There might be one between your teeth. There could be some among wage earners. There definitely are those between generations, and there’s one at your local mall. But there’s one gap that you never think about and probably never heard of—the anion gap (AG). This is a laboratory assessment of the concentration of plasma anions and cations not routinely measured in some screenings. The AG accounts for the difference between anions of chloride and bicarbonate (negatively charged) and cations of sodium (positively charged) found in your blood, and is used to check for acidosis. A value of 8 –14 mEq/L is normal, and represents the negative charges that may be contributed by other ions, including phosphate, sulfate, organic acids and plasma proteins. If your last blood test doesn’t have AG listed as such, you can calculate yours by adding the chloride to the bicarbonate, then subtracting that value from the sodium level. As with anything else on earth, there are discrepancies in acceptable values because of advances in measurement techniques and laboratory hardware (Lolekha, 2001, pp. 33-36 and pp. 87-93). Listen to your health care provider’s interpretation.
Besides detecting acid-base disorders, the AG might point to disturbances related to multiple myeloma (bone marrow-related) (Jurado, 1998), or bromide and lithium intoxication. But that’s not so common. Low values, even within the range, probably indicate laboratory error, but might depict a low albumin level (which could arise from malnutrition, overhydration, increased capillary permeability or some kind of inflammation). High levels point to acidosis, but also could be erroneous based on laboratory operator technique, cleanliness of equipment or other impediment to accuracy (Kraut, 2007).
The matter of acid-base balance is not one to be dismissed. If it strays from the pH limits of 7.35-7.45, you could pass to the great hunting ground. Notice that this is slightly alkaline (basic). The closer to 7.0, the better it is. Acidity increases when acid compounds in the blood rise. This might happen from increased consumption, increased production or decreased elimination. Acidity drops under the opposite circumstances. That means that alkalinity increases. If pH deviates too far in either direction, cells die from their own toxic wastes. The management of the pH factor is so important to the body that it regulates the balance tightly through breathing, circulation and elimination. Even obesity may be blamed on increased acidity. Acid accumulation need not be addressed in terms of protein limitation though, but in terms of increasing the consumption of fruits and vegetables. Currently, this is under deeper investigation (Berkemeyer, 2009).
It has been accepted that the regulation of pH inside and outside cells is necessary for enzyme-controlled metabolic processes. The concentration of hydrogen ions, which determines the pH of aqueous solutions, can determine the structure and function of proteins, the permeability of the cell membrane, the distribution of electrolytes, and the structure of connective tissue. Unfavorable diet composition, a controllable factor in body pH, can have long-term consequences for the occurrence and progression of a number of diseases, including cancer (Robey, 2012). Among the most studied is the impairment of bone that results from chronic low-grade metabolic acidosis (Vormann, 2008). An aggravating element of bone degradation is sodium chloride, high intake of which, combined with low potassium intake, contributes to acid-base imbalance (Frassetto, 2008) (Morris, 1006).
If we are what we eat, then many of us are walking masses of low-grade chronic, acid-induced inflammation, caused largely by eating too many simple, refined carbohydrates from grains and cereals (Rachel, 2010) (de Punder, 2013), and not so much by protein ingestion. Decade-old findings agree that the contemporary diet provides what we want instead of what we are genetically determined to need, thereby upsetting the acid-base scales (Sebastian, 2002). This is especially pertinent in the age of osteoporosis. Our skeletons hold a reservoir of alkaline mineral in the form of hydroxyapatite, the calcium-phosphorus complex that is the primary mineral component of bone. The resorption of bone is driven by acid; the replacement of bone is impeded by it (Arnett, 2008) (Brandao-Burch, 2005).
Even drinking water gets into the act. Hard water, that which contains measurable levels of magnesium and calcium especially, has biologic benefits that are probably lacking in water that is chemically softened before it reaches the spigot. Though water itself cannot be either acid or alkaline, the stuff in it can change the pH up or down. That with a higher pH is beneficial in the maintenance of calcium sufficiency (Rylander, 2008) (Burckhardt, 2008). The opposite will increase the urinary excretion of minerals.
Alkaline supplements will improve mineral balance in those who overindulge on proteinaceous comestibles and refined grains, as evidenced by studies that administered oral potassium bicarbonate (Sebastian, 1994) or potassium citrate (Jehle, 2006), where parameters of bone resorption-formation were equalized. A diet of pro-alkaline foods will do the same thing. Believe it or not, ingesting some acidic foods, such as citrus, causes the pancreas to secrete bicarbonates that neutralize the net effect of the food. But the body has limited resources, so it’s the overloads that cause problems. If a person chooses to follow an alkaline diet, he will still allow about a fourth of his plate to be acidic. Roots, crucifers, leaves, cayenne and garlic are alkaline, as are pomegranates, coconuts and citrus fruits. Meats, dairy, grains except quinoa and amaranth, and fake sweeteners are not. You can find a list on the internet. A simple habit to initiate is the 1-2-3 technique of filling the plate. One part starch, two parts protein and three parts vegetables, the latter now covering half the plate, is easy. Meatless Mondays are better if they don’t feature a pile of pasta.
