Men's Osteoporosis Support Group

A low-acid, alkaline-forming diet for improved bone health

Acid-base introduction

This is a long article. If you want to skip to the chase, you have osteoporosis and want to have a diet that gives you the best chance of maintaining or improving your BMD, then monitor your urine pH and eat foods that will get that pH to 7 or greater. Do this either through your routine medical examinations and urinalysis testing or there are pH test strips available on the Internet, and I assume elsewhere, for you to test your own urine pH. I purchased one hundred sticks from Pulse Instruments, pH 5-10, Item Code EM-9588-31 for $18.81 plus shipping. These test the pH of urine in the range of 5 to 10 so they fit our needs exactly. The diet that will bring about a urine pH of 7-8 includes eating mainly fruits, vegetables, and tubers. I'm a vegan so I eat no animal products. If I wasn't vegan I would try to minimize (or negate the effect of) meat and most dairy products along with grains, cereals and their flours. These are acid-causing in the bloodstream, which if acidic enough, can cause bone resorption as the body breaks down bone calcium compounds to buffer the acid state. Urine pH is a proxy for the acid-base state of the body. Skip to the bottom of this page for more information on potential renal acid load (PRAL), low-acid diet concept, how to use the PRAL calculator and the CRON-o-Meter to analyze the foods you eat. Or, if you want to know about the research that led me to want to try this diet, read on. (Note that Building Bone Vitality was published after I started writing this article and is reviewed in a recent Update. There is another Update with a podcast featuring one of the book's authors, Michael Castleman, interviewed on KQED's Forum. This book is suggesting the low-acid diet, which is similar to what I'm suggesting, with minor modifications).

In order to fully understand and appreciate this topic it is important to have a basic understanding of acid-base reactions. If you want more details you can read this nice explanation or other online sites. The pH of a liquid is based upon a a number from 1 to 14. The number 7 is said to be neutral--neither acidic nor basic. All numbers below 7 are acidic, and those numbers above 7 are basic, or alkaline, The pH scale is logarithmic, meaning if you go from 7 to 6, you have really changed by a factor of ten to account for the huge number of hydrogen ions that are involved in the reaction. For simplicity sake, just remember that a pH change of one or more is really a very large change.

The measurement label used when measuring acid/base is mEq. This can be thought of similar to how we label the weights of items to help us deal with them. We know that a pound of lead will be much smaller than a pound of feathers even though they are equal in weight. Or we know that it will take a smaller batch of nuts to eat 100 calories of food than if we were eating 100 calories of spinach. We can't use the weight or size of an acid or base since we are dealing with chemical ions, which can be thought of as charged particles, each with a plus or minus charge. So we use mEq to say that an acid or base has a certain number of ions (particles) that are either acid or base. If you have a solution that is 40 mEq toward the acid side, to neutralize it, you would need another solution that has -40 mEq of base. The basic ions would react with the acid ions to form a neutral solution. It doesn't matter how much the solution weighs or how much volume it takes up, simply how many mEq it contains.

The source of bicarbonate or citrate, either from diet or supplements, that I'll refer to in the rest of this Update often comes from potassium salts, and sometimes from calcium salts. For a comprehensive look at potassium go to this website.

Buffering agent. This changes the pH from a weak acid to a weak base, or vice versa. The important point I want to make here is that the skeleton, made up of calcium to a great extent, is one of the body's buffering agents. That is, in a situation where the body fluids are too acidic, calcium (and its bicarbonate ions) is released from the bones to buffer the bodily fluids to a more alkaline state. Or, in the opposite pH state where the bodily fluids are basic in nature, calcium can be incorporated into the bones and stored for when needed later to buffer an acid state. Generally we assume if the urine pH is acidic, or highly acidic, this could mean that skeletal calcium is being lost. Conversely, if the urine pH is very alkaline, we can assume calcium is being incorporated into the bones if adequate amounts are ingested and absorbed by the gut. See Osteoporos Int. 2001;12(6):493-9. Diet acids and alkalis influence calcium retention in bone. Buclin T and others. PMID: 11446566. This was a four-period, double-crossover study investigating whether a diet intervention specifically focused on acid load could modify calcium metabolism in humans. The important conclusion the authors draw for those of us with osteoporosis is, "The acid-forming diet increased urinary calcium excretion by 74% when compared with the base-forming diet (p<0.0001), both at baseline and after the oral calcium load, and C-telopeptide excretion by 19% (p=0.01), suggesting a skeletal origin for the excess calcium output. This observation confirms that renally excreted acids derived from food influence calcium metabolism, and that alkalizing nutrients inhibit bone resorption." [Bold emphasis is mine]. So this study demonstrates the buffering ability of the skeleton when the body has to deal with an acidic diet.

