|
Introduzione
Il
mantenimento di uno stabile giusto rapporto acido-base è una componente
vitale dell'omeostasi
corporea.
Oltre cento diagrammi, nomogrammi, equazioni e regole sono state
introdotti per rappresentare il rapporto acido-base: lungi dal
semplificare le cose, queste diverse rappresentazioni hanno contribuito a
complicarle a causa dell'introduzione di diversi nuovi termini e
definizioni.
Terminologia
e definizioni
Molta
gente sperimenta difficoltà a capire il rapporto acido-base.
Molte di queste difficoltà derivano dall'assenza di familiarità con la
terminologia impiegata. Se noi abbiamo una scarsa comprensione dei comuni
termini come neutro, pH, acidosi metabolica, eccesso di basi, ecc., non
deve sorprendere che abbiamo anche difficoltà a capire, i concetti, i
modelli, le sindromi descritte.
Indicatore
acido-base del pH: Piaccametro
Vedi: Terminologia
e definizioni dell'equilibrio acido-base
Continua
nel sito:
http://www.unipa.it/~lanza/gtai/acido-base/abindexit.html#Rep
vedi
anche:
http://digilander.libero.it/itisaltamura/arizona/acqua/acidibasi.htmi
Introduzione alla Medicina
Naturale
U.S. life
expectancy is about 78 years – one of the lowest
life expectancies among developed nations. Lower
than Cuba’s, and just marginally higher than
Slovenia, according to figures from the United
Nations.
China’s life
expectancy lies around 73 years, which includes
the high infant mortality rate of the rural
areas. According to the Chinese Municipal Center
for Disease Control, the life expectancy in
cities like Beijing and Shanghai is about 80
years, and Hong Kong comes in with a life
expectancy of over 82 years, despite the many
health hazards inherent with living in these
over-crowded cities.
Clues to the
Chinese secret of longevity can be found in the
streets, in the form of morning and
evening rituals, involving
large masses of people of
all ages practicing tai-chi, aerobics, games,
and even open air ballroom dancing.
Daily exercise is
widespread and woven into the Chinese culture,
offering more than just a way to burn calories.
It also enforces social interaction, limiting
the isolation that so often comes with old age
in the United States.
Tratto da:
LiveScience.com October 16, 2007
Ma
sopra tutto mangiano
riso
e non pasta e pane !
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Alimentazione e
vitamine nella terza età
La malnutrizione nella terza età è un
fenomeno molto più diffuso di quanto si possa
ritenere. Alterazioni del metabolismo, uso di
farmaci (NdR:
e
Vaccini) e
scarso appetito possono determinare carenze
vitaminiche e indurre un peggioramento del
quadro di salute generale.
La ricetta della longevità ?
Ogni anziano è in gran parte frutto della sua
storia: fondamentale è l’influenza genetica ma
più di tutto conta lo stile di vita adottato
negli anni. Se è vero che grazie alla ricerca
scientifica e all’introduzione di nuove terapie
l’aspettativa di vita è notevolmente cresciuta,
è anche vero che terza età non è sempre sinonimo
di qualità di vita.
Il processo di invecchiamento è un
fenomeno multidimensionale nel quale
hanno un ruolo ugualmente importante fattori
biologici, psicologici, sociali ed economici.
Tra questi, vanno considerati i cambiamenti
nella sfera alimentare e nutrizionale che
possono complicare il quadro di salute
generale.
A partire dalla menopausa per le donne e
dall’andropausa per gli uomini, si innesca
infatti una serie di alterazioni metaboliche che
determinano un decremento del fabbisogno
energetico, causa principale di malnutrizione.
Gli anziani mostrano generalmente indifferenza e
indolenza verso il cibo senza considerare che
con il tempo l’apparato digerente diventa meno
efficiente nell’utilizzare le proteine, le
vitamine e i minerali presenti negli alimenti.
vedi
Disbiosi
Ad aggravare la situazione, il ricorso di
molti anziani a farmaci
che possono interferire nello stato
nutrizionale, modificando il senso
dell’appetito, influendo negativamente
sull’assorbimento dei principi nutritivi e
variando il tempo di transito.
L’insieme di questi fattori può determinare
dunque carenze nutrizionali e vitaminiche
importanti che possono provocare a loro volta
patologie anche gravi. Integrare l’alimentazione
con le
vitamine (NdR: e
sali
minerali) più importanti per la terza età,
sempre sotto controllo medico, è quindi la
strategia più consigliabile per migliorare la
qualità di vita e vivere al meglio la vecchiaia.
