderly
women residents of the U.S. These findings support affirmative
answers to the questions we asked above. Can we provide
dietary guidelines for controlling dietary net acid loads
to minimize or eliminate diet-induced and age-amplified
chronic low-grade metabolic acidosis and its pathophysiological
sequelae. We discuss the use of algorithms to predict the
diet net acid and provide nutritionists and clinicians
with relatively simple and reliable methods for determining
and controlling the net acid load of the diet. A more difficult
question is what level of acidosis is acceptable. We argue
that any level of acidosis may be unacceptable from an
evolutionarily perspective, and indeed, that a low-grade
metabolic alkalosis may be the optimal acid-base state
for humans. ↑ Back To Top
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