Evolution of humans and their diet and its importance today

Am J Clin Nutr. 2002 Dec;76(6):1308-16. Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Sebastian A and others. PMID: 12450898. This is available free on the publisher's Website and it is a fascinating article, so I hope you can read it. Natural Selection works very slowly to establish traits and features that allow animals to adapt to their environment. The authors point out that the inventions of agriculture and animal husbandry have been present for less than 1% of human evolution, inadequate time to allow us to adapt to the changes these two events caused in our dietary pattern. In an examination of 159 preagriculteral diets the authors found these to be very basic-producing in nature (-88 mEq/d with 87% being net base-producing). [Note that a negative number for NEAP (net endogenous acid production) means the diet is basic in its effect on bodily fluids, or vice verse for a positive number]. The modern average American diet is calculated to have an NEAP of 48 mEq/d. Think of NEAP as being synonymous with PRAL.

This change from a base- to an acid-forming diet occurs because modern diets replaced plant foods (which have high amounts of basic bicarbonates) with cereal grains and energy-dense, nutrient-poor (EDNP) foods. The cereal grains are highly acid-forming in nature. The EDNP foods generally include fats, oils, sugars and similar highly processed foods with calories but little or no vitamins, minerals, or other nutritional value. They tend to be neutral, but they replace food that is base-forming, leading to a net acid result. Among the possible consequences of this rapid change from a base- to an acid-forming diet, the authors include the following: age-related osteoporosis, muscle wasting, calcium nephrolithiasis, sodium-chloride hypertension, exercise performance issues, infertility, age-related and disease-related chronic renal insufficiency.

I am going to cite a few of the interesting comments in the authors' discussion section of the study. Regarding the effects of cereal grains on the American diet's net acid production, "Indeed, cereal grains themselves are net acid-producing and alone accounted for 38% of the acid load yielded by the combined net acid-producing food groups in the contemporary diet (Table 1)." To highlight this even more they state, "Indeed, animal food intake could increase considerably under the circumstances without conversion of the diet to a net acid-producing one." That is, the meat, cheese, milk and yogurt and eggs in the American diet could actually increase without causing a net acid effect if the cereal grains and EDNP foods were replaced by non-grain plant foods.

There are no known modern hunter-gatherer societies where systemic acid-base equilibrium has been measured in the wild. They do, however, mention one study that found a New Guinean hunter-gatherer tribal group living in "the primitive feral condition" and finding that "urine pH of adults was usually between 7.5 and 9.0 because of potassium bicarbonate and carbonate excretion." Thus urine pH may be a proxy for the metabolic state being either acid or alkaline.

PRAL and urine pH

The Buclin and others study cited above also found that, "Serial blood and urine samples revealed that the diet affected blood pH (average difference 0.014, p-0.002) and urine pH (average difference 1.02, p<0.0001. . ." A pH difference of 1 is quite a large change that can be related to the diet. And other studies have also noted changes in urine pH from the intake of base-forming foods or chemicals.

Br J Nutr. 2008 Jun;99(6):1335-43. Epub 2007 Nov 28. Urine pH is an indicator of dietary acid-base load, fruit and vegetables and meat intakes: results from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk population study. Welch AA and others. PMID: 18042305. This study involved 363 people whose 7-day food diary's food frequency questionnaire was compared to 24-hour and casual urinalysis reports. The findings showed the low PRAL (alkaline diet) was significantly associated with a more alkaline urine pH.