Arnett TR. Extracellular pH regulates bone cell function. J Nutr. 2008 Feb;138(2):415S-418S.
Berkemeyer S. Acid-base balance and weight gain: are there crucial links via protein and organic acids in understanding obesity? Med Hypotheses. 2009 Sep;73(3):347-56.
Brandao-Burch A, Utting JC, Orriss IR, Arnett TR. Acidosis inhibits bone formation by osteoblasts in vitro by preventing mineralization. Calcif Tissue Int. 2005 Sep;77(3):167-74.
Burckhardt P. The effect of the alkali load of mineral water on bone metabolism: interventional studies. J Nutr. 2008 Feb;138(2):435S-437S.
de Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients. 2013 Mar 12;5(3):771-87. doi: 10.3390/nu5030771.
Frassetto LA, Morris RC Jr, Sellmeyer DE, Sebastian A. Adverse effects of sodium chloride on bone in the aging human population resulting from habitual consumption of typical American diets. J Nutr. 2008 Feb;138(2):419S-422S.
Hatherill M, Waggie Z, Purves L, Reynolds L, Argent A. Correction of the anion gap for albumin in order to detect occult tissue anions in shock. Arch Dis Child. 2002 Dec;87(6):526-9.
Sigrid Jehle, Antonella Zanetti, Jürgen Muser, Henry N. Hulter and Reto Krapf Partial Neutralization of the Acidogenic Western Diet with Potassium Citrate Increases Bone Mass in Postmenopausal Women with Osteopenia JASN. November 2006; vol. 17 no. 11: 3213-3222
Jurado RL, del Rio C, Nassar G, Navarette J, Pimentel JL Jr. Low anion gap. South Med J. 1998 Jul;91(7):624-9.
Kiwull-Schöne H, Kiwull P, Manz F, Kalhoff H. Food composition and acid-base balance: alimentary alkali depletion and acid load in herbivores. J Nutr. 2008 Feb;138(2):431S-434S.
Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007 Jan;2(1):162-74.
Lolekha PH, Vanavanan S, Lolekha S. Update on value of the anion gap in clinical diagnosis and laboratory evaluation. Clin Chim Acta. 2001 May;307(1-2):33-6.
Lolekha PH, Vanavanan S, Teerakarnjana N, Chaichanajarernkul U. Reference ranges of electrolyte and anion gap on the Beckman E4A, Beckman Synchron CX5, Nova CRT, and Nova Stat Profile Ultra. Clin Chim Acta. 2001 May;307(1-2):87-93.
Rachel C. Masters, Angela D. Liese, Steven M. Haffner, Lynne E. Wagenknecht, and Anthony J. Hanley Whole and Refined Grain Intakes Are Related to Inflammatory Protein Concentrations in Human Plasma J Nutr. 2010 March; 140(3): 587–594.
Morris RC Jr, Schmidlin O, Frassetto LA, Sebastian A. Relationship and interaction between sodium and potassium. J Am Coll Nutr. 2006 Jun;25(3 Suppl):262S-270S.
Roberts WL, Johnson RD The serum anion gap. Has the reference interval really fallen? Arch Pathol Lab Med. 1997 Jun;121(6):568-72.
Robey IF. Examining the relationship between diet-induced acidosis and cancer. Nutr Metab (Lond). 2012 Aug 1;9(1):72.
Rylander R. Drinking water constituents and disease. J Nutr. 2008 Feb;138(2):423S-425S.
Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med. 1994 Jun 23;330(25):1776-81.
Anthony Sebastian, Lynda A Frassetto, Deborah E Sellmeyer, Renée L Merriam, and R Curtis Morris Jr Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors Am J Clin Nutr December 2002 vol. 76 no. 6: 1308-1316
Juergen Vormann and Thomas Remer Dietary, Metabolic, Physiologic, and Disease-Related Aspects of Acid-Base Balance: Foreword to the Contributions of the Second International Acid-Base Symposium1,2 J. Nutr. February 2008 vol. 138 no. 2 413S-414S
*These statements have not been evaluated by the FDA. These products are not intended to treat, diagnose, cure, or prevent any disease.