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Under Appreciated Issues in the Treatment of Chronic Illness - Low Grade, Chronic Acidosis Combined with Potassium Deficiency-Part II

Origins and Impact of Metabolic Acidosis


09/01/2018 - Moss Nutrition Report #281

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"The happiness of most people we know is not ruined by great catastrophes or fatal errors, but by the repetition of slowly destructive little things."

Ernest Dimnet, French priest, lecturer and author (1866-1954)

INTRODUCTION

In part I of this series (The May 2018 Moss Nutrition Report), I began my review of the excellent book chapter by Sebastian et al (1) that discusses the relationship between diet and acid/alkaline balance from an evolutionary standpoint.  In part I, I primarily focused on the sections of the chapter that highlighted the biochemistry and physiology of human acid/alkaline balance in relation to diet with only a brief discussion of the evolutionary aspects.  Now I would like to focus on the sections of the chapter that address evolutionary aspects in greater detail.

However, before I do so, I would like to offer additional thoughts on the issue I discussed at the beginning of part I of this series.  Why is it that the subject of metabolic acidosis and its relationship to potassium deficiency is not receiving more attention from the functional medicine and clinical nutrition community?  For me, one reason has very much to do with the quote by Dimnet highlighted above.  I feel that we in the functional medicine and clinical nutrition community are all too often guilty of having a pre-existing agenda that complicated problems must always have complicated solutions.  Therefore, we all too often place way too much emphasis on the "great catastrophes or fatal errors" when attempting to assist patients with their health issues while under emphasizing or ignoring completely the little things patients do every day - "the repetition of slowly destructive little things" that are often a much bigger part of the causational picture.  Of course, in many ways we do a great job in focusing on some of the "slowly destructive little things" such as gluten and other food allergy issues.  However, as I am emphasizing in this series, I feel we have greatly under emphasized another equally destructive little thing - low grade, chronic metabolic acidosis and potassium deficiency.  Why?   As I mentioned in part I of this series, diagnosis and treatment of low grade, chronic metabolic acidosis and potassium deficiency rarely requires the goods and services provided by the functional medicine labs and supplement companies that sponsor the vast majority of the lectures and symposia we attend these days.  In turn, I feel simple and basic clinical issues and solutions that revolve around factors such as metabolic acidosis and potassium deficiency have fallen out of favor.  As suggested by Dimnet, if we are to improve our ability to bring happiness to our patients, we need to spend less time and effort focusing on the "great catastrophes" and "fatal errors" and spend more time and effort on "the repetition of slowly destructive little things" such as those that create and promote low-grade, chronic metabolic acidosis.

With the above in mind, I found the commentary from the publisher of The Townsend Letter, Jonathan Collin, MD, that appeared in the August/September 2018 issue quite timely and relevant.  In his commentary Collin discussed what is known as Occam's Razor.  What is Occam's Razor?  It's basically a tenet that suggests what many of us have heard repeatedly over the years in health care when confronted with the task of determining why a patient is ailing and what to do about it:

"If it looks like a duck, walks like a duck, and quacks like a duck, it's probably a duck."

In other words, the most obvious explanation of why the patient is ailing and what to do about it is usually the best in terms of efficacy, practicality, and cost effectiveness.  Of course, Collin described this principle of health care much more eloquently in his description of Occam's Razor:

"The 14th century theologian and philosopher, William of Ockham, is famous for his law of parsimony known as Occam's Razor.  As a problem-solving technique, Occam's Razor considers the hypothesis with the least number of explanations to have the highest likelihood of being truthful.  Occam's Razor frequently is used in science and medicine to explain phenomena and make a diagnosis."

Why did Collin bring up Occam's Razor in a journal devoted to alternative medicine?  He was discussing, in a special edition devoted to cancer, the idea that the traditional focus on cancer in terms of tumor aggressiveness and pathogenicity is incorrect.  A more correct and truthful way to consider cancer is the susceptibility of the terrain in which it grows and proliferates.  Collin discusses this idea in his description of the work by Kenneth Pienta, MD, an oncologist at Johns Hopkins:

"Rather than think that metastasis is based on the pathogenicity of the particular tumor cell, one should think about the terrain instead.  What is it about the organ tissue that permits the tumor cell to succeed in its tissue growth?  When the cancer cell arrives in its new environment, that organ's microenvironment changes to a milieu conducive for the tumor cell's progressive growth.  Pienta explains that we should think not about what the tumor cell is doing to us, but what we are doing to the tumor cell."

