Diet-Induced Acidosis: Is It Real and Relevant to your clients?

The article below discusses some important points on the topic of diet-induced acidosis, that we should all be aware of as Health and Fitness professionals when looking at the effects of our client’s diets on their ability to recover from injury, reduce pain and avoid disease. I’ve pulled a few brief highlights, but if you’d like to read more, the link is below.

Study on Cellular Acidosis:

British Journal of Nutrition (2010), 103, 1185–1194Pizzorno j, Frassetto LA, Katzinger J

Joseph Pizzorno 1 *, Lynda A. Frassetto 2 and Joseph Katzinger 3 1 PO Box 25801, Bastyr University, Seattle, WA 98165, USA 2 Division of Nephrology, 12 Moffitt CTSI Clinical Research Center, University of California, San Francisco, CA, USA 3 Salugenecists, 19531 7th Avenue NE, Shoreline, WA 98155, USA

Diet-Induced Acidosis: Is It Real and Clinically Relevant?

The concept of diet-induced ‘acidosis’ as a cause of disease has been a subject of interest for more than a century. The present article reviews the history of our evolving understanding of physiological pH, the physiological support for the concept of ‘acidosis’, the causes of acidosis, how it is recognized, its short-term effects as well as the long-term clinical relevance of preventative measures, and the research support for normalization of pH.

Further, we suggest differentiation of the terms ‘acidosis’ and ‘acidaemia’ as a way to resolve the conflation of these topics, which has led to confusion and controversy. The available research makes a compelling case that diet-induced acidosis, not diet-induced acidaemia, is a real phenomenon, and has a significant, clinical, long-term pathophysiological effect that should be recognized and potentially counterbalanced by dietary means.

Historic overview

The study of acid/base equilibrium and its relationship to diet and disease has been a subject of considerable speculation for at least several centuries. But before the 19th century little was known about the concepts of acids and bases, and no means were available to quantify the acid or alkaline load of foods, or the pH of physiological processes. Not until the second half of the 19th century did nutritional science began to develop, and the chemical components of food start to be analyzed. Henry Clapp Sherman’s 1919 book, Chemistry of Food and Nutrition, describes the history of nutritional studies performed up to that date (Sherman was the first to quantify nutritional acid load, in 1912).

During the next half century, a number of clinical practitioners outside of academia began to observe health improvements in their patients who were consuming unprocessed raw fruits and vegetables instead of the processed foods that were increasingly becoming the standard fare. These clinicians developed the concept that life is an equilibrium between acid and base. It was not until the 1960s, however, that input/output acid/base balance studies were performed for the first time in healthy adults and patients with chronic renal acidosis (1,2).

There is still a great deal of debate on how to define acids and bases. In the 1980s, Peter Stewart challenged traditional thought and mathematically determined that hydrogen ion and bicarbonate concentrations were dependent variables. He considered the independent variables, which by definition would determine the dependent variables, to be the strong ion difference (the difference in the net charge of cations and anions fully dissociated in solution), the partially dissociated weak acids (albumin, phosphate), and the partial pressure of carbon dioxide (PCO2) of the solution. While a full discussion of the implications of the differences between theories is beyond the scope of the present paper, of significance is the lack of consensus in the fundamental understanding of the mechanisms, as well as the practical applications of acid–base chemistry in physiological systems. A lengthy review published in January 2008 emphasizes this point(3), and excellent reviews of acid/base history are available(4,5).

Definitions: acidosis, acidaemia and diet-induced acidosis?

For the purposes of the present review, some definitions are in order, though it should be clear that most definitions are not universally accepted. The term acidosis is often used interchangeably with the term acidaemia, with the latter referring to a blood pH of less than 7·35. Correctly used, the term acidosis refers to a process, or a trend toward acidaemia, without necessarily reaching a pH of less than 7·35, or actual acidaemia.

Is acidosis a real physiological phenomenon?

The human body tends to maintain a tightly controlled pH of about 7·40 in the extracellular fluid by respiratory excretion of carbon dioxide and renal excretion of non-carbonic (non-volatile) acid or base(9). Everyday metabolism produces acid as non-volatile sulfate from amino acid catabolism, non-metabolized organic acids and phosphoric and other acids. The kidney reabsorbs all of the filtered bicarbonate (HCO 2 3) and generates new bicarbonate in the collecting duct. Under normal steady-state conditions, the net quantity of acid secreted and the consequent renal generation of new bicarbonate equals the rate of metabolic proton generation, preserving pH balance. In metabolic acidosis, either non-volatile acid accumulates, or HCO 2 3 is lost (for example, in diarrhea) and this can be happening even when the plasma HCO 2 3 is within the range considered to be normal (24–28 mmol/l)(10). While acute acid loading may only temporarily disrupt acid–base equilibrium, a chronic perturbation occurs when metabolism of the diet repeatedly releases non-carbonic acids into the systemic circulation in amounts that exceed the amount of base released concomitantly (for example, bicarbonate from combustion of organic acid salts of K in vegetable foods)(11).

What are the causes of acidosis?

The causes of metabolic acidosis include increased consumption or generation of organic acids, as well as either insufficient production of bicarbonate, or renal and/or gastrointestinal loss of bicarbonate, such as that seen in renal disease, diarrhea, pancreatic drainage and biliary fistula.

How is acidosis normalized?

The normalization of a low-grade chronic metabolic acidosis has been accomplished by two methods: change in dietary patterns and alkaline supplementation.

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