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Background: Diet can affect the body's acid-base balance due to its content of acid or base precursors. There is conflicting evidence for the role of metabolic acidosis in the development of cardiometabolic disorders, hypertension (HT), and insulin resistance (IR)., Objective: We hypothesized that dietary acid load (DAL) is associated with adverse metabolic risk factors and aimed to investigate this in the elderly., Methods: A total of 114 elderly participants were included in the study. The participants were divided into four groups, such as HT, diabetes (DM), both HT and DM, and healthy controls. Anthropometric, biochemical, and clinical findings were recorded. Potential renal acid load (PRAL) and net endogenous acid production (NEAP) results were obtained for three days, 24-hour dietary records via a nutrient database program (BeBiS software program)., Results: The groups were matched for age, gender, and BMI. There was a statistically significant difference between the groups regarding NEAP (p =0.01) and no significant difference for PRAL ( p = 0.086). The lowest NEAP and PRAL levels were seen in the control group while the highest in the HT group. Both NEAP and PRAL were correlated with waist circumference (r = 0,325, p = 0.001; r=0,231, p =0,016, respectively)., Conclusion: Our data confirmed that subjects with HT and DM had diets with greater acid-forming potential. High NEAP may be a risk factor for chronic metabolic diseases, particularly HT. PRAL could not be shown as a significantly different marker in all participants. Dietary content has a significant contribution to the reduction of cardiovascular risk factors, such as HT, DM, and obesity., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: This study aimed to investigate the association of diet quality (DQ) and dietary acid load (DAL) with insulin resistance (IR) in overweight children and adolescents., Materials and Methods: The study was conducted on 135 overweight participants aged 6-17 years. DQ was assessed using the Healthy Eating Index 2015 (HEI-2015) and the HEI-2015-TUBER, revised in accordance with the Turkey Dietary Guidelines (TUBER). Estimation of DAL was made calculating the potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores., Results: The HEI-2015-TUBER score was lower in those with IR than in those without IR (p=0.021). Higher PRAL and NEAP scores were found in those with IR (p=0.060 and p=0.044, respectively). Moreover, a one-unit increase in the HEI-2015-TUBER score and the DAL score was associated with a reduction of 4.2% and a rise of approximately 3% in IR risk, respectively., Conclusions: Healthy eating habits in overweight paediatric groups may help to reduce the IR risk, improving DQ and decreasing DAL., (Copyright © 2021 SEEN and SED. Published by Elsevier España, S.L.U. All rights reserved.)

Background & Aims: Diabetes mellitus (DM) and cardiovascular disease (CVD) are among the biggest causes of death and health expenses worldwide. A higher dietary acid load (DAL) is associated with chronic low-grade metabolic acidosis, and may increase the risk of insulin resistance (IR), DM, hypertension, and CVD mortality. However, the association between DAL and IR still lacks population-based studies to confirm laboratory findings., Methods: This is a population-based observational study including a sample of 545 individuals aged 25-64 years from Florianópolis (Southern Brazil) who participated in the EpiFloripa cohort study. All diet variables were obtained through two 24-h Food Recalls adjusted to obtain an estimate of habitual food consumption. DAL was measured by Potential Renal Acid Load (PRAL) and Net Endogenous Acid production (NEAP). Fasting blood samples were obtained from all participants. The primary outcome was IR, which was estimated by HOMA-IR. Secondary outcomes included HOMA-β, glycosylated hemoglobin, and fasting blood glucose and insulin. Multiple linear regression models adjusted for sociodemographics, lifestyle, and clinical variables were used for analysis, with exposure and outcome variables standardized as Z-scores to allow comparability of the results., Result: The mean PRAL and NEAP in the sample were 16.9 ± 4.8 and 66.1 ± 7.1 mEq/day, respectively. The average HOMA-IR score was 2.4 ± 1.6. In adjusted analyses, PRAL was positively associated with HOMA-IR, fasting insulin, and fasting blood glucose (p-value <0.05 in all cases), but not with HOMA-β or glycated hemoglobin. NEAP also showed a direct-trend relationship with HOMA-IR and fasting insulin, but not with fasting blood glucose or the other outcomes. The strongest association was between PRAL and HOMA-IR (β, 0.20; 95% CI, 0.06-0.35)., Conclusions: A higher DAL was consistently associated with higher IR and insulin levels but not with other glycaemic parameters. Apparently, β-pancreatic cells function is not affected by DAL in this population. This is the first study that describes the DAL in a population-based sample of adults in Latin America and in a middle-income country population. Further longitudinal and interventional studies are required to establish a better causal effect between DAL and IR., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2022 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)