Tra le sostanze più importanti per contrastare i
processi di invecchiamento cellulare ci sono le
vitamine antiossidanti (A, C, E), in grado di
proteggere dall’azione dannosa dei radicali
liberi: queste molecole «di scarto», prodotte a
seguito di varie reazioni chimiche che avvengono
all’interno dell’organismo, sono «instabili» in
quanto prive di un elettrone e tendono a legarsi
con cellule sane provocandone la degenerazione.
A questo riguardo, uno studio pubblicato sull’American
Journal of Clinical Nutrition ha dimostrato
che una supplementazione con
vitamina C, E, beta-carotene e zinco è
indicata nei pazienti colpiti da degenerazione
maculare senile, mentre un’altra indagine
pubblicata sul «Cochrane Database of Systematic
Reviews» ha rilevato che supplementazioni di
vitamina C possono migliorare le condizioni di
anziani affetti da polmonite.
Anche l’apporto di vitamina D è fondamentale per
preservare lo stato di salute delle ossa degli
anziani. In questi ultimi, infatti, spesso
costretti a casa e poco esposti alla luce del
sole, si osserva una riduzione della sintesi di
questa vitamina a livello epiteliale, che può
indurre stati di carenza con ripercussioni sulla
struttura ossea e sulle performance fisiche.
Non va infine trascurata l’influenza delle
vitamine sulle funzioni cognitive degli anziani.
Secondo un recente studio pubblicato anch’esso
sull’American Journal of Clinical Nutrition,
acido folico e vitamina B12 svolgono un’azione
sinergica per preservare le performance
cognitive delle persone più avanti con l’età.
By AA.VV. - Tratto da:
http://a0548.gastonecrm.it/newsletter/public/art_83.htm
Ricordiamo
che le alterazioni degli
enzimi, della
flora, del
pH digestivo e della mucosa
intestinale influenzano la salute, non
soltanto a livello intestinale, ma anche a
distanza in qualsiasi parte dell'organismo.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
DIET,
evolution and Aging - European Journal of Nutrition 4O: 200-213 (2001) ©SteinkopffVerlag2001
ORIGINAL CONTRIBUTION
L. Frassetto R. C.Morris, Jr. D. E.
Sellmeyer K.Todd A. Sebastian
Received: 1O May 2001 Accepted: 23 May 2001
Anthony Sebastian, M. D. (0)
- Box 0126
- University of California
- San Francisco, CA 94143, USA
Tel. + 1 -415/476-1160
- Fax:+ 1 -4 15/476-09 B6
- E-Mail: sebastia@gcrc.ucsf.edu
The
pathophysiologic effects of the post-agricultural
inversion of the potassium-to-sodium and
base-to-chloride ratios in the human diet
Summary
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 su-perphysiologic 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 sulfu-ric acid as an
end-product. In cross-cultural epidemiologic
stud-ies,Abelow (1] 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 iike 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 plam-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 affirma-tive 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 acido-sis and its pathophysiological sequelae.
We discuss the use of algo-evolution and aging
rithms
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 maybe
unacceptable from an evolutionarily perspective,
and indeed, that a low-grade metabolic alkalo:
sis may be the optimal acid-base state for
humans.
Keywords Acid-base-Nutrition
and evolution - Diet net acid load - Protein -
Organic anions
Introduction
The
nutritional requirements of humans were established
by natural selection during millions of years of
in which humans and their hominid ancestors
consumed foods exclusively from a menu of wild
animals and uncultivated plants [2,3]. By
contrast, the past 10,000 years - less than one
percent of hominid evolutionary time -has afforded
natural selection insufficient time to generate
adaptations and eliminate maladaptations to the
profound transformation of the human diet that occurred
during that period consequent to the inventions of
agriculture and animal husbandry, and more
recently, to the development of mouern food
production and distribution technologies [2-5].
In
comparison to the diet habitually ingested by
pre-agricultural Homo sapiens living in the
Upper Paleolithic period (40,000 to 10,000 years
ago), also referred to as the Late Stone Age, the
diet of contemporary Homo sapiens has an
overabundance of fat, simple sugars, sodium and
chloride, and a paucity of fiber, calcium and
potassium [2]. From an evolutionary nutritional
perspective, contemporary humans are Stone Agers
habitually ingesting a diet discordant with
their genetically determined metabolic machinery
and integrated organ physiology [6]. This article
discusses some of the potential consequences of
these changes.
