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Does a High Dietary Acid Content Cause Bone Loss, and Can Bone Loss Be Prevented With an Alkaline Diet?



A popular concept in nutrition and lay literature is that of the role of a diet high in acid or protein in the pathogenesis of osteoporosis. A diet rich in fruit and vegetable intake is thought to enhance bone health as the result of its greater potassium and lower "acidic" content than a diet rich in animal protein and sodium. Consequently, there have been a number of studies of diet manipulation to enhance potassium and "alkaline" content of the diet to improve bone density or other parameters of bone health. Although acid loading or an acidic diet featuring a high protein intake may be associated with an increase in calciuria, the evidence supporting a role of these variables in the development of osteoporosis is not consistent. Similarly, intervention studies with a more alkaline diet or use of supplements of potassium citrate or bicarbonate have not consistently shown a bone health benefit. In the elderly, inadequate protein intake is a greater problem for bone health than protein excess.
Special Section on Bone and Nutrition
Does a High Dietary Acid Content Cause Bone Loss, and
Can Bone Loss Be Prevented With an Alkaline Diet?
David A. Hanley*
and Susan J. Whiting
Division of Endocrinology and Metabolism, Departments of Medicine, Community Health Sciences and Oncology,
University of Calgary, Calgary, AB, Canada; and
College of Pharmacy and Nutrition, University of Saskatchewan,
Saskatoon, SK, Canada
A popular concept in nutrition and lay literature is that of the role of a diet high in acid or protein in the path-
ogenesis of osteoporosis. A diet rich in fruit and vegetable intake is thought to enhance bone health as the result of
its greater potassium and lower ‘‘acidic’’ content than a diet rich in animal protein and sodium. Consequently, there
have been a number of studies of diet manipulation to enhance potassium and ‘‘alkaline’’ content of the diet to im-
prove bone density or other parameters of bone health. Although acid loading or an acidic diet featuring a high
protein intake may be associated with an increase in calciuria, the evidence supporting a role of these variables
in the development of osteoporosis is not consistent. Similarly, intervention studies with a more alkaline diet or
use of supplements of potassium citrate or bicarbonate have not consistently shown a bone health benefit. In the
elderly, inadequate protein intake is a greater problem for bone health than protein excess.
Key Words: Acid-ash hypothesis; acid-base balance; alkaline potassium; fruits and vegetables.
In this work we examine evidence that a change in acid-
base balance through dietary means can affect bone health.
This concept is sometimes termed the ‘‘acid-ash hypothesis’
and is often promoted as an important factor in the develop-
ment of osteoporosis. This hypothesis suggests that foods
high in ‘‘acidic’’ content (e.g., animal protein and grains)
cause a chronic acidemia because of their sulfate and phos-
phate content, whereas fruits and vegetables create a more
alkaline environment because of their greater potassium-
organic anion content and may even prevent age-related
bone loss and osteoporosis. It proposes that the acidic anions
provide an increased acid load on the kidney and that the in-
creased net acid excretion (NAE) is accompanied by in-
creased calcium loss in the urine. Furthermore, proponents
of the acid-ash hypothesis suggest that, to maintain a normal
acid-base homeostasis, there is an increase in bone resorption
to buffer the excess dietary ‘‘acid.
Further credence was given to this concept when the Dietary
Reference Intake recommendation for potassium in 2005 by
the Institute of Medicine (1) made a specific reference to in-
creasing alkaline sources of potassium, that is, fruits and veg-
etables, to enhance bone health. However, recommendations
that restrict protein intake to reduce NAE, and restriction of
otherwise-healthy foods because of their ‘‘acidity.’’ may also
have implications that could be detrimental to bone health. A
recent review of the impact of acid-base balance on bone sug-
gests the proponents of the acid-ash hypothesis of osteoporosis
have underestimated the ability of the kidney and respiratory
system to deal with dietary sources of acid (2). The purpose
of this work is to examine the different types of evidence for
an acid-base effect on bone and to provide recommendations
for dietary intakes that are in-line with the evidence.
AcideBase Effects on Bone:
Observational Studies
A role for dietary vegetables and fruit on bone health has
emerged in the literature. Population-based studies have
Accepted 06/01/13.
*Address correspondence to: David A. Hanley, MD, FRCPC,
Richmond Road Diagnostic and Treatment Centre, 1820 Richmond
Road S.W., Calgary, AB T2T5C7 Canada. E-mail: dahanley@
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health, vol. 16, no. 4, 420e425, 2013
ÓCopyright 2013 by The International Society for Clinical Densitometry
reported that increased potassium intake through vegetables
and fruits is associated with increased bone mineral density.
For example, in 1999 Tucker et al, by using cross-sectional
and prospective Framingham data of subjects 69e97 yr,
showed that potassium and magnesium intakes, as well as fruit
and vegetable intake, were significantly associated with greater
bone mineral density (BMD) and with a slower rate of bone
loss, albeit the latter only in men (3). Fruit and vegetable intake
has been associated with a lower NAE, and thus, some authors
have related these studies to the concept of alkaline diets being
beneficial to bone.
Observational studies on protein, however, have not been
consistent in linking a protein-induced change in NAE to
changes in bone measures or fracture risk. Prospective as well
as intervention studies on the effect of protein intake and
BMD and/or fracture rates have almost all shown that elderly
women benefitted from an increase in protein intake (2).
Indeed, the most recent European osteoporosis guidelines
recommend a daily protein intakeof 1 g/kg body weight, a value
greater than the current dietary recommendations in the
United States and Canada (4). Thus, attempts to change NAE
by reducing protein intake may be detrimental to skeletal health.
The Dietary Approaches to Stop Hypertension (DASH)
diet, which emphasizes the intake of vegetables, fruits, and
low-fat dairy products and the avoidance of processed foods
(Table 1), may have bone benefits. In a 3-month trial among
186 middle-aged men and women, investigators reported that
the DASH diet significantly reduced biochemical markers of
bone turnover (5). However, the DASH diet does not neces-
sarily provide evidence for an acid-base effect because it
also incorporates many important healthful changes, includ-
ing sufficient calcium and protein intakes (O1000 mg and
O75 g, respectively); and a sodium intake below the upper
level of 2300 mg, which may reduce sodium-induced hyper-
A large study has corroborated the bone-health effect of in-
creasing fruits and vegetables. In the Women’s Health Initia-
tive Dietary Modification study, a low-fat and increased fruit,
vegetable, and grain educational intervention in close to
50,000 postmenopausal women was evaluated with respect
to incident hip, other site-specific, and total fractures and
self-reported falls, and, in a subset, BMD (6). After an 8-
year follow-up, the intervention group had a lower rate of
reporting 2 or more falls than did the comparison group. Al-
though few trials have been conducted in humans, many ani-
mal and cell studies indicate that a diet high in fruit supplies
carotenes, polyphenols, and other active plant compounds that
may play beneficial roles in bone metabolism (7).
