Download this article in PDF version
(Adobe PDF reader required)
Diet-Induced Acidosis: Real & Clinically Relevant
The research foundation for the clinical relevance of diet-induced metabolic acidosis has grown substantially in recent years, which led me to develop AlkaCare pH, a product designed to neutralize the adverse effects of a chronic and low-grade acidosis. In contrast to frank acidemia, which is often a consequence of disease processes such as renal failure, diet-induced acidosis typically produces very minor changes in blood pH and bicarbonate. This is primarily because compensatory responses are initiated, such as the buffering effect created by an increase in bone resorption, which effectively control these parameters within a narrow physiological range.
Yet the highly prevalent Western dietary pattern makes persistent demands upon these compensatory systems, particularly when consumed over many years. This low-grade acidosis, when present over such a long duration, creates significant clinical effects, particularly when combined with the small declines in renal function associated with aging. It is now well established that dietary choices significantly contribute to an acidotic state, as evidenced by the large European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk population study, even after adjusting for variables such as BMI, age, physical activity, and smoking status.1
A greater intake of animal-based and high sodium foods, as well as a lack of fruits and vegetables together comprised the “Western diet”, which is the primary contributing factor.2 Clinical Importance – Bone and Kidney Connections
The two areas of research with the strongest connection to dietinduced acidosis are bone integrity and kidney stone formation, with a commonality in their underlying pathophysiology. Once thought to be a passive process, it now appears that bone resorption is an active one, and it may be a subtle change in pH which is the active trigger.3 Researchers have even identified the ovarian cancer G protein-coupled receptor-1 (OGR1) as a proton sensor in bone tissue, one which activates osteoclasts in response to a more acidic environment.4
The slow loss of bone over time due to accelerated resorption is likely responsible for increased rates of osteoporosis and loss of bone mass, while the associated hypercalcemia and other changes in urine composition, such as hypocitraturia, explain the higher rate of renal stone formation. A number of studies have confirmed these relationships. In one population-based study of women between the ages of 45 and 54, a lower dietary intake of acid-producing foods correlated with greater spine and hip bone mineral density, as well as an increase in forearm bone mass, even after adjustments for related factors.5
In the Study of Osteoporotic Fractures Research cohort, a prospective trial which enrolled women over age 65, participants with a high dietary ratio of animal to vegetable protein intake (indicative of an acid producing diet) had a greater risk of hip fracture as well as more rapid femoral neck bone loss.6
Similarly, measures of dietary acid are directly associated with urinary calcium levels in both stone formers and healthy populations, and in one trial of those at heightened risk for stone formation, the potential acid load of the diet had the strongest risk for stone formation among all variables studied.7,8
A more acidic diet also reduces urinary citrate content, and increases uric acid formation.2 Metabolic Syndrome & Insulin Resistance
Perhaps the most remarkable evidence to emerge in recent years is the relationship between dietary acidosis and both insulin resistance and the metabolic syndrome. In a recent trial which examined the relationships between urinary pH and several parameters of the metabolic syndrome in over 1,000 men, a more acidic urine was found to be a characteristic of both abdominal obesity as well as the metabolic syndrome. This study found significant associations between urine pH and waist circumference, homeostasis model assessment-R, fasting plasma glucose, HbA1c, serum triglycerides, serum uric acid, as well as HDL-cholesterol.9
Dietary acid load has also been associated with an adverse cardiometabolic profile in women as well.10
These studies support earlier associations between diabetes, insulin resistance, urinary citrate excretion and urinary pH.11,12,13 Why AlkaCare pH?