J Nutr. 2008 Feb;138(2):435S-437S. The effect of the alkali load of mineral water on bone metabolism: interventional studies. Burckhardt P. PMID: 18203918. This article is also available for free at the publisher's Website. It summarizes several studies using mineral water to determine its effect on bone and bone-related factors. If mineral waters have an effect it could be related to the calcium content or to the alkaline nature of the chemicals in the water (bicarbonate mainly). The findings in another study by this group are interesting regarding this topic. Bone. 2009 Jan;44(1):120-4. Epub 2008 Sep 26. Alkaline mineral water lowers bone resorption even in calcium sufficiency: alkaline mineral water and bone metabolism. Wynn E, and others. PMID: 18926940. The participants were 30 female dieticians, mean age 26, receiving the same weighed, balanced diet but drinking one of two different mineral waters. The mineral waters were equal in calcium content but differed in bicarbonate so that water A has a PRAL of + 9.2 mEq and water B had a -11.2 mEq PRAL. The authors found, "Urinary pH and bicarbonate excretion increased with water B, but not with water A. PTH (p=0.022) and S-CTX (p=0.023) decreased with water B but not with water A." They concluded: "In calcium sufficiency, the acid calcium-rich water had no effect on bone resorption, while the alkaline water rich in bicarbonate led to a significant decrease of PTH and of S-CTX." Thus it is not necessarily the calcium content of the mineral water that affects bone-related factors, but whether it has a basic PRAL, which is verified by the urine pH as being more basic.

Burckhardt points out that most mineral waters have sulfates, which tend to be acidic. Only a few waters having an abundance of the bicarbonate ion tend to be basic. He modified the normal food-oriented PRAL formula to take into account the sulfates in mineral water, and then used PRAL to predict a mineral water's effect on the bone. After citing several studies that use this PRAL method to compare mineral waters either with a acid- or base-forming PRAL, Burckhardt concludes: "Considering all that, it appears that alkali mineral waters with a low PRAL value and a high content of bicarbonate exert an inhibitory effect on bone resorption that exceeds the effect of mineral waters that are only rich in calcium."

J Am Diet Assoc. 1995 Jul;95(7):791-7. Potential renal acid load of foods and its influence on urine pH. Remer T, Manz F. PMID: 7797810. This article describes the method to calculate the PRAL of several foods and food groups which can then be used to estimate the renal NAE (net acid excretion) and the urine pH when the foods with known PRALs are ingested. The correlation for urine pH and NAE was found to be 0.83, with 1 being an exact correlation, so the two factors are highly correlated. That means, in general, if you ingest foods with a positive (acid) PRAL, you will have a mild metabolic acidosis, and an acid urine pH. Or, if you ingest foods with a negative (basic) PRAL, you will have a basic urine pH. The more acidic or basic the foods you ingest, the more acidic or basic will be your urine pH.

Do Alkaline salts affect BMD?

J Am Soc Nephrol. 2006 Nov;17(11):3213-22. Epub 2006 Oct 11. Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia. Jehle S and others. PMID: 17035614. Note the full article is available free. This study involved postmenopausal women assigned to received 30 mEq of either oral potassium citrate (Kcitrate) or potassium chloride (KCl) daily for one year. The Kcitrate group gained almost 2% of BMD at the lumbar spine and total hip and almost 1.5% at the femoral neck. A secondary finding was a fall in blood pressure (BP) for both groups of almost 8 points systolic and 6 points diastolic measured in mmHg. Note that these were not hypotensive individuals, their blood pressure was normal going into the study. The authors conclude, "Bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as citrate, and the effect is independent of reported skeletal effects of K." [Emphasis mine]

Editor's comments. There are several interesting observations, including this: "It generally is not appreciated that the acid load that is induced by the Western diet typically is on the order of 25 to 125 mmol/d protons and is present for the entire lifespan." They note two studies that showed when they neutralized this acid load short term with alkali salts it resulted in calcium retention and bone marker changes that were compatible with decreased bone resorption in both postmenopausal women and young adults. It is presumed, but not proven, that calcium retention is because it is not being resorbed from bone by the metabolic acidosis because it has been reversed by the alkaline citrate.

Another comment the authors made suggests they don't know for sure if the BMD increased because of increased bone formation or antiresorption, so further studies will need to determine that. Noteworthy also is that the 1.9% BMD increase in the lumbar spine after one year is actually slightly greater than the 1.7% increase obtained with FDA-approved Raloxifene, which is used only in women.