The Alkaline Potassium Hypothesis
Advocates of the Alkaline Potassium Diet Hypothesis use
the Paleolithic diet as being ‘‘ideal’’ for preserving bone in-
tegrity (8). The Paleolithic diet of hunteregatherers is high
in potassium and bicarbonate precursors from vegetables
and fruit, which advocates believe counteracted the very
high protein intakes of those early humans. Herein dietary
potassium at levels of 400 mEq per day (close to 3 times
the current adequate intake for potassium) would be essential
to maintain bone integrity. In contrast, the modern western
diet is low in alkaline equivalents, and cereals, although
they are plant-based, do not provide the alkalizing effect of
fruits and vegetables. In addition, the modern western diet
is high in sodium, mainly because of processed foods. To re-
turn to a more favorable ratio of potassium (K)-to-sodium
(Na) in the diet, that is, to a ratio that is comparable with
what humans ate in preagricultural diets, both an increase
in potassium and an avoidance or severe restriction of sodium
chloride is necessary (8). Interestingly, Canadian and Ameri-
can food guide revisions have reduced the amount of cereal
grains servings and increased the amounts of fruit and vege-
table servings, that is, Eating Well with Canada’s Food Guide
(released in 2007) and MyPyramid (released in 2005). Both of
these food guides resemble the DASH diet. As illustrated in
Table 1, the DASH diet (and food guides that resemble it)
is probably the ‘‘best’ dietary pattern that can be achieved to-
day, via the use of largely unprocessed foods available in the
marketplace. By following the DASH diet, one can attain a di-
etary Na:K ratio of approximately 1:1. This ratio is a marked
improvement over dietary intakes that typically occur, that is,
w2:1, in the United States and Canada.
The Acid-Ash Hypothesis
The Acid-Ash Hypothesis is a variant of the Alkaline Potas-
sium Hypothesis. Both are premised on the argument that
acidic compounds in the diet (high protein, high phosphate,
or other ‘‘acidic’’ anions like sulfate) have an adverse effect
on bone, whereas alkaline components, such as fruit and veg-
etables, will counter this effect. Early work centered on mea-
suring NAE after consumption of diets varying in protein,
with or without variations in alkaline salts or alkaline foods
(2). However, it has never been demonstrated that, in healthy
subjects, manipulation of the diet caused any disturbance in
blood pH or bicarbonates. The ‘‘metabolic acidosis’’ predicted
with the Acid-Ash Hypothesis has remained hypothetical.
Systematic Reviews of Acid-Base and Bone
A moderately large amount of literature exists on the influ-
ence of dietary acid or alkali on bone. Although the common
theme is that a diet high in protein or phosphate would be det-
rimental to the skeleton, recent systematic reviews of this lit-
erature have not supported these premises.
The proponents of the Acid-Ash Hypothesis have sug-
gested that a diet providing high phosphate content would
be acidic and that this would result in negative calcium bal-
ance and bone loss. However, a recent meta-analysis of stud-
ies of dietary intervention with phosphate supplements found
no support for this concept (9). This analysis examined stud-
ies of phosphate supplementation that also controlled cal-
cium intake by the subjects. Control of sodium intake was
not consistent in the studies reviewed, and only one of the
studies used randomization and provided the Institute of
High Dietary Acid Content and Bone Loss 421
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health Volume 16, 2013
Medicine’s recommendations for calcium balance studies.
However, despite the variability in the quality of the studies,
regression analysis indicated that as phosphate intake in-
creased, urinary calcium decreased, irrespective of the vari-
ability in dietary calcium intake in these studies, or
whether the phosphate supplement was alkaline, neutral or
acidic. In fact, the reduction in urinary calcium excretion
was greatest with the use of acidic phosphate supplements.
However, the calcium balance was more positive with the
neutral or alkaline phosphate supplements. Very few studies
examined the effect of phosphate supplement on bone turn-
over markers or bone density; therefore, no consistent effect
could be ascertained.
This meta-analysis of the phosphate supplementation liter-
ature actually provides modest support for the opposite con-
clusion from what would be expected from the Acid-Ash
Hypothesis; that is, a high phosphate intake is associated
with increased calcium retention and a reduction in calciuria
(9). Nevertheless, the quality of the studies reviewed was not
high, and calcium balance is only a weak surrogate for long-
term effects on bone mass or bone quality.
Fenton et al also have provided 2 further meta-analyses of
literature testing the acid content of the diet on calcium bal-
ance and other bone-related outcomes (10,11). The initial
meta-analysis examined the effect of NAE on calciuria in
healthy individuals (10). In all, 25 dietary intervention studies
(of 105 reviewed) met appropriate inclusion criteria for the
meta-analysis; of note, only 2 were randomized, controlled
trials. There was a strong association between NAE and cal-
cium excretion, although 5 of the studies did not show a rela-
tionship. It was estimated that the contribution of a typical
‘‘western’ diet to NAE was 47 mEq per day, which corre-
sponded to an increase in calcium excretion of 1.6 mmol
per day. They calculated that, if diet could cause a person
to lose this much extra calcium in the urine each day, and
if the source of this calcium was bone, during an extended pe-
riod of time a clinically significant skeletal loss could occur.
However, the authors cautioned that the studies do not
Table 1
Intakes of Nutrients Important for Bone Health According to Serving Sizes of Foods of the DASH Diet
Food groups (examples
of a serving)
DASH diet
calcium intake
(foods fortified),
intake, mg
intake, mg
intake, g
Milk products
Milk, 1% (250 mL, 1 cup) 2 575 720 520 17
Cheese (50 g)
Grain products
Bread (1 slice) 7 160 950 560 21
Cereal (30 g, 1 cup)
Rice (1 cup)
Vegetable group (raw leafy vegetable)
Lettuce (1 cup) 4 200 100 970 6
Spinach (1 cup)
Fruit group
Banana (medium size) 4 95 10 1610 4
Orange (medium size)
Orange juice (1/2 cup)
Lean meat (80 g) 2 or less 50 135 550 19
Fish (80 g)
Poultry (80 g)
Egg (1) 0.6 (4 servings/week
from nuts, seeds,
and dry beans)
30 35 180 8
Cooked dry beans (125 g)
Tofu (100 g)
Peanut butter (2 tbsp-30 mL)
Total e1110 1950
4390 75
Note: Calcium, potassium, and protein are close to, or exceed, current recommendations, whereas sodium intake falls below its upper level.