The
modern dietary excess of NaCI
and
deficiency of K+ and HCOJ precursors
From
extensive data on the diets of existing
hunter-gatherer societies, and from inferences
about the nature of the Paleolithic environment,
Eaton and Konner analytically reconstructed the
Paleolithic diet and estimated the probable daily
nutrient intakes of Paleolithic humans [21. In
an estimated 3000 kilocalorie diet, meat
constituted 35 percent of the diet by weight and
plant foods, 65 percent.
Total protein intake was estimated as 251 grams
per day, of which animal protein was 191 grams,
and plant proteins, 60 grams per day. By contrast,
modern humans consume less than one-half that
amount of animal protein, and only about one-third
that
amount
of plant protein, per kilocalorie of diet consumed
[7]. Sodium intake was estimated at about 29 meq
per day, and potassium intake, in excess of 280
meq per day. By contrast, modern humans consume
between 100-300 meq of sodium per day, and about
80 meq of potassium per day.
That
is, in the switch to the modern diet, the K/Na ratio
was reversed, from 1 to 10, to more than 3 to 1.
Since food sodium is largely in the form of
chloride salts, and food potassium largely in the
fortm of bicarbonate-generating organic acid
salts, the C1/HCO3 ratio of the diet
has become correspondingly reversed. Further, the
extent to which the dietary K/Na ratio is
reversed increases with age [8], and presumably
therefore also does the CI/HCO3 ratio. Yet, the
biologic machinery that evolved to process these
dietary electrolytes remains largely unchanged,
genetically fixed in Paleolithic time [2]. Thus,
the electrolyte mix of the modern diet is
profoundly mismatched to its processing machinery
and the extent of the mismatch increases with age.
As a consequence of the diet-kidney mismatch,
contemporary humans are not only overloaded with
Na+ and Cl~ but also deficient in K+
and HCO3~. Fig. 1 demonstrates this
exchange of monovalent ions.
Adverse effects of excessive dietary sodium
chloride
Excessive
dietary sodium intake is mostly known to be
associated with elevated blood pressure.
Fig.
1 Exchange
of potassium intake for sodium (meq/day) in
transition from pre-agricultural to modern diets.
Studies
in individuals [9-11] as well as populations
[12-15] have demonstrated correlations between
dietary sodium intake and both systolic and
diastolic blood pressure. Good blood pressure
control has been linked with improvements in
cardiac, cerebral and kidney function and in
reductions in morbidity and mortality from cardiovascular
and renal disease [16-19].
Dietary
sodium is a less well-known determinant of urinary
calcium excretion. Urinary excretion of calcium is
well documented to vary directly with that of Na+
[20]. Even a moderate reduction of dietary sodium,
from 170 to 70mmol/day, could attenuate not only
hypertension but also hypercalciuria, and thereby
prevent both kidney stones and osteoporosis.
That the hypercalciuric effect of excessive
dietary sodium may be a preventable cause of
osteoporosis would seem supported by the results
of recent studies in both post-menopausal women
and adolescent girls [21,22}. Abone-demineralizing
effect of NaCl-induced hypercalciuria would also
be in keeping with the many observations made by
Nordin [23, 24] and Goulding and their associates
[25, 26], in both humans and rats.
Lack
of potassium in the diet
The
evolutionarily recent increase in dietary sodium
intake has been reciprocated by a decrease in
dietary potassium intake. It has been estimated
that our Paleolithic ancestors ate a diet
containing in excess of 200 meq potassium daily
[2]. What effects might this lack of potassium in
the diet engender ?
As
early as 1928, Addison reported that potassium
administration could lower elevated blood pressure
in humans [27], and some 40 years later,Dahlet
al.demonstrated that increasing the ratio of
potassium to sodium in the diet of salt-sensitive
hypertensive rats lowered blood pressure in a
stepwise fashion [28].
In
normotensive humans, Morris and colleagues recently
demonstrated that increases in blood pressure induced
by sodium loading could be progressively attenuated
by increasing dietary potassium intake from
30mmol/day to 120mmol/day. In this study,
potassium was given as the bicarbonate salt.
Interestingly, this decline in blood pressure
was significantly greater in the 24
African-American males than in the 14 Caucasian
males in the study [29], suggesting not just a
dietary, but a genetic component to the response
of blood pressure to potassium bicarbonate
irtgestion.