Using the KCl group in lieu of controls showed that it was the citrate anion, not the potassium cation, that led to the increased BMD. However, note that both groups had reduced BP. I didn't see a mention of it, but apparently the potassium itself reduces BP notwithstanding the anion it is paired with.

Bottom line of this study: Kcitrate increases BMD significantly when given over a one-year period to postmenopausal women in a 30 mEq daily dose.

J Clin Endocrinol Metab. 2009 Jan;94(1):96-102. Epub 2008 Oct 21. Treatment with potassium bicarbonate lowers calcium excretion and bone resorption in older men and women. Dawson-Hughes B and others. PMID: 18940881. This study is not a clear-cut example showing an alkaline potassium salt increases BMD. It did, however, show that individuals 50 years-old and older taking 67.5 mmol/day [mmol and mEq are equal for bicarbonate] of potassium bicarbonate for three months had significant reductions in urinary N-telopeptide (a biochemical marker of bone resorption) and calcium excretion. Comparatively speaking, it can be assumed that the potassium bicarbonate group would thus have increased BMD compared to the non-bicarbonate group after three months. The authors noted, "In conclusion, we have found that reducing the acidogenicity of the diet into the alkali-producing range with bicarbonate lowers calcium excretion and the bone resorption rate in healthy older men and women consuming rather typical acid-producing American diets."

N Engl J Med. 1994 Jun 23;330(25):1776-81. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. Sebastian A and others. PMID: 8190153. Note this full article is also available for free online. This study involved 18 postmenopausal women who were given oral doses of potassium bicarbonate for 18 days while on a constant diet regarding calcium and protein intake. The results showed that calcium and phosphorus balance became less negative or more positive. Serum osteocalcin (a marker of bone formation) increased and urinary hydroxyproline (a marker of bone resorption) decreased during the study. The authors concluded: "In postmenopausal women, the oral administration of potassium bicarbonate at a dose sufficient to neutralize endogenous acid improves calcium and phosphorus balance, reduces bone resorption, and increases the rate of bone formation." So this study didn't use dual-energy X-ray absorptiometry (DXA), or similar bone density testing to verify actual increases in BMD, instead using biochemical markers as proxies. It was a short study, but the results appear to correlate with those of the two previous studies discussed here regarding adding alkaline salts to the diet.

J Clin Endocrinol Metab. 2005 Jun;90(6):3528-33. Epub 2005 Mar 8. Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women. Sakhaee K and others. PMID: 15755853. This full article is also available free at the publisher's website. This study involved two forms of citrate, either used separately on in combination, and compared to placebo in a crossover study involving 18 postmenopausal women. Each arm of the study lasted two weeks. The authors noted, "Compared with placebo, combined treatment increased urinary calcium, marginally reduced sPTH, provided a clear alkali load, and reduced the bone resorption markers serum type I collagen C-telopeptide and urinary N-telopeptide by 20.4% (P < 0.0001) and 18.2% (P = 0.005), respectively." And they concluded: "In postmenopausal women, combined treatment with potassium citrate and calcium citrate inhibits bone resorption by providing an alkali load and increasing absorbed calcium." [Emphasis mine].

Editor's comments. This study found that the combination of calcium and potassium citrates took advantage of the best properties each single pill demonstrated. Particularly the calcium citrate caused a significant increase in absorbed calcium, something not seen with potassium citrate when used alone. Additionally, markers of bone formation or resorption where not affected by the potassium citrate, calcium citrate did affect some, but not all of the markers. The authors note in the discussion that is probably due to the short duration of the study that would not allow enough time for osteoblasts to respond to the medications.

Calcif Tissue Int. 2004 Apr;74(4):330-5. Effects of potassium citrate supplementation on bone metabolism. Marangella M and others. PMID: 15255069. The authors note that the beneficial effect of potassium citrate on reducing kidney stones was well document, but its effect on BMD was not so well verified. This study followed 22 postmenopausal women for three months on potassium citrate daily supplements. There was a significant net decrease in acid excretion and in urinary doxypyridinolines, hydroxyproline-to-creatinine ratios and, to a lesser extent to osteocalcin. These changes indicated that potassium citrate can reduce bone resorption to ease the potential adverse effects of chronic acidemia from protein-rich diets.