Modified from Institute of Medicine (1).
Abbr: DASH, Dietary Approaches to Stop Hypertension.
Consuming unsalted products reduces sodium intake further.
422 Hanley and Whiting
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health Volume 16, 2013
provide evidence that the source of the increase in calciuria is
bone, and there are obvious adaptive measures in the hor-
monal regulation of calcium absorption and metabolism that
could allow adaptation to an increase in urinary calcium.
These authors then went on to a meta-analysis of the liter-
ature examining the effect of interventions (diet or supple-
ments) that manipulated dietary acid/base on calcium
balance (11). The studies had to meet the following criteria:
healthy adult subjects; report change in NAE in relation to
calcium balance; randomize subjects to the order of treat-
ments; and the investigators had to follow the standard recom-
mendations for calcium balance studies (7 d of tested diet
before outcome measurement; all consumed foods were
provided to the subjects; accurate assessment of amounts con-
sumed; and laboratory analysis to confirm the calcium content
of the food). Only 5 studies met these criteria, and although
a positive relationship was seen between NAE and calcium
excretion, as in the earlier meta-analysis of 25 studies, there
was no significant relationship between NAE and calcium
balance (R2 50.003; p50.38). Therefore, the authors
concluded that changes in urinary calcium excretion do not
accurately reflect calcium balance and that the promotion of
an alkaline diet to reduce NAE in the interests of preserving
the skeleton is not justified by available evidence. Finally, the
authors of a systematic review and meta-analysis of the effect
of dietary acid on bone disease (osteoporosis), applying Hill’s
criteria of causality, reviewed 238 studies, of which 55 met
criteria for inclusion (12). The authors found the available ev-
idence does not support a causal association between dietary
acid load and osteoporosis and that there was not enough ev-
idence to support recommendation of an alkaline diet for bone
Recent Randomized Controlled Trials
To support the Alkaline Potassium Hypothesis, a number of
randomized controlled trials have been published. Only those
of 2 years’ duration that included direct measures of bone
density are examined here. There have been 3 such studies in
adult women who were given alkaline potassium as either
the citrate or bicarbonate salt alone with calcium and vitamin
D; 2 studies published bone data together in one report (13)
provided null evidence for an effect, whereas a third study
(14) provides support for the Alkaline Potassium Hypothesis.
Macdonald et al (15) completed a trial of potassium citrate
(in doses of 18.5 and 55 mEq/d) or fruit and vegetable con-
sumption (predicting 18.5 mEq/d potassium intake) in post-
menopausal women for 2 years. At the same time, Frassetto
et al (13) were testing potassium bicarbonate (in doses of
30, 60, and 90 mEq/d), also in women and for 2 years. These
authors presented the results of both studies in a single paper
wherein they presented all BMD results related to salt load;
only those with moderate salt load are plotted in Fig. 1. Over-
all, no change in bone density could be attributed to potas-
sium citrate, potassium bicarbonate, or fruit and vegetable
consumption. The authors grouped their data to determine
whether sodium intake was a factor in the lack of an effect
of alkaline potassium, and this factor proved to be of no sig-
In contrast, in a recent randomized controlled trial involv-
ing women 65e80 yr, investigators found a bone benefit of
60 mEq/d potassium citrate (14). As shown in Fig. 2, BMD
in the potassium group was 1%e2% greater than placebo;
similar results were obtained using when bone microarchitec-
ture was assessed with peripheral quantitative computed to-
mography. Biochemical markers of bone turnover indicated
less bone resorption at 6 months whereas the formation
marker was greater at 24 months of intervention. Why one
study should show clear results whereas the others could
not is not apparent. The ingestion of 60 mEq/d by the women
in the study by Jehle et al (14) study brought their mean po-
tassium intakes above the recommended level of 120 mEq/d,
Fig. 1. Mean change in BMD with 24 months treatment
with alkaline-potassium (dose as mEq/d) or as fruits and veg-
etables (F&V) in women 41e105 yr, in situation of medium
mean arterial pressure, combining data from 2 studies, n 525
or 65, depending on study. Frassetto et al (8). BMD, bone
mineral density.
Fig. 2. Mean change in BMD with 24 months’ treatment
with alkaline-potassium (dose as mEq/day), in women
65e80 yr, n 584e85 per group. Jehle et al (14). BMD,
bone mineral density.
High Dietary Acid Content and Bone Loss 423
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health Volume 16, 2013
but their sodium intakes (as measured by the use of urinary
excretion levels) remained increased at approximately 160
mEq (compared with a recommended level of 56 mEq) (1).
There is no obvious explanation why one study shows
a bone benefit of potassium and the other two do not. Jehle
et al (14) propose a link between the significant decrease in
NAE with potassium citrate and the increment in bone density
and structural parameters, but one has to question whether
a change in blood pH of 0.02 within the normal range is of
clinical significance for bone. It is possible there may be other
effects of potassium citrate independent of NAE and acid base
status. A larger and longer-term clinical trial is needed.
In this paper, attention has been given to the concept that
an alkaline diet or alkaline potassium salts promote calcium
retention. As demonstrated in the systematic reviews and
meta-analyses, there is not enough evidence to support
a causal relationship between the acid/alkali composition of
a diet and bone health. However, some studies do support
a bone benefit of a ‘‘healthy’’ diet with increased vegetable
and fruit content or supplements containing potassium bicar-
bonate or citrate: (1) epidemiologic studies in which fruit and
vegetable intake was demonstrated to be positive for BMD or
other markers of bone health; and (2) experimental studies
either in laboratory animals or human volunteers showing
that alkaline potassium salts promoted a more positive cal-
cium balance, or reduced markers of bone resorption, in com-
parison to alkaline sodium salts or to acid-forming potassium
salts. The data, however, are not clear-cut, as some clinical
trials have shown that greater potassium intake does not pro-
tect against bone loss. Also, the question has arisen as to
whether the alkaline salt must have potassium as the cation,
although sodium clearly would not benefit bone health be-
cause of other mechanisms. Thus current recommended in-
take (AI) for potassium, of 4700 mg (120 mEq) for ages
14 years and over is based, in part, on the alkaline-
potassium hypothesis. Meeting this high level of potassium
necessitates choosing a healthy diet emphasizing fruits and
vegetables with a lowered sodium intake and adequate cal-
cium, such as the DASH diet, Canada’s Food Guide, and My-
Pyramid. This dietary choice, and not intake of an alkaline
potassium salt, is more likely to help optimize bone health.