In
this same study, supplemental KHCO3 can
also override the hypercalciuric effect of dietary
NaCl-load-ing, even though such supplementation
further increases the urinary excretion of
sodium. In a recently reported metabolic study
of midd!e-aged normal men fed a diet marginally
deficient in both K+, 30 mmol/d, and
calcium, 14 mmol/d, increasing dietary NaCl from
30 to
250
mmol/d induced a 50 % increase in urinary calcium
that supplemental KHCO3 either reversed
or abolished, depending on whether it was
supplemented to 70 or 120 mmol/d, mid- and
high-normal intakes, respectively [29]. As an
apparent consequence of its demonstrated
natriuretic effect, supplemental KHCO3
also reversed and abolished, respectively,
NaCl-induced increases in blood pressure in these
men with such normotensive "salt-sensitivity"
(Fig. 2), a precursor of hypertension [30,31], In
women fed a normal K+ diet,
supplemental K-citrate prevented not only the
hypercalciuria induced by dietary NaCl-loading,
but also prevented an increase in biochemical
markers of bone resorption (Sellmeyer, D., et al,
unpublished observations).
Fig.2
Increasing dieiaiy potassium decreases mean
arterial pressure (MAP) even on high salt diets.
Specific
adverse effects of excessive dietary chloride
Although
much work has been done on the adverse effects
of dietary sodium chloride on blood pressure, very
little has been done to explore the specific role
of excessive dietary chloride. And yet.the
chloride content of the modern diet is at least as
high as the sodium content [32]. Does the exchange
of the bicarbonate we used to eat for the chloride
that we presently eat have any adverse effects?
Morris
and colleagues first demonstrated in
uninephrectomized rats given deoxycorticosterone
that while treatment with sodium as a combination
of the bicarbonate and acetate salt raised blood
pressure, treatment with sodium as the chloride
salt raised blood pressure to a significantly
higher level [33]. Luft et al. demonstrated that
sodium as the chloride salt raised blood pressure
in stroke-prone spontaneously hypertensive rats
[34] and sodium as the bicarbonate salt lowered
blood pressure in mildly hypertensive humans [35],
More recently, Morris et al. have done studies investigating
the effects of KC1 and KBC (potassiumbicarbonate)
on blood pressure, frequency of stroke and
severity of the renal lesions in the SHRSP [36].
Rats treated with KCI had significantly higher PRA
than rats treated with KBC. In each group and in
all combined, the severity of hypertension was
highly cot related with the levels of PRA (log
transformed). KCI loading induced greater
increases in BP than in control or KBC rats (Fig.
3)
The
incidence of strokes was significantly higher with
KCI than with KB/C (Table 1). In the KC1/KBC rates,
strokes occurred only in animals with SBP > 248
mmHg and with PRA > 26.5 ng/ml/h (logPRA=1.42).
Light
microscopic examination of the kidneys revealed
glomerular, tubular, interstitial, and vascular lesions
(histologically ranked in combination) similar in
quality but significantly more frequent and more
severe with KCI supplementation than either KB/C
or CTL [36]. Irrespective of dietary supplements,
renal lesions were rare in rats with SBP < 200
mmHg* The overall severity of renal lesions was
highly correlated with the level of PRA (log
transformed) (R2= 0.67, p < 0.0001).
Protein-uria was significantly greater with KCI
than either KB/C or CTL (Table 1). Creatinine
clearance was significantly greater in KB/C than
in KCI or CTL (Table 1). Morris and colleagues
concluded that the extent of renal damage and
likelihood of stroke are determined by the
severity of hypertension.
Diet
and acid-base
In
contrast to its excess chloride content, the
modern diet lacks bicarbonate and anion precursors
that generate bicarbonate on metabolism. As a
consequence, the net acid load of the
modern diet is higher than it would otherwise be.
The rest of this article will discuss this bicarbonate-deficiency-mediated
dietary acid excess.
Fig.
3
Change in systolic (SBP) and diastolic blood
pressure (DBP) with age in stroke prone
spontaneously hypertensive rats (SPSHR) treated
with a usual rat diet (CTL), or supplemented with
KCI or potassium bicarbonate. Data are presented
as median and 95% Cl.
