From: Elizabeth Childs (echilds@linex.com)
Date: Mon Dec 27 1999 - 02:50:21 MST
I ran across these in Medline and I thought they were interesting, but I'm
not qualified to interpret them properly. I'm curious what others think.
Title
Potassium bicarbonate reduces urinary nitrogen excretion in
postmenopausal women.
Author
Frassetto L; Morris RC Jr; Sebastian A
Address
Department of Medicine, University of California, San Francisco 94143,
USA.
Source
J Clin Endocrinol Metab, 82(1):254-9 1997 Jan
Abstract
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
Title
Effect of age on blood acid-base composition in adult humans: role of
age-related renal functional decline.
Author
Frassetto LA; Morris RC Jr; Sebastian A
Address
Department of Medicine, University of California, San Francisco 94143, USA.
Source
Am J Physiol, 271(6 Pt 2):F1114-22 1996 Dec
Abstract
In 64 apparently healthy adult humans (ages 17-74 yr) ingesting controlled
diets, we investigated the separate and combined effects of age, glomerular
filtration rate (GFR, index of age-related renal functional decline), renal
net acid excretion [NAE, index of endogenous acid production (EAP)], and
blood PCO2 (PbCO2, index of respiratory set point) on steady-state blood
hydrogen ion ([H+]b) and plasma bicarbonate concentration ([HCO3-]p).
Independent predictors of [H+]b and [HCO3-]p were PbCO2, NAE, and either age
or GFR, but not both, because the two were highly correlated (inversely).
[H+]b increased with increasing PbCO2, NAE, and age and with decreasing GFR.
[HCO3-]p decreased with increasing NAE and age but increased with increasing
PbCO2 and GFR. Age (or GFR) at constant NAE had greater effect on both [H+]b
and [HCO3-]p than did NAE at constant age (or GFR). Neither PbCO2 nor NAE
correlated with age or GFR. Thus two metabolic factors, diet-dependent EAP
and age (or GFR), operate independently to determine blood acid-base
composition in adult humans. 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.
Language
Eng
Unique Identifier
97151386
MESH Headings
Acid-Base Equilibrium * ; Adolescence ; Adult ; Aged ; Aging *BL/*PH ;
Bicarbonates BL ; Carbon Dioxide BL ; Chlorides BL ; Female ; Glomerular
Filtration Rate ; Human ; Hydrogen BL ; Kidney *PH ; Male ; Middle Age ;
Partial Pressure ; Protons ; Support, Non-U.S. Gov't ; Support, U.S. Gov't,
P.H.S.
Publication Type
JOURNAL ARTICLE
ISSN
0002-9513
Country of Publication
UNITED STATES
CAS Registry Number
0 (Bicarbonates); 0 (Chlorides); 0 (Protons); 124-38-9 (Carbon Dioxide);
1333-74-0 (Hydrogen)
Title
Estimation of net endogenous noncarbonic acid production in humans from diet
potassium and protein contents.
Author
Frassetto LA; Todd KM; Morris RC Jr; Sebastian A
Address
Department of Medicine and General Clinical Research Center, University of
California, San Francisco 94143, USA.
Source
Am J Clin Nutr, 68(3):576-83 1998 Sep
Abstract
Normal adult humans eating Western diets have chronic, low-grade metabolic
acidosis, the severity of which is determined in part by the net rate of
endogenous noncarbonic acid production (NEAP), which varies with diet. To
prevent or reverse age-related sequelae of such diet-dependent acidosis (eg,
bone and muscle loss), methods are needed for estimating and regulating
NEAP. Because NEAP is difficult to measure directly, we sought a simple
method to estimate it from diet-composition data. We focused on protein and
potassium contents because the production of sulfuric acid from protein
metabolism and bicarbonate from dietary potassium salts of organic acids are
the major variable components of NEAP. Using steady state renal net acid
excretion (RNAE) as an index of NEAP in 141 normal subjects eating 20
different diets, we found by multiple linear regression analysis that RNAE
[mEq/d x 10460 kJ diet (mEq/d 2500 kcal)] was predictable (R2 = 0.62) from
protein [g/d x 10460 kJ diet (g/d 2500 kcal); positive regression
coefficient, P < 0.001] and potassium [mEq/d x 10460 kJ diet (mEq/d x 2500
kcal): negative regression coefficient, P = 0.001] contents, which were not
themselves correlated. Among diets, 71% of the variation in RNAE could be
accounted for by the ratio of protein (Pro) to potassium (K) content: RNAE =
62Pro/K - 17.9 (r = 0.84, R2 = 0.71, P < 0.001). Thus, by considering both
the acidifying effect of protein and the alkalinizing effect of potassium
(organic anions), NEAP can be predicted with confidence from the readily
available contents of only 2 nutrients in foods. Provisionally, these
findings allow estimation and regulation of NEAP through diet modification.
