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Thoughts at large: Controversies in clinical nutrition and functional medicine: Issue #1 chronic low-grade metabolic acidosis - Part 1.

Author's Introduction

When I first began my work in the professional supplement industry over 30 years ago, the most frequent request I would receive from fellow practitioners was research-based yet practical and easy-to-access information on clinical use of the supplements I was selling. Based on these requests, I started writing research literature reviews that highlighted the biochemistry and clinical utility of various ingredients found in supplements. However, feedback suggested that these basic literature reviews only partially satisfied the needs of the practitioners reading these reviews. What was suggested to be an even more urgent need was clarity on the many controversies in clinical nutrition where an almost endless parade of conflicting studies was making it frustratingly difficult to decide the best way to proceed in terms of making supplemental recommendations to patients. To satisfy this need, 1 started writing literature reviews that would explore a controversy in clinical nutrition in depth with the idea that increased knowledge about the controversy would make it easier to "sort it all out" so to speak, leading to more reliable recommendations to patients and a higher percentage of positive clinical outcomes.

During these years I have also been a faithful reader of The Original Internist and have been continually impressed by the many literature reviews on some of the most pressing and controversial issues facing nutritional and functional medicine practitioners today. Recently, I was honored to receive an invitation to contribute articles to The Original Internist. I am very excited to have this opportunity to be part of the proud legacy at The Original Internist of searching for truth in health care. My first contribution addresses one of the most enduring and contentious controversies in clinical nutrition and functional medicine, chronic, low-grade metabolic acidosis and its relationship to diet.

Like many of you, over the years I have read a seemingly endless stream of literature reviews and commentaries that were designed to educate me on how to translate the complexities of fluid and electrolyte, acid/alkaline balance into an understandable body of information that could be easily and practically employed to address the needs of chronically ill patients. Unfortunately, for me, the result after reading many of these papers was even more confusion on how to convert the complexities of the biochemistry and physiology I had just read into a practical clinical intervention. Because of this, I was glad to encounter an outstanding review of the literature entitled "Diet-Induced Metabolic Acidosis" by Adeva and Souto (Adeva MM & Souto G, Clin Nutr, Vol. 30, pp. 416-421, 2011). It has added substantially to my understanding of this important yet complex aspect metabolic dysfunction in chronically ill patients. Hopefully, after you read this review, you will come to the same conclusion.

"Diet Induced Metabolic Acidosis": An Outstanding, Up to Date Review on The Impact of Diet-Induced Metabolic Acidosis on Systemic Health and Treatment Options

Before beginning my detailed review of this outstanding paper, I would like to discuss one possible bias of the authors that disturbs me. As you will see, the overall tone of the paper suggests that being acid is "bad" and being alkaline is "good." In turn, acidifying foods such as animal products and grains are "bad" and alkalizing foods such as fruit and vegetables are "good." These types of broad-based generalizations disturb me. Why? It is a generalization that is not true. For example, acidification is just as important to human physiology as is alkalinization. Therefore, while it has been said so often that it is becoming a cliche, I feel it needs to be said again; balance is the key. The truth is that acid foods are only "bad" when patients are already too acidic, either through diet and/or other mechanisms. In contrast, for a patient who is too alkaline (Yes, it does happen), acid forming foods are "good" and alkalizing foods are "bad." Of course, in reality, it is certainly true that most patients are in a state of low-grade, chronic metabolic acidosis and would benefit from increased intake of alkalizing foods. However, as I hope I have made clear, just because alkalizing foods are "good" for the majority of patients who tend to be in an acidotic state, it does not mean they are "good" for everyone.

