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The normal function of nearly all physiological processes in the body depends on maintaining the appropriate acid-base balance. The value of intracellular pH and interstitial pH strongly depends on the value of arterial blood pH, which ranges between 7.35 and 7.45 under normal physiological conditions. Diet is a major determinant of the acid load that must be excreted by the kidney to maintain acid-base balance.

Natural selection has had little evolutionary time to eliminate the maladaptations that are a consequence of the profound transformation of the human diet resulting from the inventions of agriculture and animal husbandry. When it comes to the pH and acid load in the human diet, the significant change from the hunter-gatherer civilization to now brought on by the agricultural revolution and later industrialization affected our diet in a multitude of ways such as a decrease in potassium compared to sodium, an increase in chloride compared to bicarbonate, the ratio of potassium to sodium has reversed, lowered magnesium, potassium and fiber. Modern diets are rich in saturated fat, processed foods, sodium, and phosphorus and may induce metabolic acidosis as they are not compatible with our genetically determined nutritional requirements. Faced with this constant barrage of acid our kidneys’ ability to regulate acid-base balance becomes weaker as we age. A low -low-carbohydrate high -high-protein diet with a high acid load will result in very little change in blood chemistry and pH but will result in many changes in urinary chemistry with uric acid, urinary calcium, and phosphate elevating which will increase chances for kidney stones. When we age we gradually lose the renal acid-base regulatory function and the diet-induced metabolic acidosis increases when consuming a modern diet. A low-carbohydrate high-protein diet with its increased acid load results in very little change in blood chemistry, and pH, but results in many changes in urinary chemistry. Urinary magnesium levels, urinary citrate, and pH are decreased, and urinary calcium, undissociated uric acid, and phosphate are increased. All of these burden on kidneys.u

The dietary acid load is determined ty by the balance of acid-inducing foods, such as meats, fish, eggs, cheese, and grains, and base-inducing foods, such as fruits and vegetables.

hjkhkThe modern Western-type diet is deficient in fruits and vegetables and contains excessive animal productswhich results in a net acid load to the body. To prevent accumulation of acid in the body and an increased degree of metabolic acidosis, the body has multiple systems to buffer acid including the red blood cells, muscle cells, and bone, which contains large quantities of alkaline salts of calcium. Both in vitro and in vivo studies in animals and humans suggest that bone base helps neutralize part of the dietary net acid load.

Thus, Metabolic acidosis may be exacerbated by a contemporary Western diet, which delivers a high nonvolatile acid load. The remaining acid is neutralized or stored within the body. Bone and muscle are lost to neutralize the acid as serum bicarbonate falls. Early studies suggest that lowering the dietary acid load with a reduced protein content and an increase in fruits and vegetables intake can improve the metabolic parameters of acidosis, preserve bone and muscle, and slow the glomerular filtration rate decline of the kidney. PMID: 23439373

Acidic diet and type 2diabetes

Diet-induced metabolic acidosis is a risk factor for type 2 diabetes because even a slight reduction in extracellular pH decreases the beta cell response and leads to a disruption of insulin binding to its receptor; this may lead to insulin resistance. A high dietary acidity load was associated with a higher risk of diabetes among middle-aged Danes. The increased risk of diabetes in the studies

 finding that a high dietary acidity load associates with impaired insulin sensitivity. Meanwhile fruit and vegetable consumption are associated with lower blood sugar levels, greater insulin sensitivity, and a reduced risk of type 2 diabetesPMCID: PMC6173920 Meat and fish have sulphur-containing amino acids (e.g. methionine and cysteine) which are important determinants of dietary acid load due to sulfate generation after their oxidation. Indeed, several studies have shown that the positive association between protein intake and type 2 diabetes is mainly driven by animal protein intake .PMCID: PMC5831375

The excessive release of acids into the bloodstream may also predispose to various metabolic imbalances, such as increased mineral excretion, aforementioned insulin resistance, and the stimulation of glucocorticoid hormone release. PMID: 33292308

The nutrients that release acid precursors into the bloodstream are phosphorus and proteins.

To estimate the potential acid load produced by a single food or overall diet, two measurements are used; one is potential renal acid load -PRAL and the second one is net endogenous acid production -NEAP.  Higher scores indicate diets that are acid forming.

Muscle Wasting

Evidence has shown that mild metabolic acidosis induced by an acidogenic diet led to loss of muscle tissue. Muscle wasting appears to be an adaptive response to acidosis. The acid load from diets that are rich in acid–producing protein and cereal grains relative to their content of  alkali–producing fruit and vegetables may contribute to a reduction in lean tissue mass in older adults. PMID: 1832660

Previously, the correlation between diet-acid load and metabolic disease was stronger in non-obese individuals, suggesting that it is independent of adiposity. PMID: 19667248

A high diet-dependent net acid load is independently associated with a higher risk of incident hypertension.

When examining the association between the diet-dependent net acid load and the risk of incident hypertension among 87 293 women without a history of hypertension in Nurses’ Health Study II, women with the highest acid load had an increased risk of hypertension. In order to test whether the association between acid load and hypertension is independent of its individual components, adjustments were made for intakes of protein and potassium. Results of the ratio of animal protein intake to potassium intake were similar with those of estimated diet-dependent net acid load.

A Korean National Health and Nutrition Examination Survey 2008–2011 results showed that Diet-induced acid load was associated with increased risk of CVD, independent of obesity and insulin resistance.