Editor's comments. These findings are in general agreement with the other articles noted above regarding the benefits of potassium citrate on bone. Once again the markers of bone resorption were proxies for DXA results, so keep that in mind.

J Endocrinol Invest. 2005 Mar;28(3):218-22. Long-term potassium citrate therapy and bone mineral density in idiopathic calcium stone formers. Vescini F and others. PMID: 15952405. This was a two-year study of 109 male and female subjects taking potassium citrate supplements for prevention of renal calcium stones that found increased distal radius BMD occurred with the supplements. The authors concluded: "Our results indicate that long-term treatment with K citrate increases forearm BMD in idiopathic Ca stone formers."

Editor's comments. These results are interesting and significant because they show that just alkalizing the diet with potassium citrate can increase BMD. The two-year T-score change indicated the mean T-score went from the midrange of osteopenia to the low range of normal. Logically any dietary change that alkalizes the diet should do the same thing. Since we are dealing with acid-base functions, it isn't the source of the acid or base that is so important, but its strength (pH) that should be the key. So next I want to look at any studies that examined food sources of alkali to see if they also affect bone health.

Does alkaline diet increase BMD?

Am J Clin Nutr. 1997 Jun;65(6):1831-9. Nutritional influences on bone mineral density: a cross-sectional study in premenopausal women. New SA and others. PMID: 9174480. The full study is available free online. Since this was another cross-sectional study, taking a snapshot of events at one point in time, it can't provide causality information. But it does give us a picture that relates certain variables to other variables while providing a clue as to their importance. Further studies could then seek causes of the effects noted. The participants in this study were pre-menopausal women in Scotland who had volunteered to have a BMD scan (DXA). Their current and past dietary intake was estimated with a food-frequency questionnaire and they were divided into quartiles according to various food and nutrient intakes. These were then compared to the BMD scores for individuals in each quartile. Of interest to my discussion here was that there was a significant difference in BMD of the lumbar spine in those with the highest reported intake of potassium. The authors noted, "In conclusion, the results of this study suggest that high current intakes of the nutrients potassium, magnesium, vitamin C, fiber, and zinc were associated with a higher bone mass and that a high past consumption of fruit had a positive effect on adult bone mass. These findings appear to indicate that high long-term intakes of nutrients found in abundance in fruit and vegetables may be important to bone health, possibly because of their beneficial effect on acid-base balance." [Emphasis mine].

Editor's comments. The authors said they took every precaution to use the most accurate dietary questionnaires and other steps to prevent problems with their data. That, coupled with the fact that their findings seem logical in consideration of what we know about foods that are base-producing in nature, gives strength to their argument that fruits and vegetables high in potassium are associated with greater lumbar spine BMD in premenopausal women.

Am J Clin Nutr. 2000 Jan;71(1):142-51. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? New SA and others. PMID: 10617959. The full study is available free online. This is a similar study method as used above by the New and others group. They also used markers of bone formation and resorption to validate their BMD results via DXA for the lumbar spine and femoral neck, and used peripheral quantitative computed tomography to evaluate peripheral BMD of the forearm. The results showed the women with the highest amount of fruit intake in childhood had higher BMD of the femoral neck. Higher potassium intake was also associated with higher total bone mass. Higher potassium intake was also associated with decreased values for markers of bone resorption. The authors note in the discussion, ". . .intakes of nutrients found in abundance in fruit and vegetables, namely, potassium, ß-carotene, vitamin C, and magnesium, were positively associated with bone health."

Editor's comments. These finding add credence to those of the 1997 New and others study regarding potassium intake and bone health.

Am J Clin Nutr. 2005 Apr;81(4):923-33. Low dietary potassium intakes and high dietary estimates of net endogenous acid production are associated with low bone mineral density in premenopausal women and increased markers of bone resorption in postmenopausal women. Macdonald HM and others. PMID: 15817873. The full article is available free online. Very interesting comments made in the introduction of the full article are, "At the cellular level, metabolic acidosis causes calcium efflux from bone, stimulates osteoclastic action, and inhibits osteoblastic action, whereas the opposite is true of metabolic alkalosis." This explains the mechanisms of action for either calcium removal from bone or addition to it based upon whether there is metabolic acidosis or alkalosis. Osteoclasts resorb bone, osteoblasts form bone. Thus the reason to want to have a state of metabolic alkalosis to help maintain or build BMD.