Endogenous
acid production
Endogenous
acid production can be considered as comprising
three components: 1) organic acids produced during
metabolism that escape complete combustion to
Table
1
Effects of KCI vs. KB/C in SHRSP before and
15 Weeks after initiation of dietary supplements
|
|
Age
9 Weeks (baseline)
|
|
Age
25 Weeks (15 weeks after assignment)
|
|
|
xa
|
KB/C
|
CTL
|
KCI
|
KB/C
|
CTL
|
|
SBP
(mmHg)
|
173(169/185)
|
176(173/181)
|
178(174/184)
|
248(230/258)*
|
204(197/217)**
|
226(212/235)
|
|
DBP
(mmHg)
|
124(115/130)
|
124(117/129)
|
125(118/132)
|
179067/186)*
|
144(140/156)**
|
161
(149/171)
|
|
PRA(ng/ml/hr)
|
|
|
|
17.4(&6/30.8)'-+
|
62
(4.7/1
U)
|
13.6(6.8/26.9)
|
|
Strokes
total
|
|
|
|
6/17*
|
0/15
|
1/20
|
|
Renal
lesions (overall rank)
|
|
|
|
37(13)*
|
17(13)
|
24(13)
|
|
UV-protein
(mg/d)
|
64(53/70)
|
59(51/66)
|
53(51/62)
|
251
(179/301)*
|
108(96/153)
|
147(111/172)
|
|
Creatinine
clearance
|
|
|
|
0.46(0.13)
|
0.65(0.19)**
|
0.48(0.14)
|
|
UV-Na
(mEq/d)
|
1.17(054)
|
139(036)
|
1.60(055)
|
134(0.45)
|
1.57(0.22)
|
130(030)
|
|
BW(g)
|
218(23)
|
222(22)
|
218(21)
|
319(24)
|
326(18)
|
331(13)
|
SBP, DBP, PRA, UV-Protein: median and (95%
CIJ
Renal lesions, creatinine clearance, UV-Na, BW:
mean(±SD)
1 Data not available from 2 rats who had died of
stroke.
*p
< 0.05; KCI vs. either KB/C or CTL, **p <
0.05; KB/C vs. either KCI or CTL, +p
< 0.05; KCI vs. KB/C.
Endogenous
acid production
Endogenous
acid production can be considered as comprising
three components: 1) organic acids produced during
metabolism that escape complete combustion to
carbon dioxide and water; 2) sulfuric acid (H2SO4)
produced from the catabolism of methionine and
cystine, the sulfur-containing amino acids in
dietary proteins; and 3) potassium bicarbonate
(KHCO3) produced from the metabolism of
the potassium salts of organic anions in the
vegetable foods of the diet, for example potassium
citrate and potassium malate. The potassium
bicarbonate so produced titrates sulfuric and
organic acid and thereby downregulates net
endogenous acid production (NEAP).
NEAP
then is computed as the sum of organic acid
production and sulfuric acid production minus the
in-testinally absorbed potassium salts of organic
anions that are metabolized to potassium
bicarbonate.
All
foods contain sulfur-containing amino acids, although
fruits in general contain very little; animal products
and cereal grains contain very little or no
potential base - this comes mainly from fruits and
other non-grain plant foods. Organic acid
production is driven in part by the quantity of
base-precursors in the diet, so increasing
dietary base precursors does not yield equivalent
reductions in NEAP. The greater the quantity of organic
and sulfuric acids produced from metabolism, and
the lower the amounts of potassium salts
metabolizable to bicarbonate, the greater the NEAP.
Estimating
the diet net acid load
It
is possible to quantify NEAP in normal subjects ingesting
whole food diets by measurements of the quantity
of the inorganic constituents of diet, urine and
stool, and of the total organic anion content of
the urine [37]. However, such studies are
extremely time-consuming and labor-intensive.
Kurtz et al. utilized renal net acid excretion (RNAE)
as a quantitative index of NEAP, since under
steady-state conditions there is a predictable
relation between these two variables [37,38],
and since net add excretion is more readily
measured. Nearly 90 % of the variance in net acid
excretion among the subjects was accounted for by
differences in net endogenous acid production (Fig.
4).
Measuring
RNAE to estimate NEAP of whole food diets was
first used about 90 years ago [39]. Volunteers ate
large amounts of one particular food item for
approximately one week, while doing sequential
24-hour urine collections, which were then
analyzed for ammonia, titratable acids and total
carbon dioxide - the constituents of RNAE. This
approach has a number of drawbacks; not only is
it tedious and time-consuming, but as Blatherwick
wrote in his article discussing the effects of a
boiled cauliflower diet, "It became very
distasteful after the third day, so that the
experiment was discontinued."
Fig.
4 Close
correspondence of endogenous acid production to
renal net acid excretion in normal subjects
(r=0.94, p < 0.01).
Methods
of estimating diet net acid load solely from
dietary intake have also been developed. Remer and
Manz
developed an algorithm for calculating net acid
excretion using a formula that estimated net
intestinal absorption of cations and anions,
organic acids and sul-fate. In this study, RNAE as
determined by the formula I (Cl- + P1-8-
+ SO4 + OA - Na+ - K+
- Ca2+ - Mg2+) correlated
reasonably well with the measured NAE [40]. Using
a similar formula, Remer and Manz also calculated
the potential acid load for individual food items
[41].
</ |
