Under Appreciated Issues in the Treatment of Chronic Illness – Low Grade, Chronic Acidosis Combined with Potassium Deficiency – Part VI – The Impact of Acidosis on Insulin Metabolism


In part V of this series I briefly touched on the interesting, important, and under-appreciated relationship between insulin and potassium metabolism.  Now, I would like to flip back to the other side of the potassium/metabolic acidosis coin and discuss the impact of metabolic acidosis on insulin metabolism.  As we all know, disturbances in insulin metabolism, generally expressed as either insulin resistance, hyperinsulinemia or both, can have a major impact on the course of virtually every chronic illness and factors that contribute to decreased quality of life in chronically ailing patients.  However, what many do not realize is that disturbances in insulin metabolism are more than just a function of the most commonly recognized cause, excessive intake of poor-quality carbohydrate sources.  In fact, there are many less well recognized causes of dysinsulinism, some of which have been discussed in past issues of the Moss Nutrition Report i.e., chronic inflammation and excessive psychological stress.  The less well- known cause I am going to feature in this newsletter is low grade, chronic metabolic acidosis.


Certainly, for the bulk of the patients we typically encounter, the most common cause of chronic metabolic acidosis is poor diet.  Therefore, I would like to begin this commentary with the paper “The role of dietary acid load and mild metabolic acidosis in insulin resistance in humans” by Williams et al (1).

The first quote I would like to feature from this paper provides some basic information on pH in human physiology and the impact of diet on pH dynamics:

“Under normal conditions, blood pH is maintained within a narrow physiological range.  The blood pH of arterial blood is close to 7.40, with a normal range considered to be approximately 7.35 – 7.45.  An arterial pH less than 7.35 is classified as acidaemia, whilst the underlying condition characterized by hydrogen ion retention or loss of bicarbonate or other bases, is referred to as acidosis.  The acidogenic Western diet is associated with an increase in the body’s hydrogen ion load, and has been hypothesized to lead to chronic mild metabolic acidosis, if proceeded by the failure of compensatory processes that aim to restore the homeostatic acid/base balance.   Consumption of foods with a high acid load (e.g. animal protein) results in the net production of nonvolatile acids such as hydrogen chloride (HCl) and hydrogen sulfate (H2SO4).  These acids are buffered through the excretion of carbon dioxide via the lungs, and the production of sodium salts from nonvolatile acids which are excreted by the kidneys, predominantly in association with ammonium, as NH4CL and (NH4)2SO4.  The bicarbonate generated in this process is reabsorbed and returned to the plasma, to replace the bicarbonate used to buffer the nonvolatile acid.  If acid production in the body exceeds acid excretion from the lungs and kidneys, the plasma bicarbonate and pH decrease.  Previous authors have labelled this downward shift in body pH to the lower end of the normal range as a result of dietary acid load ‘latent acidosis’, ‘diet induced acidosis’, ‘low grade acidosis’, ‘chronic metabolic acidosis’, ‘subclinical acidosis’ or ‘mild metabolic acidosis’.”

The next quote discusses the two ways metabolic acidosis actually induces insulin resistance.  The first relates to alterations in muscle metabolism and the second relates to the fact that metabolic acidosis is a physiologic stressor, thus leading to cortisol production:

“Adeva and Souto discussed how a Western diet is linked with the development of metabolic acidosis despite renal physiological alterations such as increasing renal net acid excretion (RNAE).  They hypothesized that metabolic acidosis induces insulin resistance in skeletal muscle to permit protein degradation and to generate ammonium required to promote hydrogen ion excretion, resulting in an increased risk of type 2 diabetes and hypertension.  They additionally suggest that metabolic acidosis may induce glucocorticoid production, and the resulting rise in plasma cortisol could in turn contribute to insulin resistance and proteolysis.”

Hence, in line with the allostatis/allostatic load model of illness I have discussed many times in this forum, insulin resistance induced by metabolic acidosis is not a disease per se but a response to resolve the acidotic state which can create illness if it persists too long with a great enough magnitude.  More on the allostatic relationship between acidosis and insulin metabolism later.

Souto and colleagues in the Williams et al (1) paper also suggested that metabolic acidosis induced insulin resistance could contribute to kidney dysfunction:

“Souto and colleagues further hypothesised the risk of developing renal impairment (heralded by microalbuminuria) due to metabolic acidosis induced insulin resistance, which in turn was considered to be associated with increased risk of cardiovascular disease and mortality.”