Background: Evidence suggests that changes in dietary acid load may influence body weight, body composition, and insulin sensitivity., Methods: Participants (n = 244) were randomly assigned to an intervention (vegan) (n = 122) or control group (n = 122) for 16 weeks. Before and after the intervention period, body composition was measured by dual X-ray absorptiometry. Insulin resistance was assessed with the Homeostasis Model Assessment (HOMA-IR) index and predicted insulin sensitivity index (PREDIM). Repeated measure ANOVA was used for statistical analysis., Results: Potential Renal Acid Load (PRAL) and Net Endogenous Acid Production (NEAP) decreased significantly in the vegan group with no change in the control group (treatment effect -24.7 mEq/day [95% CI -30.2 to -19.2]; p < 0.001; and -23.8 mEq/day [95% CI -29.6 to -18.0]; p < 0.001, respectively). Body weight decreased by 6.4 kg in the vegan group, compared with 0.5 kg in the control group (treatment effect -5.9 kg [95% CI -6.8 to -5.0]; Gxt, p < 0.001), largely due to a reduction in fat mass and visceral fat. HOMA-IR index decreased and PREDIM increased in the vegan group. After adjustment for energy intake, changes in PRAL and NEAP correlated positively with changes in body weight (r = +0.37; p < 0.001; and r = +0.37; p < 0.001, respectively), fat mass (r = +0.32; p < 0.001; and r = +0.32; p < 0.001, respectively), visceral fat (r = +0.19; p = 0.006; and r = +0.15; p = 0.03, respectively), and HOMA (r = +0.17; p = 0.02; and r = +0.20; p = 0.006, respectively), and negatively with changes in PREDIM (r = -0.22; p = 0.002; and r = -0.27; p < 0.001, respectively)., Conclusion: Dietary acid load as part of a plant-based diet was associated with changes in body weight, body composition, and insulin sensitivity, independent of energy intake. Mechanistic explanations suggest that the relationship may be causal., Trial Registration: ClinicalTrials.gov number, NCT03698955., Competing Interests: Declaration of competing interest All authors except for AT and RH work or have worked for the Physicians Committee for Responsible Medicine in Washington, DC, a nonprofit organization providing educational, research, and medical services related to nutrition. Dr. Barnard is an Adjunct Professor of Medicine at the George Washington University School of Medicine. He serves without compensation as President of the Physicians Committee for Responsible Medicine and the Barnard Medical Center in Washington, DC. He writes books and articles and gives lectures related to nutrition and health and has received royalties and honoraria from these sources., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Acid-base homeostasis is increasingly being recognized to play an important role in normal metabolic function. However, prospective studies on the relationship between diet-induced acid-base imbalance and insulin resistance among Asian populations have been limited. Thus, we investigated whether diet-induced metabolic acidosis was prospectively associated with insulin resistance risk in middle-aged and older Korean adults., Methods: In total, 5406 participants from the Korean Genome and Epidemiology Study without type 2 diabetes, insulin resistance, cancer, or renal diseases at baseline examination were included in this study. To estimate diet-induced metabolic acidosis, we used potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores calculated from the usual dietary intake assessed by a validated 103-item food frequency questionnaire at baseline. Multivariable Cox proportional hazard models were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of insulin resistance incidence., Results: During a mean follow-up period of 7.4 years, we documented 3449 insulin resistance cases. In the fully adjusted model, the future insulin resistance risk was significantly higher among participants in the highest quartiles of PRAL (HR: 1.30, 95% CI: 1.13-1.48, P trend  = 0.0002) and NEAP (HR: 1.30, 95% CI: 1.14-1.49, P trend  = 0.0008) than among those in the lowest quartiles. Associations were slightly strengthened among men, adults < 50 years old, obese participants, or those with low physical activity levels., Conclusions: Our findings suggested that diet-dependent acid load was positively associated with the future development of insulin resistance, suggesting effect modification by sex, age, the presence of obesity, and physical activity levels.