1. Institute of Medicine. 2005 Dietary reference intakes: sodium,
chloride, potassium and sulphate. Washington, DC: National
Academy Press.
2. Bonjour JP. 2013 Nutritional disturbance in acidebase balance
and osteoporosis: a hypothesis that disregards the essential ho-
meostatic role of the kidney. Br J Nutr 4:1e10.
3. Tucker KL, Chen H, Hannan MT, et al. 1999 Potassium, magne-
sium, and fruit and vegetable intakes are associated with greater
bone mineral density in elderly men and women. Am J Clin Nutr
4. Kanis JA, McCloskey EV, Johansson H, et al. on behalf of the Sci-
entific Advisory Board of the European Society for Clinical and
Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO)
and the Committee of Scientific Advisors of the International Os-
teoporosis Foundation (IOF). 2013 European guidance for the di-
agnosis and management of osteoporosis in postmenopausal
women. Osteoporos Int 24(1):23e57.
5. Lin PH, Ginty F, Appel LJ, et al. 2003 The DASH diet and so-
dium reduction improve markers of bone turnover and calcium
metabolism in adults. J Nutr 133:3130e3136.
6. McTiernan A, Wactawski-Wende J, Wu LL, et al. 2009 Low-fat,
increased fruit, vegetable, and grain dietary pattern, fractures,
and bone mineral density: the Women’s Health Initiative Dietary
Modification Trial. Am J Clin Nutr 89:1864e1876.
7. Shen C-L, von Bergen V, Chyua M-C, et al. 2012 Fruits and
dietary phytochemicals in bone protection. Nutr Res 32:
8. Frassetto LA, Hardcastle AC, Sebastian A, et al. 2012 No evi-
dence that the skeletal non-response to potassium alkali supple-
ments in healthy postmenopausal women depends on blood
pressure or sodium chloride. J Nutr 138:419Se422S.
9. Fenton TR, Lyon AW, Eliasziw M, et al. 2009 Phosphate de-
creases urine calcium and increases calcium balance: a meta-
analysis of the osteoporosis acid-ash diet hypothesis. Nutr J 8:41.
10. Fenton TR, Eliasziw M, Lyon AW, et al. 2008 Meta-analysis of
the quantity of calcium excretion associated with the net acid ex-
cretion of the modern diet under the acid-ash diet hypothesis.
Am J Clin Nutr 88:1159e1166.
11. Fenton TR, Eliasziw M, Lyon AW, et al. 2009 Meta-analysis of
the effect of the acid-ash hypothesis of osteoporosis on calcium
balance. J Bone Miner Res 24:1835e1840.
Key Points
A diet high in protein, providing a high phos-
phate and sulfate content, has been thought
to increase the acid load on the kidney. This in-
creased net acid excretion has been associated
with increased urinary calcium loss. Meta-anal-
yses of studies of dietary acid/base intake and
bone do not support a major influence.
Urinary calcium loss does not necessarily
mean a negative calcium balance or bone
loss. Further, a high phosphate intake is more
consistently associated with lower calcium ex-
cretion and increased calcium retention.
Evidence for alkalinizing the diet with in-
creased intake of fruits and vegetables may
be beneficial for bone, but more studies are
needed, in the form of well-conducted clinical
trials of long duration. There is contradictory
evidence of bone effects of intervention with
potassium citrate or bicarbonate supplements
from randomized clinical trials.
Nevertheless, there are compelling reasons to
promote a diet high in fruit and vegetables
for bone health. Intakes for bone health based
on dietary recommendations found in govern-
ment food guides or dietary patterns recom-
mended for chronic disease such as the
DASH diet, should be encouraged.
424 Hanley and Whiting
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health Volume 16, 2013
12. Fenton TR, Tough SC, Lyon AW, et al. 2011 Causal assessment
of dietary acid load and bone disease: a systematic review and
meta-analysis applying Hill’s epidemiologic criteria for causal-
ity. Nutr J 10:41.
13. Frassetto LA, Hardcastle AC, Sebastian A, et al. 2012 No evi-
dence that the skeletal non-response to potassium alkali supple-
ments in healthy postmenopausal women depends on blood
pressure or sodium chloride intake. Eur J Clin Nutr 66:
14. Jehle J, Hulter HN, Krapf R. 2013 Effect of potassium citrate on
bone density, mincroarchitecture, and fracture risk in healthy
older adults without osteoporosis: a randomized controlled trial.
J Clin Endocrinol Metab 98:207e217.
15. Macdonald HM, Black AJ, Aucott L, et al. 2008 Effect of po-
tassium citrate supplementation or increased fruit and vegeta-
ble intake on bone metabolism in healthy postmenopausal
women: a randomized controlled trial. Am J Clin Nutr 88:
High Dietary Acid Content and Bone Loss 425
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health Volume 16, 2013
... Using quantitative computed tomography, it has been shown that chronic metabolic acidosis in rats decreases the total bone mineral density (BMD) [16], and changing the acid-base balance by using diet can affect bone health (acid-ash hypothesis) [17]. The highest proliferation of osteoblast-like cells has been reported at pH 8.0-8.4 [18]. ...
... Although several studies have shown that potassium bicarbonate, citrate-potassium, and even bicarbonate-rich mineral water can reduce BMD [19][20][21][22] and stimulate the synthesis of osteoblastic collagen [23], but the effect of alkaline water on T-score and bone density has not yet been investigated. Also, the action mechanism of alkaline pH on bone cell proliferation and differentiation has not yet been sufficiently investigated [17,18]. It has recently been observed that there is a link between an alkaline diet and alkaline water and a lower incidence of osteoporosis., as well as the observation of some positive effects of alkaline diets containing bicarbonate and potassium citrate on bone metabolism [17,24], more studies are needed in this regard [17]. ...
... Also, the action mechanism of alkaline pH on bone cell proliferation and differentiation has not yet been sufficiently investigated [17,18]. It has recently been observed that there is a link between an alkaline diet and alkaline water and a lower incidence of osteoporosis., as well as the observation of some positive effects of alkaline diets containing bicarbonate and potassium citrate on bone metabolism [17,24], more studies are needed in this regard [17]. The purpose of this study was the effect of alkaline drinking water on bone density in postmenopausal patients with osteoporosis. ...