Is there anything more basic and fundamental to the health and optimal functioning of the terrain than fluid and electrolyte/acid-alkaline dynamics?  As we all know, optimal balance of pH and fluid/electrolyte physiology and chemistry is central to the proper function of virtually every cellular activity.  Why, then, are the functional medicine and clinical nutrition communities not addressing this important terrain issue more often and more emphatically?  Part of the answer to this question lies with the reasons I mentioned above and in part I of this series.  However, whatever the reason, as suggested by Collin and William of Ockham many years ago, we need to do a better job of avoiding the often seductive call of novelty and complexity. How can we do this?  By maintaining focus on the very basic and often simple needs of the terrain, Occam's Razor, and the fact that an animal that looks like a duck, walks like a duck, and quacks like a duck, is probably a duck.

DIET AND ACID/ALKALINE DYNAMICS FROM AN EVOLUTIONARY PERSPECTIVE

Now I would like to return to my review of the book chapter "An evolutionary perspective on the acid-base effects of diet" by Sebastian et al (1) by focusing on the sections that discuss acid-base considerations of the hunter gatherer.  The first quote I would like to feature addresses the diet of pre-agriculture humans:

"Before agriculture began, Homo sapiens habitually ate exclusively a hunter-gatherer diet similar to the one to which natural selection had fitted their genome.  The agricultural era of the last 10,000 years comprises too short a time on an evolutionary scale for natural selection to generate major genetic adaptations in response to the profound changes in the nutrient composition of the diet that resulted from the switch to the modern agricultural-based diet."

What was the specific composition of this hunter-gatherer diet?  Sebastian et al (1) continue:

"From the data on the diets of existing hunter-gatherer societies, and from inferences about the Paleolithic environment, we can construct the Paleolithic diet and the probable daily nutrient intakes of Paleolithic humans.  In an estimated 3000 kcal diet, meat constituted 35% of the diet by weight and plant foods, 65%.  Total protein intake estimates at 251 g/day, of which animal protein estimates as 191 g/day, and plant proteins, 60 g/day.  By contrast, contemporary humans consume less than one-half that amount of animal protein, and only about one-third that amount of plant protein, per kilocalorie of diet.  Na+ intake estimates at about 29 mEq/day, and K+ intake, in excess of 280 mEq/day.  By contrast, contemporary humans consume between 100 and 300 mEq of Na+ per day, and about 80 mEq of K+ per day.  Thus, in the switch to the modern diet, the K+/Na+ ratio reversed, from 1 to 10, to more than 3 to 1.  Since food from Na+ exists largely in the form of Cl_ salts, and food K+ largely in the form of HCO3-generating organic acid salts, the Cl_/HCO3_-generating organic acid salts, the Cl-/HCO3- ratio of the diet likewise reversed."

Before continuing, please notice again the very high intake of protein.  As you probably know, many in today's nutritional community would consider that level of intake way too high.  Why was it that this level of intake did not create massive metabolic imbalances?  One very likely reason is the equally high, at least by today's standards, level of potassium intake (280 mEq of potassium equals 11,200 mg).  Yes you read that right - 11,200 mg per day - almost three times as high as the current RDI of approximately 4,500 mg per day.  Why is it that this level of potassium intake did not create massive metabolic problems?  While there may be many reasons, one, as suggested above, is that the daily sodium intake was absolutely miniscule by today's standards, making the hunter-gatherer diet very much skewed towards potassium intake instead of the opposite that is seen today.  The overall effect of all of this is that there is a very low net acid production, or what is known as NEAP (Net endogenous acid production). 

Sebastian et al (1) go on to discuss this issue of net acid production in more detail by addressing the fact that the hunter-gatherer diet described above led to high levels of the base factor, bicarbonate (HCO3-):

"In addition to displacement of high HCO3-yielding plant foods by net acid-yielding cereal grains and low base-yielding legumes, displacement of high HCO3-yielding plant food by energy-dense nutrient-poor foods (e.g., separated fats, vegetable oils, refined sugars) contribute to the negative-to-positive shift in NEAP.  While removing cereal grains from the diet and substituting fruits and vegetables reduces NEAP to nearly zero, removing energy-dense nutrient-poor foods as well, and substituting fruits and vegetables, renders the diet substantially net base-producing."