Objectives: There is no clear summarised report of the association between dietary acid load components including potential renal acid load (PRAL) and net-endogenous acid production (NEAP) with cardiometabolic risk factors. In the current meta-analysis, we aimed to systematically review and summarise the eligible observational studies evaluating the association between PRAL and NEAP with blood pressure and hypertension and markers of glucose haemostasis among adults., Design and Setting: In a systematic search from PubMed, SCOPUS, Web of Sciences and Cochrane electronic databases up to May 2019, relevant studies were included in the literature review. Observational studies evaluating the association between PRAL and NEAP with the systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose, insulin, homeostatic model assessment of insulin resistance (HOMA-IR), haemoglobin A 1 C (HbA 1 C), HOMA-β and quantitative insulin check index (QUICKI) and also prevalence or odds of hypertension, hyperglycaemia and diabetes were included., Results: Total number of studies included in the 14 separate meta-analyses were as follows: Mean (SD) of SBP (PRAL, n = 12; NEAP, n = 6), mean (SD) of DBP (PRAL, n = 8; NEAP, n = 3), mean (SD) of FBS (PRAL, n = 12; NEAP, n = 5), mean (SD) of HbA 1 C (PRAL, n = 6; NEAP, n = 4), mean (SD) of HOMA-IR (PRAL, n = 7), mean (SD) of insulin (PRAL, n = 7; NEAP, n = 2); OR of type 2 diabetes mellitus (T 2 DM) (PRAL, n = 8; NEAP; n = 6), HTN prevalence (PRAL, n = 9; NEAP, n = 9), T 2 DM prevalence (PRAL, n = 7; NEAP, n = 6). According to our results, being in the highest PRAL categories was associated with higher SBP (WMD = 0.98; CI: 0.51, 1.45; P < .001), DBP (WMD = 0.61; CI: 0.089, 1.135; P = .022), insulin (WMD = -0.235, CI: 0.070, 0.400; P = .005), higher odds of diabetes (OR = 1.19; CI: 1.092, 1.311; P < .001), higher prevalence of T 2 DM (13% and 11% in highest vs lowest category). While, being in the highest category of NEAP was only associated with higher odds of diabetes (OR = 1.22; CI: 1.14, 1.31, P < .001). In subgroup analysis for finding the possible source of heterogeneity, the continent, dietary assessment tool, sample size and gender were the potent sources of heterogeneity. No association between PRAL and NEAP with HbA 1 C, HOMA-IR was reported., Conclusions: In the current meta-analysis, we found potent negative effects of high dietary acid load particularly higher PRAL scores cardiometabolic risk factors. Therefore, lower acidogenic food ingredients in the diets are suggested for the prevention of cardiovascular risk factors and diabetes., (© 2019 John Wiley & Sons Ltd.)

Background: Type 2 diabetes is a multifactorial disorder influenced by both genetic and environmental factors and is rising dramatically throughout the world. Recently, consideration to dietary acid-base load has been raised as a nutritional indicator that could have metabolic effects., Objective: The aim of this study was to systematically investigate the associations of dietary acid load indices with glucose/insulin homeostasis and type 2 diabetes in a patent based review., Methods: Systematic literature review was conducted using PubMed, Scopus and Google Scholar, from inception up to 10 January 2018. All human studies publications investigated the association of dietary acid load indices (PRAL or NEAP or Pro:K) and incidence of diabetes or glucose/insulin metabolism were included., Results: In all, 174 studies were included for the title and abstract screening. A total of 164 articles were excluded because they did not meet the inclusion criteria. Finally, 10 articles (five crosssectional studies and five cohort studies) in accordance with our inclusion criteria were chosen for further evaluations that were published between 2008 and 2017., Conclusion: Although there are some evidence of an association between dietary acid load and type 2 diabetes, definitive declarations in this regard will be needed to intervention human studies modifying acid-base dietary intake., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: It has been suggested that the acidity of the diet may be related to increased risk of type 2 diabetes. To investigate this hypothesis, we tested if the acidity of the diet, measured as the Potential Renal Acid Load (PRAL) score, was associated with incident diabetes and diabetes-related intermediary traits., Methods: A total of 54,651 individuals from the Danish Diet, Cancer and Health (DCH) cohort were included in the prospective cox regression analyses of incident diabetes over a 15 years follow-up period. Moreover, 5724 Danish individuals with baseline data from the Inter99 cohort were included in the cross sectional, multivariate and logistic regression analyses of measures of insulin sensitivity, insulin release and glucose tolerance status derived from an oral glucose tolerance test (OGTT)., Results: In the DCH cohort a trend analysis showed that quintiles of PRAL score were, after multifactorial adjustment, associated with a higher incidence of diabetes (p trend  = 6 × 10 - 7 ). HR for incident diabetes was 1.24 (1.14; 1.35) (p = 7 × 10 - 7 ) between first and fifth PRAL score quintile. In Inter99 higher PRAL score associated with insulin resistance as estimated by lower BIGTT-Si (an OGTT-derived index of insulin sensitivity) (p = 4 × 10 - 7 ) and Matsuda index of insulin sensitivity (p = 2 × 10 - 5 ) as well as higher HOMA-IR (p = 0.001). No association was observed for measures of insulin release, but higher PRAL score was associated with lower OGTT-based disposition index., Conclusions: A high dietary acidity load is associated with a higher risk of diabetes among middle-aged Danes. Although adjustment for BMI attenuated the effect sizes the association remained significant. The increased risk of diabetes may be related to our finding that a high dietary acidity load associates with impaired insulin sensitivity.

Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets results in the over-production of metabolic acids which has been associated with the development of chronic metabolic disturbances. Mild metabolic acidosis has been shown to impair peripheral insulin action and several epidemiological findings suggest that metabolic acid load markers are associated with insulin resistance and impaired glycemic control through an interference intracellular insulin signaling pathways and translocation. In addition, higher incidence of diabetes, insulin resistance, or impaired glucose control have been found in subjects with elevated metabolic acid load markers. Hence, lowering dietary acid load may be relevant for improving glucose homeostasis and prevention of type 2 diabetes development on a long-term basis. However, limitations related to patient acid load estimation, nutritional determinants, and metabolic status considerably flaws available findings, and the lack of solid data on the background physiopathology contributes to the questionability of results. Furthermore, evidence from interventional studies is very limited and the trials carried out report no beneficial results following alkali supplementation. Available literature suggests that poor acid load control may contribute to impaired insulin sensitivity and glucose homeostasis, but it is not sufficiently supportive to fully elucidate the issue and additional well-designed studies are clearly needed., Competing Interests: The authors declare no conflict of interest.

Background & Aim: Western diets rich in animal protein and poor in fruit and vegetables increase the body acid load, a predictor of type 2 diabetes risk. The relationships between dietary acid load, mild metabolic acidosis and insulin resistance remain unclear. The objective of this study was to assess the association between dietary acid load, body acid/base markers and peripheral insulin resistance at baseline and following a short-term overfeeding intervention in healthy individuals., Methods: In a cross-sectional study of 104 men and women, insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp. Plasma lactate, a marker of metabolic acidosis, was assessed and acid load scores (potential renal acid load, PRAL and net endogenous acid production, NEAP) derived from diet diaries. The cohort was grouped into lean and overweight/obese and the latter further classified as insulin-sensitive (Obsen) and insulin-resistant (Obres) based on hyperinsulinemic-euglycemic clamp glucose infusion rate (GIR, top tertile vs. bottom 2 tertiles). A subset of 40 individuals participated in an overfeeding intervention (+1250 kcal/day) for 28 days and studies repeated., Results: Obsen and Obres were matched for adiposity (BMI and fat mass, both P = 1). Fasting plasma lactate was higher in Obres (0.78 [0.63-1.14] mmol/L) compared with both lean (0.71 [0.44-0.90] mmol/L, P = 0.02) and Obsen (0.67 [0.56-0.79] mmol/L, P = 0.04) and not different between lean and Obsen (P = 0.9). Overfeeding was characterized by an increase in dietary acid load scores PRAL (P = 0.003) and NEAP (P = 0.05), a reduction in GIR necessary to maintain euglycemia (P = 0.03) and an increase in fasting plasma lactate (P = 0.02). The change in lactate was inversely associated with the change in GIR (r = -0.36, P = 0.03)., Conclusions: Mild metabolic acidosis, measured by plasma lactate, aligns with insulin resistance independent of obesity and is induced by short-term increases in energy and dietary acid load in healthy humans. Further studies are required to determine whether buffering mild metabolic acidosis improves insulin resistance and reduces diabetes risk., (Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Type 2 diabetes is increasingly being recognised as a global health crisis (World Health Organisation). Insulin resistance is closely associated with obesity and precedes the development of type 2 diabetes. However, there is now increasing evidence to suggest that diet itself may independently be associated with type 2 diabetes risk. A diet with a high acid load (or high potential renal net acid load, PRAL) can result in a decrease in pH towards the lower end of the normal physiological range, which may in turn lead to the development of insulin resistance. Conversely, reducing dietary acid load (the so called 'alkaline diet') may be protective and prevent the onset of type 2 diabetes. Here, we explore the influence of dietary acid load on the development of mild metabolic acidosis and induction of insulin resistance. Whilst large prospective cohort studies link high dietary acid load or low serum bicarbonate with the development of type 2 diabetes, the effect of a diet with a low acid (or high alkaline) load remains unclear. Further interventional studies are required to investigate the influence of dietary composition on the body's acid/base balance, insulin resistance and incidence of type 2 diabetes., (Copyright © 2015 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.)