The next two quotes again emphasize the important connection between diet and blood pH both in terms of the creation of an acidotic state as well as the impact of alkalizing foods that contain potassium and magnesium:

“A persistently high dietary acid load can lead to a decrease in blood pH towards the lower end of the normal physiological range if not adequately compensated for by homeostatic mechanisms or dietary modification.”

In addition:

“Plant-based foods such as fruit and vegetables are a key source of potassium and magnesium and have been shown to counterbalance renal net acid excretion induced by high protein intake.”

The next section of the Williams et al (1) paper provides more detail on the specifics of the relationship between acidosis and insulin metabolism:

“In healthy adults, a decrease in pH to the lower end of the normal physiological range by ammonium chloride administration, reduced insulin sensitivity. Conversely, in chronic renal failure patients, the correction of metabolic acidosis following bicarbonate treatment increased insulin sensitivity.  Increased renal net acid excretion, decreased urinary pH, increased sulphate excretion as well as serum markers of metabolic acidosis, including low bicarbonate, high anion gap (the difference between measured anions and cations in serum) and increased lactate (a small component of the anion gap) have consistently been associated with insulin resistance and type 2 diabetes risk.”

Next, the authors expand on the relationship between lactate, acidosis, and glucose metabolism:

“In a large prospective study of overweight individuals, an elevation in lactate concentration at rest was found to be an early indicator of glucose impairment.  This rise in lactate, an indicator of metabolic acidosis, within the normal physiological range was predictive of type 2 diabetes incidence in the Atherosclerosis Risk in Communities (ARIC) study.”

How else might metabolic acidosis affect insulin metabolism?  As you will see, it affects insulin binding and signaling mechanisms:

“In a study of cultured rat myoblasts, a decrease in extracellular pH was found to disrupt insulin binding and reduce the phosphorylation of Akt, a downstream target in the insulin signaling pathway.”

In the next section of the Williams et al (1) paper assessment modalities are discussed in terms of using metabolic acidosis clinical measurements to predict the acid load of the diet:

“In healthy individuals, renal net acid excretion has been shown to be highly predictive of protein and potassium content of the diet and is thus a reliable index of dietary acid load.”

In addition, renal net acid excretion can also be used as an assessment tool, along with other laboratory measurements, to determine risk for type 2 diabetes:

“Increased renal net acid excretion, as well as other measures of mild metabolic acidosis, including low serum bicarbonate, high anion gap, and low urinary pH, have been associated with an increased risk of type 2 diabetes.”


The next paper I would like to review is “The effects of systemic and local acidosis on insulin resistance and signaling” by Baldini and Avnet (2), which provides more detail on the relationship between acidosis and insulin metabolism.  The first set of quotes I would like to feature discusses the acidosis seen with many diabetics.  Unlike the diet induced acidosis highlighted in the Williams et al (1) paper which suggested that the acidotic state is related to HCl and H2SO4 production, the acidosis seen with diabetics may be related to the presence of excess lactic acid:

“Hyperlactatemia is a recurrent clinical feature of diabetic patients and has been directly associated with acidosis through a cause-and-effect relationship.”

However, the excess lactic acid may not be just a function of excess production.  It may also be due to decreased metabolism:

“In a clinical context, lactic acidosis can occur either due to excessive production of lactate at the tissue level or impaired lactate metabolism.”

In addition, somewhat confusing the issue from an assessment standpoint, many patients with excess lactic acid may still have a normal serum pH:

“Notably, hyperlactatemia may also occur with a normal serum pH…”

Why would diabetics demonstrate increased levels of lactate?  The reason has to do with the fact that insulin resistance is not the only insulin/glucose dysregulation issue seen with these patients.  In addition, increased serum glucose levels lead to increased production of insulin, which stimulates glycolysis.  Baldini and Avnet (2) note:

“One of the major functions of insulin is a stimulatory effect on glycolysis that occurs when there is a rise in the level of circulating glucose.  In turn, glycolysis causes lactic acid production.”

The next section of the Baldini and Avnet (2) paper directly addresses the cause and effect relationship between acidosis and insulin resistance:

“pH is known to modify insulin activity, and that acidification is considered as a mechanism of insulin resistance.”