In simpler terms, what does this all mean?  A high protein diet, even at levels seen with the hunter-gatherer, is not inherently acid producing.  Rather, it becomes a net acid producer only because the intake of base-producing fruits and vegetables is way too low:

"In other words, the mistakenly adjudged 'high' protein intakes of the modern diet does not make it net acid-producing; rather it becomes net acid-producing because of 'low' intakes of high base-yielding plant foods in preference to 'high' intakes of cereal grains, legumes, and energy-dense nutrient-poor foods."

How often do we hear about the dangers of the high protein diet?   Even though, as many of you know through my past writings and lectures, I am an avid advocate of the idea that most people in the US would experience health benefits by increasing dietary protein intake above the usual and customary levels, I will readily admit that protein intake levels can be excessive at some point.  However, as Sebastian et al (1) so eloquently point out, what most in the clinical nutrition community think of as "excessive" in terms of dietary protein intake is actually an issue of too little alkaline, plant-based food intake.  In the next quote, Sebastian et al (1) discuss the benefits of a high protein intake when combined with high alkaline, plant-based diet:

"Indeed, high protein intakes have desirable effects, for example an anabolic effect on bone, owing to substrate (amino acid) provision for building bone matrix, and a stimulatory effect that increases the bone growth-promoting factor, insulin-like growth hormone-I.  Since metabolic alkalosis also has anabolic effects on bone and since metabolic acidosis reduces serum IGF-I levels, the combination of a net base-producing/alkalosigenic diet and a high protein diet might optimize peak bone mass achievement and eliminate age-related declines in bone mass."

The next quote emphasizes the authors' suggestion that the health problems we tend to associate with a diet too high in acidifying factors and more likely associated with the fact that the diet is too low in alkalizing factors:

"The switch from the ancestral net base-producing diet to the modern net acid-producing diet imposed a double jeopardy on modern humans, one due to a loss of potentially beneficial base input to the body, another due to a net addition of pathogenic acid to the body - crossing the neutral zone from base- to acid-land.  In considering the acid-base effects of diet, we need to consider not only the potential negative effects of chronic diet-induced metabolic acidosis but also loss of the potential positive effects of chronic diet-induced metabolic alkalosis."

Should we be making an effort to induce a state of metabolic alkalosis in our patients and the population in general?

From a traditional and even nutritional medicine standpoint, our basic education seemed to emphasize that both a state of metabolic acidosis and metabolic alkalosis should be avoided.  Sebastian et al (1), as I have been suggesting, have a very different viewpoint on this issue.  The next few quotes go into much more detail as to why, according to the authors, a chronic state of metabolic alkalosis is preferable.  First, consider the following:

"From an evolutionary nutritional perspective...it appears that the optimal diet of humans supplies an excess of HCO3-generating precursors relative to H+-generating precursors."

Furthermore:

"We may then regard a stone age-type net base-producing diet as the evolutionary optimal human diet.  From this perspective, diet-induced chronic low-grade K+-replete metabolic alkalosis would constitute the natural and optimal systemic acid-base state of humans."

In the next quote the authors discuss the idea I suggested above that we need to reframe our traditional thinking that metabolic alkalosis is a pathologic state:

"Clinicians may express skepticism that K+-replete alkali-loading metabolic alkalosis, however mild, confers optimal systemic acid-base status.  Clinicians view metabolic alkalosis as a 'disorder,' caused by pathological conditions, in which the associated alkalemia and hyperbicarbonatemia injure the body.  However, the adverse effects of metabolic alkalosis depend on the severity of the accompanying alkalemia and increase in plasma [HCO3-], and the associated state of body K+ stores."

In fact, many allopathic practitioners routinely induce metabolic alkalosis with commonly prescribed drugs:

"Clinicians often (if unintentionally) induce sustained low-grade metabolic alkalosis, for example, with thiazide treatment of hypertension or calcium nephrolithiasis, and do not consider it imperative to treat the low-grade alkalosis, though they sometimes do indirectly, by administering KCl when overt hypokalemia coexists.  In thiazide treatment of calcium nephrolithiasis, some clinicians recommend supplementing with dietary K+ with its alkalinizing salts (e.g., potassium citrate), which sustains the low-grade metabolic alkalosis.  Alkalinizing salts of potassium have the advantage of both increasing urinary citrate excretion (an inhibitor of stone formation) and amplifying the thiazide reduction of urinary calcium excretion."

