I am trying to understand if there is some truth in the acid-base diet
theory. I've been reading different opinions on the net.

Anyway, I see there are studies on Pubnet about acid-base balance in diet.
What do you make of this article, for instance?

http://www.nutrition.org/cgi/content/full/128/6/1051
The Journal of Nutrition Vol. 128 No. 6 June 1998, pp. 1051-1053
Excess Dietary Protein Can Adversely Affect Bone1,2

Uriel S. Barzel3 and Linda K. Massey*, 4

Division of Endocrinology and Metabolism, Department of Medicine,
Montefiore Medical Center and The Albert Einstein College of Medicine,
Bronx, NY 10467 and * Food Science and Human Nutrition, Washington State
University, Spokane, WA 99201

      ABSTRACT
The average American diet, which is high in protein and low in fruits and
vegetables, generates a large amount of acid, mainly as sulfates and
phosphates. The kidneys respond to this dietary acid challenge with net
acid excretion, as well as ammonium and titratable acid excretion.
Concurrently, the skeleton supplies buffer by active resorption of bone.
Indeed, calciuria is directly related to net acid excretion. Different food
proteins differ greatly in their potential acid load, and therefore in
their acidogenic effect. A diet high in acid-ash proteins causes excessive
calcium loss because of its acidogenic content. The addition of exogenous
buffers, as chemical salts or as fruits and vegetables, to a high protein
diet results in a less acid urine, a reduction in net acid excretion,
reduced ammonium and titratable acid excretion, and decreased calciuria.
Bone resorption may be halted, and bone accretion may actually occur.
Alkali buffers, whether chemical salts or dietary fruits and vegetables
high in potassium, reverse acid-induced obligatory urinary calcium loss. We
conclude that excessive dietary protein from foods with high potential
renal acid load adversely affects bone, unless buffered by the consumption
of alkali-rich foods or supplements.
KEY WORDS: humans · protein · bone · acid · potassium

This paper will discuss the effects of dietary protein on acid-base
metabolism and ultimately on urinary calcium and bone. Although important,
heredity, exercise and dietary calcium and phosphate per se will not be
considered. Because the factors discussed are not related to sex hormones,
findings apply equally to both genders.

Bone is a very large ion exchange buffer system. Green and Kleeman (1991)
reported that 80% of total body carbonate is in the hydration shell, the
water surrounding bone, as are 80% of citrate and 35% of sodium, which can
serve to buffer excess acid. Ninety-nine percent of the calcium is in bone.
Bone responds to acid by an acellular, physicochemical reaction with the
rapid release of carbonate, citrate and sodium from the hydration shell. In
response to chronic acid stress such as is imposed by an acid-ash diet,
cellular responses mobilize bone and calcium as a buffer.

An acid-ash diet is a diet that creates acid in the process of its
metabolism. The average American diet, which is high in protein and low in
fruits and vegetable, can generate over 100 mEq of acid daily, mainly as
phosphate and sulfate (Remer and Manz 1994). Acid generated by diet is
excreted in the urine. Foods such as fish and meat have a high potential
renal acid load (PRAL) (Table 1). Many grain products and cheeses also have
a high PRAL. In contrast, milk and non-cheese dairy products such as yogurt
have a low PRAL. Fruits and vegetables have a negative PRAL, which means
that they supply alkali-ash.


View this table:
http://www.nutrition.org/cgi/content-nw/full/128/6/1051/T1

     Table 1. Average potential renal acid loads (PRAL) of certain food
groups and combined foods1

An example of a food product that yields high levels of acid for the body
to dispose of is a cola drink. Phosphoric acid is one of the ingredients
listed on the cola container. The pH of cola is ~3.0, ranging from 2.8 to
3.2. The human kidney can excrete urine with a pH no lower than 5. If one
ingests and fully absorbs a beverage with a pH of 3, one has to dilute it
100-fold to achieve a urinary pH of 5. Thus, a can containing 330 mL of
cola would result in 33 L of urine! This does not happen because the body
buffers the acid of the soft drink. For full buffering, 1 L of cola
requires some four tablets of Tums, which contain 16 mEq of carbonate as
the calcium salt.

A relevant comparison of the metabolic effects of acid phosphate and
neutral phosphate was published by Lau et al. (1979). Young healthy adults
consumed identical diets plus 2 g of phosphate, either acidic or neutral.
The total phosphate ingested was identical, but the acid phosphate group
ingested an excess of 24 mEq H+. Net urinary acid and calcium excretion
were measured. Urinary calcium excretion per day was 52 mg greater in
subjects consuming acid phosphate than in those ingesting neutral
phosphate. Clearly, it is not how much phosphate is consumed that affects
urinary calcium, but whether it is in a chemically neutral or acid form.