This population-based study used samples of 11,601 subjects aged 40–79. Individual CVD (cardiovascular disease) risk was evaluated using atherosclerotic cardiovascular disease (ASCVD) risk equations in subjects without prior CVD. Acid–base status was assessed with both the PRAL and the dietary acid load (DAL) scores derived from nutrient intake. Results showed that individuals in the highest PRAL tertile had a significant increase in 10 year ASCVD risks (and tended to belong to the high-risk (10 year risk >10 %) group compared to those in the lowest PRAL tertile. The association between higher PRAL score and high CVD risk was stronger in the middle-aged group. Furthermore, individuals in unhealthy condition with lower PRAL scores had comparable ASCVD risk to people in the higher PRAL group that were in favorable physical condition. In addition, elevated PRAL scores were associated with high ASCVD risk independent of obesity, exercise, and insulin resistance. Similar trends were observed with DAL scores.

When they evaluated the PRAL score and the risk according to BMI as well as insulin resistance/ insulin sensitive groups more substantial correlations were observed in lean individuals and in the insulin sensitive group. Moreover, there was no significant difference in risk of ASCVD between lean subjects with higher PRAL scores and those in the overweight group in the lowest PRAL tertile, suggesting that CVD risk of lean individuals would increase if diet-induced acid loads were elevated. In addition, if sedentary individuals lowered their intake of dietary acid, they might exhibit comparable CVD risks with people who regularly exercised. While obesity and exercise are major contributing factors to CVD risk, diet-induced acid load might modify these effects.

Moreover, the association between diet-induced acid load and CVD risk with respect to muscle mass seems compelling. There has been some evidence that sarcopenia could influence CVD, such as increased arterial stiffness and inflammatory markers in people with sarcopenia (muscle loss). PMID: 27565571

Long-term dietary potential renal acid load during adolescence and the likelihood of nonalcoholic fatty liver disease in young women.  

the findings suggest that higher dietary acidity in adolescence may be associated with lipid accumulation in the liver for females. PMID: 22223573

the detrimental effects of ‘acid’ from the diet on bone mineral have been demonstrated. The use of our skeleton as a source of ‘buffer’ which contributes to both the preservation of the body's pH and defense of the system against acid–base disorders has been proposed and studied over the last few decades.

References

Dawson-Hughes B, Harris SS, Ceglia L. Alkaline diets favor lean tissue mass in older adults. Am J Clin Nutr. 2008 Mar;87(3):662-5. doi: 10.1093/ajcn/87.3.662. PMID: 1832660

Frassetto, L., Banerjee, T., Powe, N., & Sebastian, A. (2018). Acid Balance, Dietary Acid Load, and Bone Effects-A Controversial Subject. Nutrients, 10(4), 517. https://doi.org/10.3390/nu10040517 PMID: 29690515

Han, E., Kim, G., Hong, N., Lee, Y. H., Kim, D. W., Shin, H. J., Lee, B. W., Kang, E. S., Lee, I. K., & Cha, B. S. (2016). Association between dietary acid load and the risk of cardiovascular disease: nationwide surveys (KNHANES 2008-2011). Cardiovascular diabetology, 15(1), 122. https://doi.org/10.1186/s12933-016-0436-zPMID: 27565571

New S. A. (2003). Intake of fruit and vegetables: implications for bone health. The Proceedings of the Nutrition Society, 62(4), 889–899. https://doi.org/10.1079/PNS2003310 PMID: 15018489

Krupp, D., Johner, S. A., Kalhoff, H., Buyken, A. E., & Remer, T. (2012). Long-term dietary potential renal acid load during adolescence is prospectively associated with indices of nonalcoholic fatty liver disease in young women. The Journal of nutrition, 142(2), 313–319. https://doi.org/10.3945/jn.111.150540 PMID: 22223573

Schwalfenberg G. K. (2012). The alkaline diet: is there evidence that an alkaline pH diet benefits health?. Journal of environmental and public health, 2012, 727630. https://doi.org/10.1155/2012/727630PMID: 22013455

Scialla, J. J., & Anderson, C. A. (2013). Dietary acid load: a novel nutritional target in chronic kidney disease?. Advances in chronic kidney disease, 20(2), 141–149. https://doi.org/10.1053/j.ackd.2012.11.001PMID: 23439373

Sebastian, A., Frassetto, L. A., Sellmeyer, D. E., Merriam, R. L., & Morris, R. C., Jr (2002). Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. The American journal of clinical nutrition, 76(6), 1308–1316. https://doi.org/10.1093/ajcn/76.6.1308 PMID: 12450898

Gæde, J., Nielsen, T., Madsen, M. L., Toft, U., Jørgensen, T., Overvad, K., Tjønneland, A., Hansen, T., Allin, K. H., & Pedersen, O. (2018). Population-based studies of relationships between dietary acidity load, insulin resistance and incident diabetes in Danes. Nutrition journal, 17(1), 91. https://doi.org/10.1186/s12937-018-0395-1 PMCID: PMC6173920

Kiefte-de Jong JC, Li Y, Chen M, Curhan GC, Mattei J, Malik VS, Forman JP, Franco OH, Hu FB. Diet-dependent acid load and type 2 diabetes: pooled results from three prospective cohort studies. Diabetologia. 2017 Feb;60(2):270-279. doi: 10.1007/s00125-016-4153-7. Epub 2016 Nov 17. PMCID: PMC5831375 

Zhang, L., Curhan, G. C., & Forman, J. P. (2009). Diet-dependent net acid load and risk of incident hypertension in United States women. Hypertension (Dallas, Tex. : 1979), 54(4), 751–755. https://doi.org/10.1161/HYPERTENSIONAHA.109.135582 PMID: 19667248