Where else has modern medicine employed therapeutic metabolic alkalosis?  Sebastian et al (1) continue:

"Independently of thiazides, inducing and sustaining a mild metabolic alkalosis with chronic alkali loading is recommended in treatment for calcium nephrolithiasis in patients with idiopathic hypocitraturia.  Clinicians also induce mild metabolic alkalosis with alkali loading as standard treatment for patients on chronic hemodialysis, to minimize or prevent the diet-induced metabolic acidosis that ordinarily occurs between dialysis sessions."

SPECIFIC DISEASE STATES CAUSED OR CONTRIBUTED TO BY METABOLIC ACIDOSIS

Bone wasting and osteoporosis

Sebastian et al (1) point out an extensive body of research that makes it clear that chronic metabolic acidosis presents a major negative impact on bone health.  What follows is a series of quotes from the authors that make this association unmistakably clear.  This first quote points out the role of bone in maintaining optimal alkaline reserve when the body is confronted with an acidotic challenge:

"Metabolic acidosis reduces bone mass.  Bone serves as an ion exchange reservoir that can release K+ and Na+ in exchange for H+.  Bone also provides a large reservoir of base in the form of alkaline salts of calcium (phosphates, carbonates), which it releases into the systemic circulation in response to acid loads.  The liberated base mitigates the severity of the acidosis, and thus contributes to systemic acid-base homeostasis.  The liberated calcium and phosphorus disappear into the urine, without compensatory increase in gastrointestinal absorption, and thus bone mineral content declines."

The next quote points how we can, via laboratory evaluation, determine if bone is being actively used to counter and acidotic state, leading to bone loss:

"In humans, urinary hydroxyproline excretion increases, providing evidence that organic bone matrix resorption increases during acid loading contributing to acid-base homeostasis, since it results in less utilization of extracellular base for bone formation."

What evidence exists that supports this proposed intimate connection between maintenance of acid/alkaline balance and bone physiology?  The authors state:

"Two lines of evidence indicate that chronic low-grade diet-induced acidosis imposes a chronic drain on bone: (a) stability of blood acid-base equilibrium in the face of continuing positive external balance of acid, and, (b) amelioration of negative calcium and phosphorus balances, reduction of bone resorption, and stimulation of bone formation attendant to short-term neutralization of the dietary acid load.  Longer-term (3 months) partial neutralization of the diet net acid load with potassium citrate also reduces bone resorption, and long-term (3 years) administration of potassium bicarbonate causes a persisting reduction in urine calcium excretion."

The next quote discusses how the kidney and bone act as a team to counteract an acid challenge:

"When the body generates net acid endogenously, the acidified blood reaches bone and kidney concurrently, and both respond by adding new base to the systemic circulation, each according to its sensitivity and capacity.  To whatever extent bone supplies base in response to its encounter with the acid-loaded blood, to that extent the kidney sees less acid (as reflected by lesser blood acidity and higher plasma [HCO3-], and therefore, in the steady state, the kidney does not receive the full signal to generate new HCO3- equal to the full rate of endogenous acid production.  Not surprising then the kidney does not 'keep up' with endogenous acid production."

Therefore, as noted in the quote above, bone is the primary organ system that copes with an acid challenge.  The kidney is secondary.  Unfortunately, the way bone copes with an acid load is self- destruction.  Is it surprising then that, in country where intake of high acid foods is predominant, bone loss is so prevalent?  Also, it should be no surprise then that, in the face of a high acid diet, calcium supplements, since they do not deal with the cause of bone loss, will have only a limited impact on preventing, reducing, or reversing bone loss.

Lastly, consider this sobering statistic concerning how a fairly small amount of endogenous acid production can seriously deplete bone density over a lifetime:

"...bone need contribute base at no more than 2% of endogenous acid production to substantially demineralize itself over decades of adult life."

Chronic metabolic acidosis and muscle wasting

Over the years I have discussed in several newsletters how the loss of muscle mass seen with sarcopenia can contribute to chronic metabolic acidosis.  How about the reverse scenario?  Can chronic metabolic acidosis contribute to muscle wasting?  Sebastian et al (1) point out:

"In diseases that cause chronic metabolic acidosis, protein degradation in skeletal muscle accelerates, inducing negative nitrogen balance.  These effects result from the acidosis itself, not its cause, nor from sequelae of the underlying acidosis-producing disorder, because they occur with widely differing acidosis-producing conditions and because alkali administration reverses them."