Full-text available
Objectives: Postmenopausal women are predisposed to osteoporosis, and those on acidic diets are at a higher risk, because it has been demonstrated that such diets have adverse effects on bone health. In this study, the effect of alkaline drinking water on bone mineral density was evaluated in postmenopausal women with osteoporosis. Methods: One hundred postmenopausal women with osteoporosis (T-score ≤ -2.5) were equally divided into an intervention group and a control group (n = 50 each). The intervention group received calcium D (daily), alkaline drinking water (1.5 L daily with pH 8.6 ± 0.3), and Osteofos tablet (70 mg weekly), whereas the control group received only calcium D and Osteofos tablet for 3 months. T-scores of the femur and spine bones were obtained using bone densitometry before and 3 months after the intervention. Results: After the intervention, the mean T-scores of the femur and spine bones significantly increased in both the control and intervention groups (P < 0.05). However, the mean changes in the spine T-score were significantly higher in the intervention group (0.39 ± 0.07) than in the control group (0.08 ± 0.01) (P < 0.05). No significant differences were observed in the mean changes in the femur T-score between the two groups. Conclusion: Our findings demonstrate that drinking alkaline water improves spine T-scores in postmenopausal women with osteoporosis. Hence, alkaline water can be used to treat osteoporosis due to increased bone density in postmenopausal women. Long-term interventions are necessary to confirm the effects of alkaline water on femur density.
... Vegetables with higher carbohydrates (eg. potato) are considered a so-called alkaline diet [14], Their increased consumption can have negative effects but in a balanced diet, they do have a role [15,16]. Lemon, lime, and grapefruit are highly recommended without any justification. ...
... This dietary restriction can result in cardiovascular diseases, tumour, diabetes, etc. [17,18,19]. Alkaline diets and supplements have not shown benefits to bone health [15]. The allowance of fish consumption is positive based on the nutritional fact, because of their eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and beneficial fatty acid (omega-3). ...
Full-text available
The stomach of animals plays a significant role throughout life. After taking food, the nutrients of those foods maintain all biological processes. The stomach is a reservoir for storing food for several hours. If digestion within the stomach hampers, the entire body will undergo many ailments. Evolutionary changes in the stomach of various animals (herbivores, carnivores, and omnivores) to understand the quality or nature of the stomach based on their food. Based on some articles, oral communication, and an effective questionnaire proved that in a northern region of Bangladesh (Saidpur town under Nilphamari District), out of 60 families, 85% of family members were affected by acidity problems where 37% of college students (17-19 years) due to their excess taking of oily and spicy foods. On the other hand, their regular food intake showed 80% acidic, 7.5% neutral, and 12.5% alkaline food.
... Vegetables with higher carbohydrate content (e.g. potato) fall under total prohibition in the so-called alkaline diet (Young and Young, 2006), which is quite radical in the sense of diets, it can narrow the possible food sources down significantly (their increased consumption can have negative effects, but in a balanced diet, they do have their role) (Hanley and Whiting, 2013;Fenton and Fenton, 2016). ...
... Despite the fact that acid loading or a protein-rich diet might be associated with an increase in calciuria, there is no exact evidence linking these factors to osteoporosis. Further, studies of alkaline diets and supplements have not shown benefits to bone health (Hanley and Whiting, 2013). ...
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Several misconceptions exist about foods and nutrition. Many believe, that the human body can “acidify”, thus, an “alkaline diet” should be followed. The acid-base balance is a characteristic of a normally functioning human body. Throughout our metabolic processes, acids and substances with acidic pH are produced continuously, which, in the case of a healthy person, does not affect the pH of the human body. In those rare cases, when an overall pH imbalance evolves in the human body due to its life-threatening nature, it requires urgent medical intervention. Furthermore, it cannot be influenced by dietary interventions. This paper highlights evidence regarding acidification and the acid-base balance, with special attention to certain food groups. Foodstuffs have different specific pH value (acid-base character), they can be acidic, alkaline, or neutral in elemental state. Beside their chemical nature, the effect they have on the human body depends on the mechanism of their metabolism, as well. Diet and ingredients have direct and indirect effects on the human body's intracellular and extracellular compartments (especially blood and urine), still they do not influence its pH significantly. Alkaline diets were born in the absence of evidence-based information and/or the misunderstanding and wrong interpretation of the available and up-to-date scientific facts. The convictions of consumers and the promotion of the alkaline diet lack the scientific basis, so it can be harmful or even dangerous in the long run. In summary, scientific evidence on the efficacy or prophylactic effects of an alkaline diet is not available.
... Oxidation of the sulphur-containing amino acids, methionine and cysteine content of them is involved in the formation of hydrogen ions, which subsequently promotes systemic acidity [12]. Bone, as a primary buffer system, is critical to correcting acid-base imbalances by releasing alkaline salts [13,14]. It should be noted that calcium is one of the most important components of bone mineral content (BMC) and is essential for ensuring bone health [15]. ...
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Background & Aims Dietary patterns that promote mild metabolic acidosis may have a negative effect on bone and muscle, and a high dietary acid load (DAL) may be detrimental to skeletal muscle mass and bone mineral content. However, the association between skeletal muscle mass and bone mineral content with dietary acid load has not been consistently reported in previous studies. The objective of the study was to evaluate the association of potential renal net acid load (PRAL) and net endogenous acid production (NEAP) with bone mineral content and skeletal muscle mass in pre-menopause women with overweight or obesity in Iran. Method Three hundred and ninety women with a body mass index (BMI) of 25 were included in this cross-sectional study. We used a validated 147-item semi-quantitative food frequency questionnaire (FFQ) for evaluating the dietary intake. Based on the dietary data, potential renal net acid load (PRAL) and net endogenous acid production (NEAP) were calculated. Muscle mass and bone mineral content were estimated by a bioelectrical impedance analyzer (BIA). Results After controlling for potential confounders, we discovered a significant linear relationship between PRAL (β = -0.027, 95%CI = -0.049 to -0.004, P = 0.02) and NEAP (β = -0.05, 95%CI = -0.097 to -0.003, P = 0.03) and skeletal muscle mass index. However, there was no significant difference between SMM and BMC across PRAL and NEAP tertiles. Conclusion PRAL and NEAP were found to be inversely related to skeletal muscle mass index among overweight/obese women. Further research is required to establish whether this relationship is important for musculoskeletal health in these populations.
... The alkaline diet itself was the attempt for people to balance acid-base equilibrium in the body, after high consumption of an acidic diet that mostly involved animal-based food. Previous studies showed diverse and unclear results of alkaline diet impact to health benefit after intervention in some groups of community [26][27][28][29]. ...