Similar findings were reported by Breslau et al. (1988). They compared
vegetarian, ovovegetarian and animal protein diets. Although total protein,
phosphorus, sodium, potassium and calcium content of all of these diets was
not different, the animal protein diet contained 6.8 mmol more sulfate.
Urinary pH was more acidic, 6.17 vs. 6.55, and net acid excretion was 27
mEq/d higher in those consuming the animal protein diet; both urinary
phosphate and sulfate were higher. Daily urinary calcium was 47 mg higher
when those young adults were consuming an animal protein diet vs. the
vegetarian diet.

The effect of a higher protein, acid-ash diet has also been shown in
elderly people who participated in a study in which they ate 0.8 or 2 g
protein/kg body weight (Licata et al. 1981). Urinary calcium nearly doubled
with the higher protein diet, increasing from 90 ± 17 to 171 ± 22 mg/d.
Calcium balance was positive (+40 ± 35 mg/d) when subjects consumed the low
protein diet but negative (-64 ± 35 mg/d) when they consumed the high
protein diet.

Recently, Appel et al. (1997) reported the effect of a high fruit and
vegetable diet in an 8-wk study of >350 people. Dietary protein was a
constant percentage of energy, whereas dietary calcium was somewhat lower
in the control diet (443 vs. 534 mg/d), and dietary potassium and magnesium
were higher in the experimental diet (4700 vs. 1700 mg/d and 423 vs. 176
mg/d, respectively). An increase in fruit and vegetable intake from 3.6 to
9.5 daily servings decreased urinary calcium from 157 ± 7 to 110 ± 7 mg/d,
a drop of 47 ± 6 mg/d, whereas urinary calcium of controls dropped only 14
± 6 mg/d. This was not an effect of salt, because urinary sodium decreased
by only 232 mg/d (7%) in the intervention group, and increased by 142 mg/d
(5%) in the control group. Fruits and vegetables are the major source of
buffer in the diet (Table 1).

Population studies further confirm the effect of urinary acidity on urinary
calcium excretion. Hu et al. (1993) studied women in five different Chinese
counties. Urinary calcium excretion was lower when the urine was more
alkaline; more acidic urine was associated with a higher urinary calcium.

Strong evidence that the effects of high protein diets are mediated through
changes in acid-base balance comes from studies in which the acid loads of
dietary protein are neutralized with bicarbonate. Only two studies with
this design have been published to date. Lutz (1984) supplemented a high
protein diet (102 g) with bicarbonate and looked at the effect on urinary
calcium and calcium balance. Subjects were in negative calcium balance
while consuming 102 g protein/d, but the bicarbonate supplement decreased
urinary calcium by 66 mg/d and balance was slightly positive. Subjects had
similar calcium balances when consuming either the high protein (102 g)
diet plus bicarbonate or a moderate protein (44 g) diet. A more elaborate
study was conducted by Sebastian et al. (1994) who studied a 96-g protein
diet in women. During KHCO3 supplementation, urinary calcium fell and
calcium balance was more positive.

A study in adult rats assessed bone formation and resorption by
microradiography (Barzel and Jowsey 1969). Rats fed ammonium chloride for 1
y had increased resorption of bone and decreased amounts of femoral bone,
~15-20%. A similar effect was also seen when the rats consumed a low
calcium diet. Bone resorption was increased in rats consuming ammonium
chloride regardless of the calcium content of the diet, and total bone was
smaller than in the controls fed the same diet. Rats fed a low calcium diet
who received bicarbonate experienced high bone formation and deposited
about the same amount of bone content as rats fed a regular calcium diet.
Ammonium chloride as a source of acid caused bone resorption and decreased
total bone, whereas bicarbonate increased bone formation and increased
total bone, thus protecting the rat's skeleton from the negative effects of
a low calcium diet. More recently, the effects of acid ingestion on rat
bones were duplicated with histomorphometry and bone markers by Myburgh et
al. (1989).

Overall, these studies show us that the effects of adding buffer to a high
protein diet are as follows: 1) urine pH falls; 2) urinary net acid
excretion, titratable acidity and ammonia excretion decrease; 3) calciuria
decreases; and 4) total bone increases. On the other hand, when the body is
challenged with a dietary acid load, the kidneys excrete more acidic urine,
and the organism also turns to the skeleton for additional buffer.