The Western Diet and the Creation of Low-Grade Chronic Metabolic Acidosis

The first quote I would like to present from this excellent paper by Adeva and Souto discusses the nature of the problem: "Contemporary human diet in industrialized countries is deficient in fruits and vegetables and contains excessive animal products and sodium chloride. Fruits and vegetables are abundant in potassium salts of metabolizable anions, including citrate and malate, which consume hydrogen ions when metabolized, having an alkalizing effect. "

Specifically, what is it about animal products and cereal grains that makes them so acid forming? The authors point out:

"Animal proteins and cereal grains contain sulfur-containing amino acids (methionine, homocysteine, and cysteine) whose oxidation generates sulfate, a non-metabolizable anion that constitutes a major determinant of the daily acid load. The content of these amino acids is from 2 to 5 fold higher in meat and eggs than in grains and legumes. The accompanying anions for potassium are chiefly phosphate and chloride in animal products and cereals, making these nutrients more acidogenic than fruits and vegetables. The modern western diet based on animal products generates an acid load not compensated by the shortage of fruit and vegetables causing a lifespan state of unnoticed and growing metabolic acidosis. "

Before continuing, I would like to comment on two of the points made in the preceding quote. First, please note that two amino acids that we in clinical nutrition and functional medicine discuss quite often in terms of their importance due to their antioxidant and detoxifying properties are also major inducers of the daily acid load. Therefore, we must consider methionine and cysteine ingestion, as with every other substance we ingest, from a hormetic standpoint where issues of dosage are just as important, if not more so, than just knowing that methionine and cysteine are "good" for enhancing free radical quenching and optimizing detoxification pathways. Second, please note again that the main form of supplemental potassium found in the marketplace, potassium chloride, is acid-forming. In turn, use of potassium chloride would be contraindicated when considering the use of a potassium containing supplement as part of an alkalizing regimen.

The Role of the Kidney in Dealing with an Increased Systemic Acid Load

As we all know, for every environmental stressor, the body must generate some sort of response to deal with this stressor. Furthermore, as has been documented repeatedly in the many papers being written on allostatic load, if this response goes on too long, it can play as big a role in creating chronic sickness as the original environmental stressor, and sometimes more so. In human physiology, the kidney plays a major role in responding to and dealing with an increased diet-induced acid state. How does the kidney perform this function? Unfortunately, the answer to this question is one of the most complicated and difficult to understand processes in human biochemistry and physiology. However, I feel that the description by Adeva and Souto does a fairly good job of making this process somewhat easier to understand than the usual paper or text on acid/alkaline physiology. Hopefully, you agree: "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."

Therefore, in simpler terms, to deal with a diet-induced acid load, the kidney attempts to restore acid/alkaline balance by utilizing several pathways:

* It sends non-metabolizable ions such as sulfate into the urine

* It retains citrate, an alkalinizing, metabolizable anion

* It produces ammonia

* It sends ammonia into the urine

Of course, as I pointed out above, every response by the body to environmental stressors carries with it some potentially adverse metabolic consequences, where, for the most part, as I mentioned, the metabolic adversity will be expressed clinically if the response goes on too long. With this thought in mind, what is the impact of the above actions taken by the kidney to restore acid/alkaline balance?

"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 and risk factors for calcium stone disease."

In simpler terms, the efforts by the kidney to deal with the acid load lead to the following:

* Lowered urine pH

* Since the alkaline anion citrate is being retained to deal with the acid load, there is too little citrate in the urine

* Excessive levels of calcium in the urine

* Increased nitrogen and phosphate in the urine

* What can happen if these phenomena go on too long?

* The low urine pH can lead to the creation of uric acid stones

* The low citrate and elevated calcium in the urine can lead to the creation of calcium stones

What is the net result concerning acid/alkaline balance and urine composition? Adeva and Souto note:

"Persons consuming a diet based on animal protein have higher kidney net acid excretion and more acidic urinary pH than persons on a plant-based diet. The urinary excretion of sulfate, phosphate, and uric acid is also higher in persons on the animal protein diet, compared with the vegetarian diet."

