Diet-induced metabolic acidosis

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Diet-induced metabolic acidosis

María M. Adevab, Corresponding Author Contact Information, E-mail The

Corresponding Author and Gema Soutoa

a Clinical Center of the National Institutes of Health, Washington DC, USA

b Hospital General Cardona, c/ Pardo Bazán s/n 15406 Ferrol, La Coruña,

Spain

Received 17 November 2010;

accepted 16 March 2011.

Available online 9 April 2011.

Summary

The modern Western-type diet is deficient in fruits and vegetables and contains

excessive animal products, generating the accumulation of non-metabolizable

anions and a lifespan state of overlooked metabolic acidosis, whose magnitude

increases progressively with aging due to the physiological decline in kidney

function. In response to this state of diet-derived metabolic acidosis, the

kidney implements compensating mechanisms aimed to restore the acid-base

balance, such as the removal of the non-metabolizable anions, the conservation

of citrate, and the enhancement of kidney ammoniagenesis and urinary excretion

of ammonium ions. These adaptive processes lower the urine pH and induce an

extensive change in urine composition, including hypocitraturia, hypercalciuria,

and nitrogen and phosphate wasting. Low urine pH predisposes to uric acid stone

formation. Hypocitraturia and hypercalciuria are risk factors for calcium stone

disease. Even a very mild degree of metabolic acidosis induces skeletal muscle

resistance to the insulin action and dietary acid load may be an important

variable in predicting the metabolic abnormalities and the cardiovascular risk

of the general population, the overweight and obese persons, and other patient

populations including diabetes and chronic kidney failure. High dietary acid

load is more likely to result in diabetes and systemic hypertension and may

increase the cardiovascular risk. Results of recent observational studies

confirm an association between insulin resistance and metabolic acidosis

markers, including low serum bicarbonate, high serum anion gap, hypocitraturia,

and low urine pH.

Keywords: Metabolic acidosis; Ammonium ions; Citrate; Insulin resistance

Abbreviations: DASH, dietary approaches to stop hypertension; NEAP, net

endogenous acid production; RNAE, renal net acid excretion; TA, titratable acid;

HOMA-IR, homeostasis model assessment–insulin resistance; NHANES, national

health and nutrition examination surveys

http://www.sciencedirect.com/science/article/pii/S0261561411000604