Background & Aims: Acid-base imbalance has been suggested to play an important role in certain cardio-metabolic abnormalities, including type 2 diabetes; however, epidemiological evidence linking dietary acid load to glucose metabolism is lacking. We examined the association of dietary acid load with markers of insulin resistance (IR), insulin secretion, and blood glucose status among Japanese workers., Methods: The study subjects were 1732 workers, aged 19-69 years, who completed a health survey at a periodic checkup. Dietary intake was assessed using a validated brief diet history questionnaire. Potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores were derived from nutrient intake. A multilevel linear regression model was used to estimate the means of fasting insulin, fasting plasma glucose, homeostatic model assessment of IR (HOMA-IR) score, homeostatic model assessment of β-cell function (HOMA-β) score and glycated hemoglobin (HbA1c) level with adjustment for potential confounding variables., Results: PRAL was positively associated with HOMA-IR score (Ptrend = 0.045); the multivariable-adjusted means (95% confidence intervals) for the HOMA-IR scores for the lowest through the highest quartiles of PRAL were 0.88 (0.82-0.94), 0.92 (0.86-0.98), 0.92 (0.86-0.98), and 0.94 (0.88-1.01). A similar association was observed between NEAP and HOMA-IR scores (Ptrend = 0.03). In the stratified analyses, these positive associations were confined to subjects with lower BMIs (<23 kg/m(2)) (Ptrend = 0.03 and 0.01 for PRAL and NEAP, respectively). NEAP score was positively associated with HOMA-β score (Ptrend = 0.03). Dietary acid load score was not appreciably associated with fasting glucose or HbA1c levels., Conclusions: The present findings suggest that high dietary acid load is associated with IR among apparently healthy adults., (Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Diet affects the body’s acid-base balance by providing acid or alkali precursors in the metabolism. The importance of the acid-base balance of the diet for cardiovascular diseases, which have become the most important cause of morbidity on the global scale, has started to take its place in the literature. The prediction of endogenous acid production in dietary acid-base balance is expressed as dietary acid load. Although the available information about the effect of dietary acid load on cardiovascular diseases is limited, possible mechanisms are indicated as excessive calcium and magnesium excretion from the kidneys, reduced urinary citrate excretion, and excessive cortisol production. Metabolic acidosis has an important role in the development of cardiometabolic abnormalities, especially insulin resistance. Studies examining the relationship between dietary acid load and cardiovascular disease are limited and there is an inconsistency between studies. Practices for determining risk factors for cardiovascular diseases and preventing their effects are very important for the protection and improvement of health. Considering dietary acid load when planning a diet for individuals with cardiovascular diseases can help increase the effectiveness of the diet. The purpose of this review is to examine the effect of dietary acid load on cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Metabolic effects of high diet acid load (DAL) have been studied for years in adults, although only recently in children. Contemporary diets, especially those of Western societies, owe their acidogenic effect to high animal-origin protein content and low contribution of base-forming elements, such as fruits and vegetables. This imbalance, where dietary acid precursors exceed the body’s buffering capacity, results in an acid-retaining state known by terms such as “eubicarbonatemic metabolic acidosis,” “low-grade metabolic acidosis,” “subclinical acidosis,” or “acid stress”. Its consequences have been linked to chronic systemic inflammation, contributing to various noncommunicable diseases traditionally considered more common in adulthood, but now have been recognized to originate at much earlier ages. In children, effects of high DAL are not limited to growth impairment caused by alterations of bone and muscle metabolism, but also represent a risk factor for conditions such as obesity, insulin resistance, diabetes, hypertension, urolithiasis, and chronic kidney disease (CKD). The possibility that high DAL may be a cause of chronic acid-retaining states in children with growth impairment should alert pediatricians and pediatric nephrologists, since its causes have been attributed traditionally to inborn errors of metabolism and renal pathologies such as CKD and renal tubular acidosis. The interplay between DAL, overall diet quality, and its cascading effects on children’s health necessitates comprehensive nutritional assessments and interventions. This narrative review explores the clinical relevance of diet-induced acid retention in children and highlights the potential for prevention through dietary modifications, particularly by increasing fruit and vegetable intake alongside appropriate protein consumption.A higher resolution version of the Graphical abstract is available as Supplementary informationA higher resolution version of the Graphical abstract is available as Supplementary informationGraphical abstract: Metabolic effects of high diet acid load (DAL) have been studied for years in adults, although only recently in children. Contemporary diets, especially those of Western societies, owe their acidogenic effect to high animal-origin protein content and low contribution of base-forming elements, such as fruits and vegetables. This imbalance, where dietary acid precursors exceed the body’s buffering capacity, results in an acid-retaining state known by terms such as “eubicarbonatemic metabolic acidosis,” “low-grade metabolic acidosis,” “subclinical acidosis,” or “acid stress”. Its consequences have been linked to chronic systemic inflammation, contributing to various noncommunicable diseases traditionally considered more common in adulthood, but now have been recognized to originate at much earlier ages. In children, effects of high DAL are not limited to growth impairment caused by alterations of bone and muscle metabolism, but also represent a risk factor for conditions such as obesity, insulin resistance, diabetes, hypertension, urolithiasis, and chronic kidney disease (CKD). The possibility that high DAL may be a cause of chronic acid-retaining states in children with growth impairment should alert pediatricians and pediatric nephrologists, since its causes have been attributed traditionally to inborn errors of metabolism and renal pathologies such as CKD and renal tubular acidosis. The interplay between DAL, overall diet quality, and its cascading effects on children’s health necessitates comprehensive nutritional assessments and interventions. This narrative review explores the clinical relevance of diet-induced acid retention in children and highlights the potential for prevention through dietary modifications, particularly by increasing fruit and vegetable intake alongside appropriate protein consumption.A higher resolution version of the Graphical abstract is available as Supplementary informationA higher resolution version of the Graphical abstract is available as Supplementary information [ABSTRACT FROM AUTHOR]