Of course, as with bone loss, muscle loss with chronic metabolic acidosis is not a random, isolated occurrence.  Rather, it is a coordinated response by the body to counteract the acidotic state.  The authors comment:

"Acidosis-induced proteolysis serves acid-base homeostasis, just as acidosis-induced osteolysis does.  With increased skeletal release of amino acids, including glutamine and amino acids, the liver converts to glutamine (the major source for renal synthesis of ammonia [NH3]), the kidney can greatly increase excretion of H+ (as ammonium ions [NH4])."

In simpler terms, amino acids released from muscle during acidosis-induced muscle breakdown travel to the liver to promote increased glutamine production.  This glutamine, in turn, travels to the kidney, promoting increased excretion of acidifying hydrogen ions. 

Chronic metabolic acidosis and renal dysfunction

Can chronic metabolic acidosis contribute to renal dysfunction?  Sebastian et al (1) point out:

"The question has arisen whether the metabolic acidosis that typically occurs during chronic progressive renal diseases in turn accelerates the progression of renal injury and functional decline.  We believe the question is germane because it prompts the question whether chronic diet-induced metabolic acidosis contributes to the pathogenesis of the renal structural and functional decline that occurs normally with aging.

Chronic metabolic acidosis contributes to the progression of renal disease putatively by at least five potential acidosis-inducible renal pathologies: (a) intrarenal calcium salt deposition (skeletal calcium mobilization and reduced renal citrate concentrations; (b) renal cellular hypertrophy (metabolic sequelae of acidosis); (c) intrarenal complement-induced cytotoxicity initiated and sustained by increased local concentrations of NH3; (d) amino acid-induced hemodynamic injury (accelerated protein catabolism); and, (e) intrarenal oxidant damage (hypermetabolism)."

THE IMPACT OF METABOLIC ALKALOSIS ON SPECIFIC ORGAN SYSTEMS

Bone

As described above, chronic metabolic acidosis has a significant detrimental effect on bone health.  Conversely, chronic metabolic alkalosis appears to have a very positive impact on bone health, as noted by Sebastian et al (1).  In the first of several quotes I would like to present on this relationship, the authors state the following:

"Metabolic alkalosis, by contrast, reduces calcium efflux from bone, and both suppresses osteoclastic bone resorption and stimulates osteoblastic bone formation.  Those effects occur linearly with medium pH values above 7.40 (effected by increasing medium [HCO3-]), suggesting that even minimal degrees of alkalosis show anabolic and antiresorptive effects.  Those in vitro findings also suggest that inducing and sustaining a low-grade systemic metabolic alkalosis with appropriate amounts of dietary base might amplify the antiosteoporotic effects of simply neutralizing the diet net acid load with smaller amounts of base.  Alkalosis-producing base input may augment bone also through renal conservation of calcium.  Reduced urinary calcium excretion produced by alkali loading linearly correlates with the alkali load over a broad range..."

The authors than go on to discuss the effects on bone health when potassium-based alkali loading is employed:

"A small increase in the ratio of osteoblastic bone formation to osteoclastic bone resorption, such as might accompany low-grade K+ alkali-loading metabolic alkalosis, might tip the scales just enough to equalize the unfavorable formation-resorption coupling and prevent bone mass decline, or tip them enough even to increase bone mass."

Evidence of this can be seen in the skeletal remains of the hunter-gatherer populations who had a higher dietary alkaline content when compared with ancient agriculture-based populations:

"Observations on the skeletal remains of stone age humans provide some clues.  Ancestral Homo species exhibit increased cortical thickness of their femurs, relative to body mass, and strength or rigidity.  Prehistoric hunter-gatherer femurs show greater density that those from prehistoric periodic agriculturists, and bone density in the hunter-gatherers remained relatively stable with age compared to the agriculturists."

Next Sebastian et al (1) point out the favorable impact of an alkaline diet on initial bone development:

"A more favorable bone formation-resorption coupling ratio secondary to chronic dietary net base input might also facilitate acquisition of bone during growth and development, leading to higher peak bone mass.  Consider the finding that very large intermittent doses of alkali given to children with HCO3-wasting renal tubular acidosis, required to sustain complete correction of metabolic acidosis, greatly accelerated bone growth."