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Objectives There are many water types available on the market. They are widely known in public with health claims. The questions are, are those claims are scientifically proven or those are just testimonies from the consumers or overclaimed by the producers. This study aims to systematically review evidences on the health effects of alkaline, oxygenated, and demineralized water in comparison with mineral water among healthy population. Contents Data were obtained from databases PubMed, Cochrane, Scopus, EBSCO, dan Science Direct since January 2000 until July 2022. There were 10 eligible articles, consisted of two articles on alkaline, four articles on oxygenated, and four articles on demineralized water, that furtherly being analyzed. Summary Compared to consumption of mineral water, consumption of alkaline and oxygenated water did not show any significant difference on gut microbiota, urine pH, blood parameter, or fitness parameter. While, consumption of demineralized water in the long term resulted in lower quality of certain nutrient intake. Outlook Recent evidences do not prove any additional health effects of alkaline, oxygenated, or demineralized water compared to mineral water. In contrast, demineralized water consumption in the long run was proven to lead to adverse effect.
Urinary stone disease (USD) is a common condition that affects approximately one in eleven adults [1]. Relapse rates in adults have been shown to be up to 50% within 5–10 years with as many as 75% of patients forming another stone within 20 years [1, 2]. Urinary stone morbidity is associated with the excruciating pain of acute stone episodes as well as urinary tract obstruction and infection. Data has linked USD with multiple systemic disease states including chronic kidney disease (CKD) [3]. In addition, adults with USD have higher rates of cardiovascular disease (CVD) including coronary artery disease, hypertension, acute myocardial infarction (MI), and stroke [4, 5]. Correlation has been found between USD and decreased bone mineral density (BMD) and increased skeletal fracture rates [6, 7]. The exact mechanisms behind the association of stone, bone, and vascular disease are unknown. Inflammation has indirectly been implicated by the association of common inflammatory metabolic conditions including diabetes, obesity, hypertension, and dyslipidemia with USD as well as CVD and bone disease [8]. The natural history of whether urinary stones precede cardiovascular or bone disease development is unclear; however, stone forming children and young adults have shown evidence of early atherosclerosis and suboptimal BMD with increased risk of skeletal fractures [9–11].
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While osteoporosis is a chronic disease caused by multiple factors, it is also a risk factor for fractures. At present, numerous risk factors for osteoporosis and secondary fractures have been identified, including sunlight, physical fitness, gender, age, trauma, dietary habits, tobacco, alcohol, drugs, air quality, and genetics. Despite that factors such as long winters, short daylight hours, less daily physical activity, air pollution, low calcium and high salt diet, and sedentary lifestyle could negatively impact the bones of residents in the alpine regions of northern China, the direct effect of low-temperature stimulation on bone growth and development remains unclear. In this study, by reviewing current research progress related to osteoporosis and fracture risk in northern China, we proposed appropriate preventive measures for different risk factors to reduce the occurrence of osteoporosis and fracture in cold areas of northern China.
Objectives Dietary protein intake is of great significance for the bone health of middle-aged and elderly people. This study is aimed to explore the relationships between dietary protein intake and the risk of osteoporosis in middle-aged and older individuals among US population.Methods Based on the National Health and Nutrition Examination Survey (NHANES), this study includes a total of 20497 participants during 2005–2008, and identify 4707 middle-aged and older people aged 45 years or above. Demographic data and relevant dietary intake information are acquired through in-home management questionnaires. The logistic regression models are established to identify the odds ratio (OR) and 95% confidence interval (CI) of OP in each quartile category of energy-adjusted dietary protein intake. The receiver operating characteristic (ROC) curve is applied to explore the optimal cut-off value of daily dietary protein intake for predicting risk of OP.Results442 participants with OP are identified among 4707 middle-aged and older people, and the dietary protein intake of OP group is significantly lower than that of non-OP group (P<0.001). The logistic regression analysis shows that with the increase of daily dietary protein intake, the prevalence of OP in each quartile category decreases gradually (P<0.001). This trend is not altered in univariate model (P<0.001), as well as the adjustments for the covariates of age and BMI (Model 1, P<0.001), the covariates of sex (Model 2, P=0.036), the covariates of smoking, drinking alcohol, education, ratio of family income to poverty, hypertension and diabetes (Model 3, P<0.001), and the covariates of dietary intake (Model 4, P=0.008). Moreover, we also identify that the daily dietary protein intake of 61.2g is the optimal cut-off value for predicting risk of OP.Conclusion In general, among US population, the lower daily dietary protein intake is positively related to the ascending risk of OP in middle-aged and older individuals.
In Kapitel. 8 wird das Konstrukt der Anionenlücke bzw. der albumin-korrigierten Anionenlücke zur Unterscheidung einer Additions- von einer Subtraktionsazidose vorgestellt. Weiterhin wird die therapeutisch wichtige Unterscheidung zwischen chloridsensitiven und chloridresistenten Alkaloseformen erläutert. Eine andere Einteilung erfolgt anhand der Ursache bzw. Pathogenese in Additions- und Subtraktionsalkalosen. Störungen des Elektrolyt- und Wasserhaushaltes gehen mit Veränderungen des Säuren-Basen-Haushaltes (SBH) einher. Dilutionsazidosen respektive Kontraktionsalkalosen entstehen durch Volumenschwankungen oder Veränderungen des Kochsalzbestandes. Hypokaliämien sind mit einer Alkalose und Hyperkaliämien mit Azidose verbunden. Auch die Homöostase im Kalzium-Phosphat-Haushalt ist mit dem SBH verknüpft. Zuletzt werden die Anionenlücke im Urin als Differenzierungsmöglichkeit eines Bikarbonat-Verlustes und die diagnostische Bedeutung der osmotischen Lücken in Serum bzw. im Urin besprochen.
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Unlabelled: Guidance is provided in a European setting on the assessment and treatment of postmenopausal women at risk of fractures due to osteoporosis. Introduction: The International Osteoporosis Foundation and European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis published guidance for the diagnosis and management of osteoporosis in 2008. This manuscript updates these in a European setting. Methods: Systematic literature reviews. Results: The following areas are reviewed: the role of bone mineral density measurement for the diagnosis of osteoporosis and assessment of fracture risk, general and pharmacological management of osteoporosis, monitoring of treatment, assessment of fracture risk, case finding strategies, investigation of patients and health economics of treatment. Conclusions: A platform is provided on which specific guidelines can be developed for national use.