Interestingly, the authors go on to point out that, in the past, it was thought that the insulin resistance caused by acidosis was mainly a function of the production of ketone bodies (ketoacidosis).  However, subsequent research has demonstrated that acidosis due to any cause will impair insulin sensitivity.

What is the mechanism of acidosis induced insulin resistance?  One aspect is a reduction of insulin receptor binding:

“Acid-induced insulin resistance has been observed in several cell types.  A possible very simple reason for this effect is reduced insulin binding to its receptor at high proton concentrations.  Igarashi et al. have elegantly shown that in adipocytes, lowering of extracellular pH is associated with a reduced insulin binding rate (up to 70%).”


“Acidosis…has the potential to directly affect the insulin-stimulated glucose uptake by interfering with the first step of the insulin signaling pathway, the insulin receptor activation, which, as a consequence, might impair the downstream insulin receptor signaling.”

Acidosis, dysinsulinism, and inflammation

As we all know by now, there’s always more to the story with virtually every metabolic imbalance and that “more to the story” portion generally involves inflammation.  Can an acidotic state increase production of inflammatory mediators?  Of course, the answer is yes:

“Tissue acidification (pH decrease of at least 0.5-1.0 pH unit) is commonly associated with inflammation.”

What is the impact on insulin activity?

“Activation of inflammatory pathways by acidosis can, in turn, impair glucose metabolism and cause systemic insulin resistance.”

Which pro-inflammatory factors are most involved in adversely affecting insulin metabolism?  As with many other metabolic imbalances with which we are familiar, IL-1, IL-6 and NF-κB are predominant:

“Notably, IL-1, which is a major proinflammatory cytokine, is present at increased levels in patients with diabetes mellitus, and could promote β-cell destruction and alter insulin sensitivity.  Likewise, IL-6 has been suggested to be involved in the development of obesity-related and diabetes mellitus Type 2-related insulin resistance.  The action of IL-6 on glucose homeostasis is also complex, and integrates central and peripheral mechanisms.  Overall, these data demonstrate that acidosis has the potential to indirectly cause insulin resistance via the activation of NF-κB pathways and the release of inflammatory cytokines, an already well-known cause of chronic inflammation in diabetic patients.”

From the conclusion of the Baldini and Avnet paper (2) I would like to highlight two key quotes:

“Acidosis modulates insulin sensitivity and resistance in many different and complex ways.  Notably, the timing of exposure to acidosis is a crucial factor in this context, since acute and chronic effects of acidosis may have completely opposite effects.”

Finally, the authors point out that dietary modifications may be an important intervention with diabetic patients who are experiencing acidosis-induced insulin resistance and glucose metabolism imbalances:

“For diseases associated with insulin resistance, like for type 2 diabetes, decreasing dietary acid load may be an achievable alternative and a relevant route to improve glucose homeostasis and prevention on a long-term basis.”

Acidosis, dysinsulinism, and cortisol

As we all know by now, any discussion on chronic illness and its relationship to dysinsulinism, acidosis, and inflammation would not be complete without understanding the role of another ubiquitous participant in metabolic dysfunction, cortisol.  The impact of cortisol in acidosis-induced dysinsulinism was discussed in the paper “Insulin sensitivity and glucose homeostasis can be influenced by metabolic acid load” by Della Guardia et al (3).  The first quote I would like to feature from this paper discusses the impact of acidosis-induced increased cortisol on insulin metabolism:

“Other physiological responses to metabolic acidosis, including increased cortisol levels, have been proposed as causative mechanisms for insulin resistance.  Cortisol acts as anti-insular hormone, being capable of inhibiting insulin signaling in peripheral tissues, such as skeletal muscle and adipocytes.”

The next quote discusses the relationship between pH and cortisol secretion in more detail:

“Cortisol secretion is stimulated by low pH to increase the plasmatic clearance of excess hydrogen ions.  In this respect, Buehlmeier et al. – pooling results from randomized trials – observed an overall decrease of adrenal-glucocorticoids secretion following alkali supplementation, although the effects on cortisol levels was not specifically investigated.  As cortisol acts as an anti-insular hormone, the augmentation of its circulating levels as a result of mild-metabolic acidosis may account for worsening insulin sensitivity.”

