Protein May Adversely Affect Bone

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The Journal of Nutrition Vol. 128 No. 6 June 1998, pp. 1051-1053

 

http://www.nutrition.org/cgi/content/full/128/6/1051

 

Protein May Adversely Affect Bone

 

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

References

 

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. Food such as meat have a high

potential renal acid load (PRAL) (Table 1). Many refined grain products and

cheeses also have a high PRAL. In contrast, 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.

 

 

 

 

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.

 

 

Moderators Note: This would not be advisable as Tums carries with it some very

unhealthy additives, for instance aluminum which carries a known link to

Alheimers, etc..

 

 

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 physiologynot 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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osteoclasts by small changes in extracellular pH near the physiological range.

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