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Abstract Background Acid-base homeostasis is increasingly being recognized to play an important role in normal metabolic function. However, prospective studies on the relationship between diet-induced acid-base imbalance and insulin resistance among Asian populations have been limited. Thus, we investigated whether diet-induced metabolic acidosis was prospectively associated with insulin resistance risk in middle-aged and older Korean adults. Methods In total, 5406 participants from the Korean Genome and Epidemiology Study without type 2 diabetes, insulin resistance, cancer, or renal diseases at baseline examination were included in this study. To estimate diet-induced metabolic acidosis, we used potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores calculated from the usual dietary intake assessed by a validated 103-item food frequency questionnaire at baseline. Multivariable Cox proportional hazard models were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of insulin resistance incidence. Results During a mean follow-up period of 7.4 years, we documented 3449 insulin resistance cases. In the fully adjusted model, the future insulin resistance risk was significantly higher among participants in the highest quartiles of PRAL (HR: 1.30, 95% CI: 1.13–1.48, P trend = 0.0002) and NEAP (HR: 1.30, 95% CI: 1.14–1.49, P trend = 0.0008) than among those in the lowest quartiles. Associations were slightly strengthened among men, adults

Abstract Background It has been suggested that the acidity of the diet may be related to increased risk of type 2 diabetes. To investigate this hypothesis, we tested if the acidity of the diet, measured as the Potential Renal Acid Load (PRAL) score, was associated with incident diabetes and diabetes-related intermediary traits. Methods A total of 54,651 individuals from the Danish Diet, Cancer and Health (DCH) cohort were included in the prospective cox regression analyses of incident diabetes over a 15 years follow-up period. Moreover, 5724 Danish individuals with baseline data from the Inter99 cohort were included in the cross sectional, multivariate and logistic regression analyses of measures of insulin sensitivity, insulin release and glucose tolerance status derived from an oral glucose tolerance test (OGTT). Results In the DCH cohort a trend analysis showed that quintiles of PRAL score were, after multifactorial adjustment, associated with a higher incidence of diabetes (p trend = 6 × 10− 7). HR for incident diabetes was 1.24 (1.14; 1.35) (p = 7 × 10− 7) between first and fifth PRAL score quintile. In Inter99 higher PRAL score associated with insulin resistance as estimated by lower BIGTT-Si (an OGTT-derived index of insulin sensitivity) (p = 4 × 10− 7) and Matsuda index of insulin sensitivity (p = 2 × 10− 5) as well as higher HOMA-IR (p = 0.001). No association was observed for measures of insulin release, but higher PRAL score was associated with lower OGTT-based disposition index. Conclusions A high dietary acidity load is associated with a higher risk of diabetes among middle-aged Danes. Although adjustment for BMI attenuated the effect sizes the association remained significant. The increased risk of diabetes may be related to our finding that a high dietary acidity load associates with impaired insulin sensitivity.