Before continuing, please note again the first sentence of the above quote that highlights a key point about allostatic responses that I have been emphasizing repeatedly over the years.  Cortisol increases in response to an acidotic state is not a manifestation of disease per se as traditional medical and nutritional thinking might surmise.  Instead, it is a response by the body to rid itself of excess, acid-producing hydrogen ions.  However, in line with allostatic load concepts which suggest that the magnitude and duration of the response to a stressor (in this case excess levels of acidic hydrogen ions) determines whether the response will be an improvement or detriment to health, a cortisol response to increased levels of hydrogen ions will eventually lead to the development of insulin resistance if the cortisol levels are too high and persist for too long.

The next quote I would like to feature discusses the intriguing question.  Since, as we know, potassium bicarbonate reduces metabolic acidosis, based on the above relationship between metabolic acidosis and cortisol, will potassium bicarbonate supplementation also reduce elevated cortisol levels?  As noted in the following quote, the answer is, indeed, yes:

“…Maurer and colleagues reported a slight decrease in cortisol levels following supplementation with KHCO3 in healthy individuals.”

Muscle metabolism, acid/alkaline balance and dysinsulinism

As I have discussed repeatedly in my writings and lectures over the years, due to the fact that most insulin receptors are located on muscle, muscle is the primary determinant of insulin sensitivity/resistance.  Could acid/alkaline balance play a role in influencing this relationship?  This question was also addressed by Della Guardia et al (3). 

The authors begin this discussion by emphasizing the important role of muscle in insulin metabolism:

“Preservation of skeletal muscle mass and functionality is critical for glucose homeostasis as it is the primary site of insulin-stimulated glucose uptake.  Insulin sensitivity and β-cell functionality are dependent on muscle health, and a metabolically active muscular system has been shown to improve glycemia and insulin sensitivity in healthy and diabetic subjects.  Reduced muscle mass and strength is commonly associated with obesity and insulin resistance, in addition to other chronic metabolic perturbations, and abnormalities in insulin signal transduction have been associated with reduced activity of insulin-dependent glucose transport in skeletal muscles in diabetic patients.”

How can metabolic acidosis affect this relationship?  The authors comment:

“To this end, muscle insulin-insensitivity accelerates muscle degradation by affecting insulin signaling, and end-stage kidney failure patients, suffering from mild metabolic acidosis, exhibit significant muscle loss compared with health subjects.  Conversely, alkali salt supplementation offsets the acidosis-induced muscle mass wasting.”

The next quote makes it clear that, in line with the allostatic relationship between cortisol and metabolic acidosis discussed above, loss of muscle due to metabolic acidosis is not just a detrimental outcome but a response to cope with the excess acidity.  As noted in the following quote, ammonia (NH3) released from muscle during muscle breakdown will act as an alkalizing factor to promote disposal of acidic hydrogen ions:

“Protein and amino-acid degradation would provide energetic substrates and increase NH3 availability to promote hydrogen-ions disposal via the kidneys.”

With the above in mind, it would make sense that an alkaline diet would promote preservation of muscle mass:

“…Welch et al. reported a slight positive association between a more alkaline diet, lean mass, and muscle parameters.  A prospective cohort study conducted on approximately 3000 individuals found slower muscle mass wasting among persons over 65 with a lower net endogenous acid production (NEAP)…across four years.”

Similarly, supplementation of alkalizing potassium bicarbonate (KHCO3) had a similar positive effect on muscle metabolism:

“A short-term supplementation with KHCO3 (60-120 mmol/day) for 18 days in 14 healthy postmenopausal women reduced urinary total nitrogen levels.  Similarly, two studies reported that KHCO3 was sufficient to reduce nitrogen excretion in middle-aged or older subjects.  Since urinary nitrogen can reflect the rate of protein degradation in physiological conditions…the authors suggest that supplementation may be effective for the preservation of muscle protein.  Interestingly, in one of the investigations mentioned, supplementation with alkali salt was correlated with increased muscle performance (+70% of power measured with one rep at leg press) in women >50 years-old, whereas in men did not elicit any effect.”