Language
Eng
Unique Identifier
98403802
MESH Headings
Acidosis ET ; Adolescence ; Adult ; Aged ; Bicarbonates *ME/UR ; Comparative
Study ; Dietary Proteins *ME ; Energy Intake ; Female ; Human ; Male ;
Middle Age ; Potassium AD/*ME ; Predictive Value of Tests ; Regression
Analysis ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S.
Publication Type
JOURNAL ARTICLE
ISSN
0002-9165
Country of Publication
UNITED STATES
CAS Registry Number
0 (Bicarbonates); 0 (Dietary Proteins); 7440-09-7 (Potassium)
Title
Normal diet NaCl variation can affect the renal set-point for plasma
pH-(HCO3-) maintenance [see comments]
Author
Cogan MG; Carneiro AV; Tatsuno J; Colman J; Krapf R; Morris RC Jr; Sebastian
A
Address
Department of Medicine, University of California, San Francisco 94143.
Source
J Am Soc Nephrol, 1(2):193-9 1990 Aug
Abstract
In humans who are ingesting abundant NaCl, blood pH (pHb) and plasma
bicarbonate concentration [HCO3-)p) change little or imperceptibly in
response to the ingestion of alkali salts. We tested the hypothesis that
such tight homeostatic regulation is an artifact of eating a culturally
imposed NaCl-enriched diet, not a fundamental physiological trait of humans.
In five normal men ingesting a constant acid-producing diet with a low
intrinsic NaCl content (0.15 mEq/kg of body weight per day), we measured
plasma and urine acid-base composition during four 7-day periods in which
the diet was supplemented as follows: no supplements----NaHCO3
only----NaHCO3 plus NaCl----NaCl only. Each sodium supplement was 2.0
mmol/kg body weight per day. With no supplements, pHb was 7.43 +/- 0.005 and
(HCO3-)p was 25.0 +/- 0.4 mEq/L. When NaHCO3 only was added, pHb rose 0.02
(to 7.45 +/- 0.004; P less than 0.01) and (HCO3-)p rose nearly 4 mEq/L (to
28.9 +/- 0.6 mEq/L, P less than 0.001). The rise in (HCO3-)p was sustained
predominantly by an increased rate of renal bicarbonate reabsorption. When
NaCl was added, (HCO3-)p returned to the earlier level, despite continued
NaHCO3 supplementation (24.9 +/- 0.6 mEq/L), and remained there when NaHCO3
supplementation was subsequently stopped (24.1 +/- 0.5 mEq/L). Thus, tight
homeostatic regulation of plasma acid-base composition in response to a
change in dietary base occurred only when dietary NaCl was abundant. To our
knowledge, this is the first study in normal humans that demonstrates that
diet NaCl variations within the normal range significantly influence plasma
acid-base composition.(ABSTRACT TRUNCATED AT 250 WORDS)
Language
Eng
Unique Identifier
91370771
MESH Headings
Acid-Base Equilibrium PH ; Adult ; Bicarbonates AD/*BL/UR ; Diet ;
Homeostasis PH ; Human ; Hydrogen-Ion Concentration ; Kidney PH ; Male ;
Middle Age ; Sodium AD ; Sodium, Dietary *AD ; Support, Non-U.S. Gov't ;
Support, U.S. Gov't, P.H.S.
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