This is another cross-sectional study that compared the bone density across quartiles for 3226 peri- and early-postmenopausal women. They found a 6-8% increase in markers of bone resorption in the quartile with the lowest potassium intake and the highest net endogenous acid production (NEAP). A difference of 8% in BMD was observed between the highest and lowest quartiles of potassium intake in the premenopausal group. The conclusions were: "Dietary potassium, an indicator of NEAP and fruit and vegetable intake, may exert a modest influence on markers of bone health, which over a lifetime may contribute to a decreased risk of osteoporosis."

Editor's comments. An 8% difference in BMD doesn't sound like that much, but that is probably equal to two or three years of gain with one of the bisphosphonates, so not insignificant either. It would have been more impressive had the association gone for all women in the study. The authors suggest that this failure may be due to physical characteristics of some women in the lowest quartile.

The Buclin T and others study cited above is also an example of diet affecting factors of bone formation or resorption. It infers that long term a base-forming diet would reduce loss of skeletal calcium in comparison to what an acid-forming diet would do. But that hasn't been shown yet. It would be great to see a long-term study that included DXA to evaluate the effect on BMD of the two diets. I'm looking for such a study, but no luck finding one yet.

Am J Clin Nutr. 1999 Apr;69(4):727-36. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Tucker KL and others. PMID: 10197575. This is available as free full text also. The was a cross-sectional and 4-year longitudinal study of members of the Framingham Study comparing diet and BMD at several sites. The authors found, "Greater potassium intake was significantly associated with greater BMD at all 4 sites for men and at 3 sites for women (P < 0.05). Magnesium intake was associated with greater BMD at one hip site for both men and women and in the forearm for men. Fruit and vegetable intake was associated with BMD at 3 sites for men and 2 for women. Greater intakes of potassium and magnesium were also each associated with less decline in BMD at 2 hip sites, and greater fruit and vegetable intake was associated with less decline at 1 hip site, in men. There were no significant associations between baseline diet and subsequent bone loss in women." This led them to conclude that an alkaline-forming diet had beneficial effects on bone density.

Editor's comments. These results are similar to those above regarding the value of potassium and other elements of a base-producing diet to benefit bone metabolism. Had all the correlations remained constant for each gender and each bone site the findings would have been stronger. Perhaps future research will shed light on that. But this study adds weight to the notion that base-forming foods benefit bone mineral density, while certainly not proving it.

Diet options to affect bone mineralization

If you want to use the PRAL concept and urine pH to test for its effectiveness, check with your healthcare provider first if you are in doubt. I'm not a nutritionist or a physician and am not giving medical advice. You should particularly verify that increasing your daily intake of potassium would have no negative effect on your health, modify or interfere with any medications you are taking, etc.

The previously discussed studies are suggestive that a diet with the ability to alkalize the blood/serum should be beneficial for bone health while maintaining a state of mild metabolic alkalosis, as humans did for the first 99% of their evolution. The strongest studies are related to using salts of potassium or calcium, either the citrate or carbonate. Likely this is because it is easier to get reliable compliance and other results with a daily pill or two rather than trying to control the entire daily food intake. But, because there is a strong correlation between PRAL and urine pH this should afford a fairly simple way for anyone interested in using diet to maintain a mild state of metabolic alkalosis. That is, eat and drink items that are known to have a negative PRAL, and then verify that is working by testing your urine pH. It should definitely be 7 or greater, and I strive for the 7-8 range personally.

There are at least four ways to use the PRAL concept. Keep in mind that PRAL values are calculated for 100 grams of each item, which is about 3.5 ounces. Thus if you eat 7 ounces, double the PRAL value. If you eat 1ounce, cut it by about 2/3s, etc.

1) Just eat more fruits and vegetables than you are now, and/or fewer meats and grains and dairy products. Based upon the urine pH you have, adjust accordingly.