Skeletal Muscle

Similar to bone, there is evidence that metabolic alkalosis can benefit skeletal muscle status:

"In children with HCO3-wasting renal tubular acidosis treated with large amounts of alkali, bone growth accompanied a generalized growth acceleration, including skeletal muscle."

Sebastian et al (1) then comment on the relationship between muscle and metabolic alkalosis from a Paleolithic perspective:

"To completely prevent age-related declines in muscle mass might require restoring the diet to its Paleolithic net base-producing state, with it associated low-grade metabolic alkalosis.  Administration of alkalosis-producing doses of exogenous base in humans can greatly reduce renal excretion of urea while concomitantly decreasing serum urea concentration, suggesting that alkali-loading alkalosis increases body nitrogen stores, of which skeletal muscle owns the lion's share."

Kidney stones

As was noted above, metabolic acidosis promotes formation of kidney stones.  Conversely, as noted by the authors, metabolic alkalosis can have a very positive effect with stone formers:

"By inducing a low-grade metabolic alkalosis without associated K+ depletion, moderate dietary net base loading (e.g., with KHCO3 or fruits and vegetables) also would be expected to increase excretion of citrate, which by chelating calcium reduces its availability for stone formation.  We predict that by both greatly increasing citrate excretion and greatly decreasing total calcium excretion, habitual ingestion of a moderate net base-producing potassium-rich diet (e.g., 50-100 mEq endogenous net base production and 200-250 mEq potassium intake per day) will completely prevent expression of the underlying defect(s) in patients with idiopathic hypercalciuria, both as hypercalciuria and as recurrent stone formation."

Please note that 200 mEq of potassium intake is equal to 8000 mg, which is approximately twice the recommend dietary intake.  Therefore, this approach to dealing with kidney stones must be considered as a limited time therapeutic intervention that should only be initiated after thorough patient evaluation, which includes appropriate laboratory testing. 

OVERALL CONCLUSIONS BY SEBASTIAN ET AL

In concluding their book chapter, Sebastian et al(1) reiterate their emphatic contention that our desire to emulate the Paleolithic diet must go beyond the usual emphasis on dietary protein.  We must also emulate the emphasis of the hunter-gatherer diet on the plant-based, high potassium, alkalizing foods:

"The ancestral human diet yielded net base because base input from plant-source foods exceeded input from animal-source foods.  Diets rich in base-producing plant foods contain abundant K+.  Indeed, we estimate that the K+ content of ancestral hominid diets as three to four times greater than that of contemporary diets."

SOME FINAL THOUGHTS

As we all know, during the last 10-20 years ingestion of the high protein, Paleolithic diet has been emphasized by many in the clinical nutrition and functional medicine community.  In contrast, many in this community have taken the opposing position that dietary protein at these levels could pose a risk to health.  I would maintain that our increasing fascination and focus on complexity that I have discussed in the first two installments of this series has blinded us to a simple and basic "see the forest before the trees" concept that has been so eloquently described by Sebastian et al (1):

Many advocates of the Paleolithic diet do not realize that the Paleolithic diet is more than just a matter of protein.  Equally important, if not more so, is the often ignored simple reality that the Paleolithic diet was also incredibly high in plant-based, high potassium alkaline foods.  Therefore, while the protein aspect of the Paleolithic diet is key for the promotion of good health, what may be even more important is plant-based, alkalizing aspect.

In short, any adverse effects of the Paleolithic diet are much more likely due to too little potassium-based alkalizing foods rather than too much protein.  Of course, the real irony is that this is really nothing new to most of us.  Why don't we focus on this issue more?  As I mentioned in the beginning of this installment, it may be that our attention has been diverted in various educational venues away from the simple truth suggested by Dimnet - that answers to our patients' health issues lie not so much with the complexity of  "great catastrophes" and "fatal errors" that often require expensive lab tests to diagnose and high-priced supplements to treat but with the simple and ordinary "repetition of slowly destructive little things" that can be diagnosed and treated very often with basic and inexpensive modalities.  

In part III of this series I will be exploring still more research on the adverse heath impact of chronic metabolic acidosis.

REFERENCES

  1. Sebastian A et al. An evolutionary perspective on the acid-base effects of diet. In: Gennari FJ et al, ed. Acid-Base Disorders and Their Treatment Boca Raton: Taylor & Francis; 2005:241-92.

 

 

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