As you might expect, other environmental factors besides dietary composition from an animal/plant standpoint do impact on acid/alkaline balance. One of these factors is sodium chloride intake, as noted by the authors:

"Dietary sodium chloride also influences systemic acid-base status, being an independent negative predictor of plasma bicarbonate. Excessive consumption of animal proteins and sodium chloride with insufficient ingestion of plant-based foods increases the body acid load and induces metabolic acidosis by accumulation of non-metabolizable anions, predominantly sodium and chloride."

In addition, as you might expect, metabolic acidosis has an impact on sodium and chloride metabolism, creating still another metabolic vicious circle:

"Metabolic acidosis promotes chloride (and sodium) urinary loss, inducing negative sodium chloride balance, with secondary activation of the renin-angiotensin-aldosterone system and subsequent rise in plasma and urine aldosterone concentration."

Thus, as the above quotes point out, salt (sodium chloride) plays an important role in acid/alkaline physiology that is often under appreciated. On one hand, as with animal protein, excess intake of sodium chloride can contribute to an acidotic situation. On the other hand, metabolic acidosis can lead to loss of sodium chloride in the urine, with consequent activation of factors involved in blood pressure determination. Therefore, I feel it is logical to hypothesize that acid/alkaline optimization is one of many important factors that needs to be addressed with patients who demonstrate suboptimal blood pressure readings.

Another factor that plays a role in determining acid/alkaline balance is the aging process, due to progressive decline in kidney function:

"The magnitude of the lifespan diet-induced metabolic acidosis escalates progressively with advancing age probably due to the decline in kidney function occurring with aging. There is a gradual increase in blood hydrogen ion concentration in healthy humans from youth to old."

With all of the above in mind, the authors provide an overview of how the kidney responds to an acidic diet: "In response to the metabolic acidosis imposed by the acidogenic diet, the kidney implements adaptive processes aimed to restore the acid-base balance, including amplification of the urinary excretion of non-metabolizable ions, such as chloride, phosphate and sulfate, the conservation of metabolizable anions, such as citrate, and the activation of the urinary excretion of ammonium ions to expand both hydrogen ion and anion elimination."

In addition:

"In response to the diet-induced metabolic acidosis, the urinary excretion of anions such as sulfate, chloride, and phosphate increases and there is also urinary loss of calcium. "

The interrelationship between the body's efforts to deal with an acidic diet and other metabolic processes

As we all are beginning to realize, in a world where chronic illness is becoming increasingly complex, optimal treatment of chief complaints in chronically ill patients requires that we abandon our traditional ways of addressing metabolic imbalances where we largely considered them in isolation, focusing purely on alkalizing or restoring glycemic imbalance or detoxifying, etc. Instead we must realize that all metabolic processes are interactive in ways that are sometimes difficult to comprehend. Nevertheless, even though we may not understand all the interactions, I feel it is important to at least recognize their existence and do our best to address all metabolic issues that may be present in any one chronically ill patient. With this thought in mind, please consider the following quote that addresses acid-forming elements in the diet and their interaction with insulin metabolism:

"The urinary excretion of sulfate correlates strongly and directly with animal protein content, being higher in individuals consuming animal protein-based diets than in subjects on vegetarian diets. Urinary sulfate excretion is inversely correlated with urine pH and has been found significantly greater in insulin resistant subjects compared to persons with normal insulin sensitivity in univariate analysis of a cross-sectional study of healthy subjects, suggesting a link between animal dietary protein, endogenous acid production and insulin resistance."

In part II of this commentary on chronic, low-grade metabolic acidosis, I will continue my review of this outstanding paper on the subject by Adeva and Souto, presenting still more interesting and sometimes overlooked interrelationships between acid/alkaline physiology and key metabolic pathways that are often functioning suboptimally in our chronically ill patients.

by: Jeffrey Moss, DDS, CNS, DACBN
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Author:Moss, Jeffrey
Publication:Original Internist
Date:Sep 1, 2016
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