In the next section of their paper, Della Guardia et al (3) emphasize the important relationship between acid/alkaline balance and glucose/insulin metabolism that I discussed above in my review of the Williams et al (1) paper:

“Cross-sectional studies on large groups of individuals are likely to indicate a direct relationship between markers of acid load (or acid-imbalance) and insulin sensitivity or glycemic control.  This is in accordance with the observation that consuming higher quantities of fruit and vegetables (low amount of dietary acid load) reduces the risk of developing insulin resistance and diabetes.  Increased net acid excretion, as well as other measures of mild metabolic acidosis (e.g., low serum bicarbonate, high anion gap, and low urinary pH) have been associated with an increased risk of diabetes T2.   In a large epidemiological investigation (NHANES), lower bicarbonate plasmatic levels and higher anion gap have been independently associated with decreased insulin-sensitivity in women aged 30-55.  Similarly, elevated plasma bicarbonate measured in 630 white, overweight women not suffering from metabolic conditions was associated with reduced risk of diabetes T2 (self-reported diagnosis) after adjusting for BMI, creatininemia, and history of hypertension.”

Della Guardia et al (3) conclude with the following overview statements:

“The data reviewed here strongly suggests an association between glucose metabolism and acid load biochemical markers.  Findings which propose an active role of diet-induced acidosis in the regulation of insulin sensitivity are in accordance with experimental data showing that in models of metabolic acidosis, such as end-stage kidney failure, insulin sensitivity can be restored via alkali supplementation.  Dietary acid load may be modulated through specific dietary adjustments and the results discussed above are in line with the observation that plant-based diet consumption is an effective management for glucose-imbalance and metabolic disturbances.”

Furthermore, concerning mechanism of action:

“As reported, a significant body of evidence supports the critical role of acidosis in the disruption of peripheral insulin activity through the interference with its receptor binding and intracellular insulin-signal transduction.”


The Baldini and Avnet (2) paper reviewed above discussed the relationship between serum lactate levels and metabolic acidosis.  From a clinical standpoint, is serum lactate useful in diagnosing BOTH acid/alkaline imbalance and insulin resistance?  This question was addressed by the study “Dietary acid load, metabolic acidosis and insulin resistance – Lessons from cross-sectional and overfeeding studies in humans” by Williams et al (4).

In this study, 40 overweight individuals (20 men and 20 women aged 37 ± 2 years ingested a high calorie diet (1250 kcal/day above baseline energy requirements) for 28 days.  The diet consisted of 45% fat, 15% protein, and 40% carbohydrate.  In addition, the diet contained significant amounts of acid producing processed foods.  As you will see, in this population ingesting a high calorie, high acid diet, fasting plasma lactate levels, an indicator metabolic acidosis, were significantly higher in the insulin resistant subjects:

“…circulating lactate, a small component of the anion gap, is a surrogate of body acid/base balance.  Elevations in plasma lactate within the normal range are indicative of mild metabolic acidosis and predictive of type 2 diabetes incidence in the Atherosclerosis Risk in Communities (ARIC) study.  In the present study, fasting plasma lactate was higher in obese insulin resistant individuals compared to obese insulin sensitive individuals matched for BMI, total body fat and central abdominal fat, suggesting that lactate is higher in insulin resistant individuals regardless of adiposity.”

Given that elevated or high normal plasma lactate is an indicator for metabolic acidosis and low dietary potassium and magnesium is a significant cause of metabolic acidosis, could elevated or high normal plasma lactate indicate a need for additional dietary potassium and magnesium?  According to Williams et al (4), the answer is yes:

“Plant-based foods such as fruit and vegetables are a key source of potassium and magnesium, major contributors to the dietary alkali load.  In patients with chronic renal disease, supplementation of the diet with fruit and vegetables has been reported to have a comparable effect to oral sodium bicarbonate in correcting metabolic acidosis over a one year trial.  This is supported in the present study, where elevations in plasma lactate during overfeeding were inversely associated with dietary intake of potassium and magnesium.”

Williams et al (4) conclude their paper with the following statement:

“Mild metabolic acidosis, as indicated by circulating lactate, (i) aligns with insulin resistance independent of adiposity and (ii) is induced by short-term increases in energy and dietary acid load in healthy humans.”

For those of you who routinely use functional medicine testing with your patients, lactate is included in the Genova organic acids panel.  Therefore, if your routine assessment methodologies are inconclusive for the presence of low grade, chronic metabolic acidosis, insulin resistance, and/or the need for increased dietary potassium and magnesium, lactate measurements included with the Genova organic acids panel may be very helpful in this regard.


As noted above, potassium deficiency can certainly contribute to insulin resistance.  However, with that stated, can we also infer that potassium supplementation can improve insulin sensitivity, particularly in cases where it is not absolutely certain that a state of potassium deficiency actually exists?  This question was answered by the paper “Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study” by Conen et al (5). 