2). Use the estimated PRAL values for general food categories that I list here. Eat more of the ones with a low PRAL, and fewer of the ones with the high PRAL, test your urine pH and modify as needed. From my previous Newsletter here is my list of general food categories and their PRAL: Fats and oils have no PRAL; fish have 7.9; fruits and juices have -3.1 (except dried fruits have a much lower number, e.g., raisins -21); bread has 3.5; flour 7.0; noodles 6.7; meat has 9.5; milk has 1.0; soft cheese has 8.0; hard cheese has 23.6, and vegetables have -2.8. There are two items not on any of the lists I've seen elsewhere that are important for their alkalizing ability: molasses and sun-dried tomatoes. Any brand of (preferably unsulfured) molasses is good with a Tbsp being about -7.71. But Wholesome Organic Molasses brand is -17.85 per Tbsp. The PRAL of sun-dried tomatoes is about -58.36. It is possible to buy sun-dried tomatoes online for between $4 and $5 per pound in the U.S. This sounds expensive, but realize that a pound of sun-dried tomatoes is made from 20 pounds of whole tomatoes. I usually pay at least $1 a pound for whole tomatoes, and often more. Meaning the sun-dried variety is almost 75% cheaper than whole tomatoes when considering the nutrient value, not the weight. That means we pay about an extra 75% for the water in the whole tomatoes compared to the sun-dried version. And I've seen no other food item that comes close to the alkalizing effect of sun-dried tomatoes.

3) Use other resources to get specific PRAL values of foods, such as this site which has considerable information. Calculate or estimate the PRAL of each food you eat to be sure you have a negative value daily. Test your urine pH to verify you are in the desired pH range.

4) Use a PRAL spreadsheet calculator similar to mine in conjunction with CRON-o-METER to calculate the exact PRAL for foods. Here is the PRAL calculator:

You can see that Food and Amount are just for your own edification, they aren't part of the formula. What I have done is used the CRON-o-METER to insert the amount of the food and its name, then it gives me the Protein, Phosphorus, etc. which I type in those cells. the PRAL value calculates with each cell's data entry.

The above is an example of the CRON-o-METER's (CoM) calculations for 100 g of some food. There are two tabs that are used: General for the grams of protein and Minerals for the milligrams of the other items. Examples for how the CRON-o-METER is used for the dried apricots are shown below in the graphic.

To get here I clicked on Add Serving, typed in Apricots and then clicked on the Apricots, dried, sulfured, uncooked. Then I left the lower block on g (grams), but could have hit the down arrow to select cups, each or whatever other options that were there. Then I click on Add, and this is what I have when I click on the General tab. From there I type the protein amount in the PROTEIN G column on the spreadsheet PRAL calculator. Next we'll go to the Minerals tab as below. (Note if you make a mistake when you enter a food, you can right click on it and delete, then start over. Or you can double click on the item, e.g., grams, and then modify what you entered.)

From here I can get all the other values I need for the PRAL calculation, once they are all entered in the correct columns, the calculated PRAL automatically comes up.

If you add another food item to the list above, what will happen is that the totals in the tabs below will be for the combination of both (or however many items you have added) immediately after you add each new item to the food list. To see what any single item contributes by itself, just click on it. If you then want to see the total amount again for all or some items, use the control key for the PC or the command key for the Mac and click on each item while holding that key until they are all selected.

The other thing I do with the CoM is to make new recipes for foods that I create. Go to Food, Create New Recipe and then start adding foods to the list. I try to name the new food, "My something food" so that it will be easy to find my creations by just starting the search with the word "My" each time. I also like to put the PRAL of my recipe in the name so I won't have to recalculate it later. This can be educational if you eat a lot of grains. Start the new recipe with your old grain item, e.g., oatmeal, maybe with some oat bran. Then add some fruits, e.g., banana, dried apricots or prunes, strawberries, etc., to see how many it takes to alkalize the oatmeal. Obviously you have to enter you nutrient total in the spreadsheet PRAL calculator as you add each new food to get the effect of the addition.

I hope this is helpful for anyone wanting to try the low-acid diet as a means to improving bone health. Discuss this with your physician first, if you then agree to try this diet, get some urine pH test strips, and use the information here to make your diet one that is consistently low-acid-forming in nature. Ideally a starting test for biochemical markers of bone breakdown and/or formation would be helpful. Then after a few months have those tested again to see if there are improvements: reduced markers of bone resorption and increased markers of bone formation. Then follow the results with DXA to see if BMD increases. I'd like to hear about your results if you move to an alkalizing diet or if you have questions, send an email.

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