The Western, diet rich in acidogenic foods (e.g., meat, fish and cheese) and low in alkaline foods (e.g., vegetables, fruits and legumes), is deemed to be a cause of endogenous acid production and elevated dietary acid load (DAL), which is a potential cause of metabolic acidosis. Multiple authors have suggested that such a dietary pattern increases the excretion of calcium and magnesium, as well as cortisol secretion. In addition, it is associated with decreased citrate excretion. All of these seem to increase blood pressure and insulin resistance and may contribute to the development of cardiometabolic disorders. However, there are inconsistencies in the results of the studies conducted. Therefore, this narrative literature review aims to present the outcomes of studies performed in recent years that investigated the association between DAL and the following cardiometabolic risk factors: blood pressure, hypertension, carbohydrate metabolism and lipid profile. Study outcomes are divided into (i) statistically significant positive association, (ii) statistically significant inverse association, and (iii) no statistically significant association.

Aims/hypothesis: Studies suggest a potential link between low-grade metabolic acidosis and type 2 diabetes. A western dietary pattern increases daily acid load but the association between diet-dependent acid load and type 2 diabetes is still unclear. This study aimed to assess whether diet-dependent acid load is associated with the risk of type 2 diabetes. Methods: We examined the association between energy-adjusted net endogenous acid production (NEAP), potential renal acid load (PRAL) and animal protein-to-potassium ratio (A:P) on incident type 2 diabetes in 67,433 women from the Nurses' Health Study, 84,310 women from the Nurses' Health Study II and 35,743 men from the Health Professionals' Follow-up Study who were free from type 2 diabetes, cardiovascular disease and cancer at baseline. Study-specific HRs were estimated using Cox proportional hazards models with time-varying covariates and were pooled using a random effects meta-analysis. Results: We documented 15,305 cases of type 2 diabetes during 4,025,131 person-years of follow-up. After adjustment for diabetes risk factors, dietary NEAP, PRAL and A:P were positively associated with type 2 diabetes (pooled HR [95% CI] for highest (Q5) vs lowest quintile (Q1): 1.29 [1.22, 1.37], p <0.0001; 1.29 [1.22, 1.36], p <0.0001 and 1.32 [1.24, 1.40], p <0.0001 for NEAP, PRAL and A:P, respectively). These results were not fully explained by other dietary factors including glycaemic load and dietary quality (HR [95% CI] for Q5 vs Q1: 1.21 [1.09, 1.33], p <0.0001; 1.19 [1.08, 1.30] and 1.26 [1.17, 1.36], p <0.0001 for NEAP, PRAL and A:P, respectively). Conclusions/interpretation: This study suggests that higher diet-dependent acid load is associated with an increased risk of type 2 diabetes. This association is not fully explained by diabetes risk factors and overall diet quality. [ABSTRACT FROM AUTHOR]

Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets results in the over-production of metabolic acids which has been associated with the development of chronic metabolic disturbances. Mild metabolic acidosis has been shown to impair peripheral insulin action and several epidemiological findings suggest that metabolic acid load markers are associated with insulin resistance and impaired glycemic control through an interference intracellular insulin signaling pathways and translocation. In addition, higher incidence of diabetes, insulin resistance, or impaired glucose control have been found in subjects with elevated metabolic acid load markers. Hence, lowering dietary acid load may be relevant for improving glucose homeostasis and prevention of type 2 diabetes development on a long-term basis. However, limitations related to patient acid load estimation, nutritional determinants, and metabolic status considerably flaws available findings, and the lack of solid data on the background physiopathology contributes to the questionability of results. Furthermore, evidence from interventional studies is very limited and the trials carried out report no beneficial results following alkali supplementation. Available literature suggests that poor acid load control may contribute to impaired insulin sensitivity and glucose homeostasis, but it is not sufficiently supportive to fully elucidate the issue and additional well-designed studies are clearly needed.