Fortunately, supplementation with the acid-neutralizing minerals found in AlkaCare pH reverses many of the adverse effects of the diet-induced acidosis described above. AlkaCare pH contains clinically relevant doses of calcium, magnesium and potassium primarily complexed to citrate, and when taken together have synergistic effects than when used individually. For example, a cross-over trial demonstrated greater benefit on markers of bone resorption when calcium citrate and potassium citrate were taken together than when used in alone.14 Similarly, potassium citrate and magnesium appear to have greater efficacy for reducing renal stone formation when used in combination, and citrate itself has a synergistic physiological effect, in addition to enhancing mineral absorption.15,16,17
A number of trials have shown that alkaline therapy can reverse the bone loss associated with dietary induced acidosis, and have demonstrated increases in bone mass in prospective and controlled clinical trials.18,19
Patients given alkaline therapy to treat their kidney stones have also seen increases in bone mineral density, highlighting the benefit of targeting this shared metabolic abnormality versus treating these diseases individually.20
Finally, AlkaCare pH combines these citrate-bound alkaline minerals with a proprietary berry blend rich in antioxidants to protect against reactive oxygen species, now known to be an important mediator of age-related bone loss.21,22 Conclusion
One of the most subtle components of a Western diet may nonetheless affect a wide-ranging number of conditions, including osteoporosis, renal stone formation, insulin resistance and the metabolic syndrome, all of which may have shared components underlying their pathophysiology. Alkacare pH combines synergistic nutrients, including citrate-bound alkaline minerals and proprietary antioxidants to address this widespread pathology and reverse the underlying dysfunction. Bioclinic Naturals has rigorous standards for quality and integrity of its products, with up to 400 quality control tests to ensure supplements of the highest purity and efficacy. References
Welch A.A., et al., (2008) 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. Br J Nutr 99, 1335–1343
Adeva M.M., Souto G. (2011) Diet-induced metabolic acidosis. Clin Nutr. 2011 Aug; 30(4): 416-21.
Arnett T.R., (2008) Extracellular pH regulates bone cell function. J Nutr 138, 415S–418S.
Frick K.K., et al., (2009) Metabolic acidosis increases intracellular calcium in bone cells through activation of the proton receptor OGR1. J Bone Miner Res 24, 305–313.
New S.A., et al., (2004) Lower estimates of net endogenous non-carbonic acid production are positively associated with indexes of bone health in pre-menopausal and perimenopausal women. Am J Clin Nutr 79, 131–138.
Sellmeyer D.E., et al., (2001) A high ratio of dietary animal to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal women. Study of Osteoporotic Fractures Research Group. Am J Clin Nutr 73, 118–122.
Trinchieri A., et al., (2006) Effect of potential renal acid load of foods on urinary citrate excretion in calcium renal stone formers. Urol Res 34, 1–7.
Lemann J. Jr., (1999) Relationship between urinary calcium and net acid excretion as determined by dietary protein and potassium: a review. Nephron 81, Suppl. 1, 18–25
Otsuki M., et al., (2011) Association of urine acidification with visceral obesity and the metabolic syndrome. Endocr J. 58(5): 363-7.
Murakami K., et al., (2008) Association between dietary acid-base load and cardiometabolic risk factors in young Japanese women. Br J Nutr. Sep;100(3): 642-51.
Cupisti A., Meola M., D’Alessandro C., et al., (2007) Insulin resistance and low urinary citrate excretion in calcium stone formers. Biomed Pharmacother 61, 86–90
Daudon M., Traxer O., Conort P., et al., (2006) Type 2 diabetes increases the risk for uric acid stones. J Am Soc Nephrol 17, 2026–2033.
Maalouf N.M., Cameron M.A., Moe O.W., et al., (2007) Low urine pH: a novel feature of the metabolic syndrome. Clin J Am Soc Nephrol 2, 883–888
Sakhaee K., Maalouf N.M., Abrams S.A., et al., (2005) Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women. J Clin Endocrinol Metab 90, 3528–3533.
Kato Y., Yamaguchi S., Yachiku S., et al., (2004) Changes in urinary parameters after oral administration of potassium- sodium citrate and magnesium oxide to prevent urolithiasis. Urology 63, 7–12.
Schwille P.O., Schmiedl A., Herrmann U., et al., (1999) Magnesium, citrate, magnesium citrate and magnesium-alkali citrate as modulators of calcium oxalate crystallization in urine: observations in patients with recurrent idiopathic calcium urolithiasis. Urol Res 27, 117–126.
Ettinger B., et al., (1997) Potassium-magnesium citrate is an effective prophylaxis against recurrent calcium oxalate nephrolithiasis. J Urol 158, 2069–2073.
Sebastian A., et al., (1994) Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med 330, 1776–1781.
Jehle S., et al., (2006) Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia. J Am Soc Nephrol 17, 3213–3222.
Vescini F., et al., (2005) Long-term potassium citrate therapy and bone mineral density in idiopathic calcium stone formers. J Endocrinol Invest 28, 218–222.
Mazière C., et al., (2010) Oxidized low density lipoprotein inhibits phosphate signaling and phosphate-induced mineralization in osteoblasts. Involvement of oxidative stress. Biochim Biophys Acta. Nov; 1802(11): 1013-9.
Manolagas S.C., (2010) From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. Endocr Rev. Jun; 31(3): 266-300.