In this study 11 overweight subjects demonstrating both impaired fasting glucose and impaired glucose intolerance (prediabetes) were evaluated.  The composition of the group was 7 males and 4 females aged 47-63 years.  The subjects were divided into two groups with one group ingesting 3600 mg of potassium as potassium chloride per day for two weeks followed by placebo ingestion for two weeks.  The other group ingested 3600 mg of potassium as potassium citrate per day for two weeks followed by placebo ingestion for two weeks.

The results were quite interesting in that potassium supplementation improved insulin secretion and insulin sensitivity even when there was no evidence of potassium deficiency.  Even more interesting, though, is that only the potassium citrate and not the potassium chloride demonstrated this effect.  This should not be surprising given that, as I have stated in previous newsletters, the alkalizing effect is extremely important, and chloride is a known acidulator.  The authors comment:

“The results of this placebo-controlled, randomized cross-over pilot study demonstrate that even in the absence of overt, pre-existing K+ depletion, K+ supplementation improved beta-cell function (measures of insulin secretion) in subjects with prediabetes.  The insulin-sensitizing and hypotensive effect, however, critically depended on citrate as the accompanying anion.”

Would potassium bicarbonate (Bicarbonate is also an alkalizing factor) have the same impact?  Since citrate is converted to bicarbonate in the body (6), in my opinion it is highly likely.


When I started writing this newsletter series in May of 2018, I stated that my primary incentive for writing it was the impression I had that the functional medicine community was overly enamored with the latest high-tech functional medicine tests and supplements.  In turn, it appeared to me that this love affair with “the latest, greatest, and most expensive” was crowding out at many, if not most of the major functional medicine symposia, discussions of the foundations of clinical nutrition that have reliably and cost effectively improved patient health over the years.  The aspect of this oversight that upset and confounded me the most was the foundational issue of fluid and electrolyte balance with an emphasis on low grade, chronic metabolic acidosis and its intimate relationship with potassium, a nutrient that appears to have fallen off the face of the earth, judging from how many functional medicine symposia lecturers actually discuss it to any great extent.  Why was I so confounded and upset about this nutritional issue in particular?  As I hope I have demonstrated to you in this series, the reason is the massive discrepancy between the sheer immensity of the amount of published research on the subject and the amount of people in the functional medicine community who are focusing on and employing this research in their lectures and practices to a significant extent.

It is my hope that this newsletter series has convinced you that this discrepancy can no longer be tolerated.  For, as I have tried to demonstrate, not only are issues relating to low grade, chronic metabolic acidosis and potassium deficiency central to the quality of life issues being experienced by many, if not most chronically ill patients, these issues can be addressed quite successfully using low-tech, low-cost assessment modalities, simple and practical lifestyle corrections, and basic and quite affordable supplemental protocols. 

In closing, I look forward to hearing from you, the readers of these newsletters, on ways that focusing on low grade, chronic metabolic acidosis specifically and fluid and electrolyte imbalances in general have played a role in improving the health and quality of life of your patients.  For, perhaps, if enough of us “in the trenches” speak up, the organizers of major functional medicine symposia and the lecturers they partner with will finally get the message that low cost, low tech, back to basics nutrition is just as vital to the successful practice of functional medicine and clinical nutrition as the latest and greatest, if not more so.

Moss Nutrition Report #288 – 11/01/2019 – PDF Version


  1. Williams R et al. The role of dietary acid load and mild metabolic acidosis in insulin resistance in humans. Biochimie. 2016;124:171-7.
  2. Baldini N & Avnet S. The effects of systemic and local acidosis on insulin resistance and signaling. Int J Mol Sci. 2019;20(126).
  3. Della Guardia L et al. Insulin sensitivity and glucose homeostasis can be influenced by metabolic acid load. Nutrients. 2018;10(618).
  4. Williams RS et al. Dietary acid load, metabolic acidosis and insulin resistance – lessons from cross-sectional and overfeeding studies in humans. Clin Nutr. 2016;35:1084-90.
  5. Conen K et al. Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study. J Diabetes and Its Complications. 2016;30:1158-61.
  6. Naka T & Bellomo R. Bench-to-bedside review: Treating acid-base abnormalities in the intensive care unit – the role of renal replacement therapy. Critical Care. 2004;8(2):108-14

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