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The nutritional acid load hypothesis of osteoporosis is reviewed from its historical origin to most recent studies with particular attention to the essential but overlooked role of the kidney in acid-base homeostasis. This hypothesis posits that foods associated with an increased urinary acid excretion are deleterious for the skeleton, leading to osteoporosis and enhanced fragility fracture risk. Conversely, foods generating neutral or alkaline urine would favour bone growth and Ca balance, prevent bone loss and reduce osteoporotic fracture risk. This theory currently influences nutrition research, dietary recommendations and the marketing of alkaline salt products or medications meant to optimise bone health and prevent osteoporosis. It stemmed from classic investigations in patients suffering from chronic kidney diseases (CKD) conducted in the 1960s. Accordingly, in CKD, bone mineral mobilisation would serve as a buffer system to acid accumulation. This interpretation was later questioned on both theoretical and experimental grounds. Notwithstanding this questionable role of bone mineral in systemic acid-base equilibrium, not only in CKD but even more in the absence of renal impairment, it is postulated that, in healthy individuals, foods, particularly those containing animal protein, would induce 'latent' acidosis and result, in the long run, in osteoporosis. Thus, a questionable interpretation of data from patients with CKD and the subsequent extrapolation to healthy subjects converted a hypothesis into nutritional recommendations for the prevention of osteoporosis. In a historical perspective, the present review dissects out speculation from experimental facts and emphasises the essential role of the renal tubule in systemic acid-base and Ca homeostasis.
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Modern diets have been suggested to increase systemic acid load and net acid excretion. In response, alkaline diets and products are marketed to avoid or counteract this acid, help the body regulate its pH to prevent and cure disease. The objective of this systematic review was to evaluate causal relationships between dietary acid load and osteoporosis using Hill's criteria. Systematic review and meta-analysis. We systematically searched published literature for randomized intervention trials, prospective cohort studies, and meta-analyses of the acid-ash or acid-base diet hypothesis with bone-related outcomes, in which the diet acid load was altered, or an alkaline diet or alkaline salts were provided, to healthy human adults. Cellular mechanism studies were also systematically examined. Fifty-five of 238 studies met the inclusion criteria: 22 randomized interventions, 2 meta-analyses, and 11 prospective observational studies of bone health outcomes including: urine calcium excretion, calcium balance or retention, changes of bone mineral density, or fractures, among healthy adults in which acid and/or alkaline intakes were manipulated or observed through foods or supplements; and 19 in vitro cell studies which examined the hypothesized mechanism. Urine calcium excretion rates were consistent with osteoporosis development; however calcium balance studies did not demonstrate loss of whole body calcium with higher net acid excretion. Several weaknesses regarding the acid-ash hypothesis were uncovered: No intervention studies provided direct evidence of osteoporosis progression (fragility fractures, or bone strength as measured using biopsy). The supporting prospective cohort studies were not controlled regarding important osteoporosis risk factors including: weight loss during follow-up, family history of osteoporosis, baseline bone mineral density, and estrogen status. No study revealed a biologic mechanism functioning at physiological pH. Finally, randomized studies did not provide evidence for an adverse role of phosphate, milk, and grain foods in osteoporosis. A causal association between dietary acid load and osteoporotic bone disease is not supported by evidence and there is no evidence that an alkaline diet is protective of bone health.
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The acid-ash hypothesis posits that increased excretion of "acidic" ions derived from the diet, such as phosphate, contributes to net acidic ion excretion, urine calcium excretion, demineralization of bone, and osteoporosis. The public is advised by various media to follow an alkaline diet to lower their acidic ion intakes. The objectives of this meta-analysis were to quantify the contribution of phosphate to bone loss in healthy adult subjects; specifically, a) to assess the effect of supplemental dietary phosphate on urine calcium, calcium balance, and markers of bone metabolism; and to assess whether these affects are altered by the b) level of calcium intake, c) the degree of protonation of the phosphate. Literature was identified through computerized searches regarding phosphate with surrogate and/or direct markers of bone health, and was assessed for methodological quality. Multiple linear regression analyses, weighted for sample size, were used to combine the study results. Tests of interaction included stratification by calcium intake and degree of protonation of the phosphate supplement. Twelve studies including 30 intervention arms manipulated 269 subjects' phosphate intakes. Three studies reported net acid excretion. All of the meta-analyses demonstrated significant decreases in urine calcium excretion in response to phosphate supplements whether the calcium intake was high or low, regardless of the degree of protonation of the phosphate supplement. None of the meta-analyses revealed lower calcium balance in response to increased phosphate intakes, whether the calcium intake was high or low, or the composition of the phosphate supplement. All of the findings from this meta-analysis were contrary to the acid ash hypothesis. Higher phosphate intakes were associated with decreased urine calcium and increased calcium retention. This meta-analysis did not find evidence that phosphate intake contributes to demineralization of bone or to bone calcium excretion in the urine. Dietary advice that dairy products, meats, and grains are detrimental to bone health due to "acidic" phosphate content needs reassessment. There is no evidence that higher phosphate intakes are detrimental to bone health.
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The acid-ash hypothesis posits that protein and grain foods, with a low potassium intake, produce a diet acid load, net acid excretion (NAE), increased urine calcium, and release of calcium from the skeleton, leading to osteoporosis. The objectives of this meta-analysis were to assess the effect of changes in NAE, by manipulation of healthy adult subjects' acid-base intakes, on urine calcium, calcium balance, and a marker of bone metabolism, N-telopeptides. This meta-analysis was limited to studies that used superior methodological quality for the study of calcium metabolism. We systematically searched the literature and included studies if subjects were randomized to the interventions and followed the recommendations of the Institute of Medicine's Panel on Calcium and Related Nutrients for calcium studies. Five of 16 studies met the inclusion criteria. The studies altered the amount and/or type of protein. Despite a significant linear relationship between an increase in NAE and urinary calcium (p < 0.0001), there was no relationship between a change of NAE and a change of calcium balance (p = 0.38; power = 94%). There was no relationship between a change of NAE and a change in the marker of bone metabolism, N-telopeptides (p = 0.95). In conclusion, this meta-analysis does not support the concept that the calciuria associated with higher NAE reflects a net loss of whole body calcium. There is no evidence from superior quality balance studies that increasing the diet acid load promotes skeletal bone mineral loss or osteoporosis. Changes of urine calcium do not accurately represent calcium balance. Promotion of the "alkaline diet" to prevent calcium loss is not justified.