Aims/hypothesis: We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods: An observational survey with prospective follow-up including 911 non-diabetic Swedish men aged 70-71 years was carried out. The gold standard euglycaemic-hyperinsulinaemic clamp technique and the OGTT were used to determine insulin sensitivity and beta cell function, respectively. Diabetes incidence was assessed during 18 years of follow-up. Renal function was estimated from serum cystatin C concentrations. Dietary acid load was calculated as potential renal acid load (PRAL) and net endogenous acid production (NEAP) algorithms from 7 day food records. Adequate dietary reporters were identified by Goldberg cut-offs. Results: PRAL and NEAP were not associated with insulin sensitivity or beta cell function. Underlying kidney function or consideration of dietary adequate reporters did not modify these null findings. During follow-up, 115 new cases of diabetes were validated. Neither PRAL nor NEAP was associated with diabetes incidence. Conclusions/interpretation: Our results do not support the hypothesis that dietary acid load influences insulin sensitivity, beta cell function or diabetes risk. Interventional studies modifying acid-base dietary intake are needed to further elucidate a possible role of acid load in the development of type 2 diabetes. [ABSTRACT FROM AUTHOR]

The Western, diet rich in acidogenic foods (e.g., meat, fish and cheese) and low in alkaline foods (e.g., vegetables, fruits and legumes), is deemed to be a cause of endogenous acid production and elevated dietary acid load (DAL), which is a potential cause of metabolic acidosis. Multiple authors have suggested that such a dietary pattern increases the excretion of calcium and magnesium, as well as cortisol secretion. In addition, it is associated with decreased citrate excretion. All of these seem to increase blood pressure and insulin resistance and may contribute to the development of cardiometabolic disorders. However, there are inconsistencies in the results of the studies conducted. Therefore, this narrative literature review aims to present the outcomes of studies performed in recent years that investigated the association between DAL and the following cardiometabolic risk factors: blood pressure, hypertension, carbohydrate metabolism and lipid profile. Study outcomes are divided into (i) statistically significant positive association, (ii) statistically significant inverse association, and (iii) no statistically significant association. [ABSTRACT FROM AUTHOR]

Aims/hypothesis Studies suggest a potential link between low-grade metabolic acidosis and type 2 diabetes. A western dietary pattern increases daily acid load but the association between diet-dependent acid load and type 2 diabetes is still unclear. This study aimed to assess whether diet-dependent acid load is associated with the risk of type 2 diabetes. Methods: We examined the association between energy-adjusted net endogenous acid production (NEAP), potential renal acid load (PRAL) and animal protein-to-potassium ratio (A:P) on incident type 2 diabetes in 67,433 women from the Nurses’ Health Study, 84,310 women from the Nurses’ Health Study II and 35,743 men from the Health Professionals’ Follow-up Study who were free from type 2 diabetes, cardiovascular disease and cancer at baseline. Study-specific HRs were estimated using Cox proportional hazards models with time-varying covariates and were pooled using a random effects meta-analysis. Results: We documented 15,305 cases of type 2 diabetes during 4,025,131 person-years of follow-up. After adjustment for diabetes risk factors, dietary NEAP, PRAL and A:P were positively associated with type 2 diabetes (pooled HR [95% CI] for highest (Q5) vs lowest quintile (Q1): 1.29 [1.22, 1.37], ptrend <0.0001; 1.29 [1.22, 1.36], ptrend <0.0001 and 1.32 [1.24, 1.40], ptrend <0.0001 for NEAP, PRAL and A:P, respectively). These results were not fully explained by other dietary factors including glycaemic load and dietary quality (HR [95% CI] for Q5 vs Q1: 1.21 [1.09, 1.33], ptrend <0.0001; 1.19 [1.08, 1.30] and 1.26 [1.17, 1.36], ptrend <0.0001 for NEAP, PRAL and A:P, respectively). Conclusions/interpretation This study suggests that higher diet-dependent acid load is associated with an increased risk of type 2 diabetes. This association is not fully explained by diabetes risk factors and overall diet quality.