The long-term consequence of a small change in calcium balance is
substantial. A 50-mg increase in urinary calcium loss per day will result
in a 18.25-g loss per year, or 365 g over 20 y. Because the average adult
female skeleton contains 750 g calcium at its peak, this is a loss of one
half of total skeletal stores! For a male with a store of 1000 g calcium,
this is about one third of the total.

Both Bushinsky (1996) and Arnett and Sakhaee (1996) have documented that
osteoclasts and osteoblasts respond independently to small changes in pH in
the culture media in which they are growing. A small drop in pH causes a
tremendous burst in bone resorption. Sebastian et al. (1994) noted small
changes in blood pH and CO2 levels that would be considered within the
normal range during the potassium supplementation described above, but
would be sufficient to affect bone metabolism.

Dietary salt is known to affect urinary calcium excretion. It is generally
poorly appreciated that the anion accompanying sodium is important to the
overall effect of salt on calcium metabolism (Massey and Whiting 1996).
When Berkelhammer et al. (1988) replaced sodium chloride with equimolar
sodium acetate in patients receiving total parenteral nutrition who had
marked hypercalciuria, urinary calcium decreased markedly and calcium
balance became positive. The blood pH was 7.37 with sodium chloride and
7.46 with sodium acetate. It was the chloride or acetate, not the sodium,
that determined the blood pH and the degree of urinary calcium excretion.
They confirmed observations by others that urinary calcium paralleled total
acid excretion.

The effects of dietary protein may be greater as we age. Aging kidneys
cannot generate ammonium ions and excrete hydrogen ions as well as young
kidneys do. High dietary acidity yields a lower blood pH in the elderly
(Frassetto et al. 1996). In fact, a review of the literature reveals that
older people have higher blood H+ and lower blood bicarbonate (Frasetto and
Sebastian 1996). Parathyroid hormone (PTH) levels are higher in older
adults. PTH influences plasma CO2 as well as plasma phosphate levels; the
total buffering capacity is decreased when PTH is elevated (Barzel 1981).
Overall, we can conclude that the elderly have decreased renal ability to
excrete free acid, as well as elevated PTH, both of which promote acidosis.
Therefore, the elderly may be more sensitive to the effect of acidic diets,
and this would mean that they require more buffer than younger people for
the same dietary acid load. When the elderly are given supplements of
calcium citrate, lactate or carbonate, it is not the calcium but the
accompanying anion that benefits their bones. Over time, it is the balance
of dietary acid and base that determines calcium balance; remember that
different food sources of protein differ greatly in their acidogenic
effects (Remer and Manz 1995).

Bone and mineral investigators should look at acid-base effects of diet and
use appropriate methods to quantitate these effects. The 24-h urine
collection in a metabolic unit as part of total calcium balance measurement
is the gold standard of acid-base research. The 24-h collection of urine in
an ambulatory setting, as used by Appel et al. (1997), is a second choice
method. Hu et al. (1993) used a 12-h, overnight collection in a community
study. Another approach to evaluate the acid-base effect of a diet is to
quantitate the net acid content of each dietary item (Remer and Manz 1995).
There is also a need to develop convenient methods for quantitating urinary
acid excretion. A possible simplified approach could be based on key
dietary and urinary components. For example, Frassetto et al. (1997) found
that the dietary protein to potassium ratio predicts net acid excretion.
Net renal acid excretion, in turn, predicts urinary calcium excretion.

In summary, a diet high in acid-ash protein causes excessive urinary
calcium loss because of its acid content; calciuria is directly related to
urinary net acid excretion. Alkali buffers, whether chemical salts or
dietary fruits and vegetables, reverse this urinary calcium loss.

Overall, the evidence leaves little doubt that excess acidity will create a
reduction in total bone substance. This is normal physiology---not
pathology. This is a mechanism of Homo sapiens to protect himself against
acidosis. The ability to buffer the acidosis of starvation or a high meat
diet gave a survival advantage in a hunter-gatherer society. Modern peoples
are now eating high protein, acid-ash diets and losing their bones. The
study by Appel et al. (1997) shows that increasing buffering capacity by
increasing fruit and vegetable intake is a practical way to counteract the
acidity generated by the dietary protein, reduce calciuria and consequently
improve calcium balance.

      FOOTNOTES
1   Presented at the Annual Meeting of the American Society for Bone and
Mineral Research, September 10, 1997, Cincinnati, OH.
2   The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 USC section 1734 solely to indicate
this fact.
3   To whom reprint requests should be addressed.
4   To whom correspondence should be addressed.

Manuscript received 27 January 1998. Revision accepted 9 March 1998.

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