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The effects of dietary changes on osteoporosis, low bone density, and frequent falls are unestablished. We assessed the effect of the Women's Health Initiative Dietary Modification low-fat and increased fruit, vegetable, and grain intervention on incident hip, total, and site-specific fractures and self-reported falls, and, in a subset, on bone mineral density (BMD). Postmenopausal women (n = 48,835) aged 50-79 y (18.6% of minority race-ethnicity) were randomly assigned to receive the Dietary Modification intervention (40%, n = 19,541) (daily goal: < or =20% of energy as fat, > or =5 servings of vegetables and fruit, and > or =6 servings of grains) or to a comparison group that received no dietary changes (60%; n = 29,294). After a mean 8.1 y of follow-up, 215 women in the intervention group and 285 women in the comparison group (annualized rate: 0.14% and 0.12%, respectively) experienced a hip fracture (hazard ratio: 1.12; 95% CI: 0.94, 1.34; P = 0.21). The intervention group (n = 5423; annualized rate: 3.44%) had a lower rate of reporting > or =2 falls than did the comparison group (n = 8695; annualized rate: 3.67%) (HR: 0.92; 95% CI: 0.89, 0.96; P < 0.01). There was a significant interaction according to hormone therapy use; those in the comparison group receiving hormone therapy had the lowest incidence of hip fracture. In a subset of 3951 women, hip BMD at years 3, 6, and 9 was 0.4-0.5% lower in the intervention group than in the comparison group (P = 0.003). A low-fat and increased fruit, vegetable, and grain diet intervention modestly reduced the risk of multiple falls and slightly lowered hip BMD but did not change the risk of osteoporotic fractures. This trial was registered at as NCT00000611.
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The acid-ash diet hypothesis of osteoporosis suggests that acid from the modern diet causes a demineralization of the skeleton, and mobilized bone calcium is excreted. A systematic approach has not been used to summarize the findings of the numerous studies about the hypothesis. The purpose of this meta-analysis was to estimate the quantity of net acid excretion and calciuria associated with the modern diet, to assess the association between acid excretion and calcium excretion, and to assess the influence of urine preservatives on calcium measurement. We systematically searched for trials of the acid-ash hypothesis and conducted a meta-analysis. Twenty-five of 105 studies met the inclusion criteria. The estimated quantity of net acid excretion from the weighted average of the control diets from 11 studies was 47 mEq/d. The increase in urinary calcium with a change in renal net acid excretion depended on whether the urine was acidic or alkaline (P < 0.001). A significant linear relation was observed between net acid excretion and calcium excretion for both acidic and alkaline urine (P < 0.001). The estimated change in urine calcium associated with a change of 47 mEq of net acid excretion in acidic urine was 1.6 mmol/d (66 mg/d) of calcium. Evidence suggests a linear association between changes in calcium excretion in response to experimental changes in net acid excretion. However, this finding is not evidence that the source of the excreted calcium is bone or that this calciuria contributes to the development of osteoporosis.
Osteoporosis is a disease of bone characterized by loss of bone matrix and deterioration of bone microstructure that leads to an increased risk of fracture. Cross-sectional studies have shown a positive association between higher fruit intake and higher bone mineral density. In this review, we evaluated animal and cellular studies of dried plum and citrus and berry fruits and bioactive compounds including lycopene, phenolics, favonoids, resveratrol, phloridzin, and pectin derived from tomato, grapes, apples, and citrus fruits. In addition, human studies of dried plum and lycopene were reviewed. Animal studies strongly suggest that commonly consumed antioxidant-rich fruits have a pronounced effect on bone, as shown by higher bone mass, trabecular bone volume, number, and thickness, and lower trabecular separation through enhancing bone formation and suppressing bone resorption, resulting in greater bone strength. Such osteoprotective effects seem to be mediated via antioxidant or anti-inflammatory pathways and their downstream signaling mechanisms, leading to osteoblast mineralization and osteoclast inactivation. In future studies, randomized controlled trials are warranted to extend the bone-protective activity of fruits and their bioactive compounds. Mechanistic studies are needed to differentiate the roles of phytochemicals and other constitutes in bone protection offered by the fruits. Advanced imaging technology will determine the effective doses of phytochemicals and their metabolites in improving bone mass, microarchitecture integrity, and bone strength, which is a critical step in translating the benefits of fruit consumption on osteoporosis into clinical data.
Context: The acid load imposed by a modern diet may play an important role in the pathophysiology of osteoporosis. Objective: Our objective was to evaluate the skeletal efficacy and safety and the effect on fracture prediction of K-citrate to neutralize diet-induced acid loads. Design and setting: We conducted a randomized, double-blind, placebo-controlled trial at a teaching hospital. Subjects: Subjects included 201 elderly (>65 yr old) healthy men and women (t-score of -0.6 at lumbar spine). Intervention: Intervention was 60 mEq of K-citrate daily or placebo by mouth. All subjects received calcium and vitamin D. Outcome measures: The primary outcome was change in areal bone mineral density (aBMD) at the lumbar spine by dual-energy x-ray absorptiometry after 24 months. Secondary endpoints included changes in volumetric density and microarchitectural parameters by high-resolution peripheral quantitative computed tomography in both radii and both tibiae and fracture risk assessment by FRAX (Switzerland). Results: K-citrate increased aBMD at lumbar spine from baseline by 1.7 ± 1.5% [95% confidence interval (CI) = 1.0-2.3, P < 0.001] net of placebo after 24 months. High-resolution peripheral quantitative computed tomography-measured trabecular densities increased at nondominant tibia (1.3 ± 1.3%, CI = 0.7-1.9, P < 0.001) and nondominant radius (2.0 ± 2.0%, CI = 1.4-2.7, P < 0.001). At nondominant radius, trabecular bone volume/tissue volume increased by 0.9 ± 0.8%, (CI = 0.1-1.7), trabecular thickness by 1.5 ± 1.6% (CI = 0.7-2.3), and trabecular number by 1.9 ± 1.8% (CI = 0.7-3.1, for all, P < 0.05). K-citrate diminished fracture prediction score by FRAX significantly in both sexes. Conclusions: Among a group of healthy elderly persons without osteoporosis, treatment with K-citrate for 24 months resulted in a significant increase in aBMD and volumetric BMD at several sites tested, while also improving bone microarchitecture. Based on the effect on fracture prediction, an effect on future fractures by K-citrate is possible.
Background/objectives: In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture. Subjects/methods: We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n=266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low- or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined. Results: Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: -0.6 ± 2.8% and -1.5 ± 2.4%, respectively (P=0.027); spine: -0.5 ± 3.4% and -2.6 ± 3.5%, (P<0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium- or potassium-lowering effects on blood pressure did not alter the results. Conclusions: Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.