Connection of Diet, Urine pH, and Diseases
A urine pH is an indicator of your overall health and well-being. It gives insights into important clues as to what’s going on in your body. According to the American Association for Clinical Chemistry, our normal urine pH ranges between 4.5 and 8. The higher the number, the more alkaline your pH is. The lower the number, the more acidic your pH is.
Numerous factors can disturb the urine pH level including diet, some medications, certain health conditions, and environmental toxins.
Excessive acid in the body fluids can result in metabolic acidosis. The abundance of acid in the body occurs when kidneys are unable to remove extra acid or when too much acid is produced in the body, stimulated by a number of reasons-primarily your food choices.
There are several types of metabolic acidosis like diabetic acidosis, hyperchloremic acidosis, Lactic acidosis, and diet-induced acidosis.
Some lifestyle choices and health issues can cause your blood pH to shift dramatically and lead to alkalosis. An imbalance in bicarbonates, kidney stones, eating disorders, Proteus urinary tract infection, and dehydration are some of the reasons for alkalosis.
Diet-induced metabolic acidosis.
Excessive intake of acidic food can induce acidosis. In fact, if you are experiencing some other kind of acidosis then the situation can worsen by consuming high acid diet. Some foods are acidic due to the high level of amino acids that contain sulfur which is present in eggs, meat, and dairy products. In addition, salt can also make it hard for kidneys to remove extra acid. Other than that, grains, sugar, excessive caffeine, processed foods, sodas, and other sweetened beverages are suggested to avoid metabolic acidosis.
People prefer a modern diet lacking in vegetables and fruits and rich in excessive animal products. These animal products generate an accumulation of non-metabolized anions and trigger the state of overlooked metabolic acidosis, whose tendency increases with aging because of physiological decline in kidney function. In response to diet-derived metabolic acidosis, kidneys implement the compensating mechanism to restore the acid-base balance, such as conservation of citrate, removal of piled-up anions, spur in kidney ammonia genesis, and excretion of ammonium ions through urine.
These processes lower the urine pH and change its composition including hypocitraturia, hypercalciuria, excessive nitrogen, and phosphate excretion. Low urine pH can increase the chances of uric acid stone formation. Similarly, hypocitraturia and hypercalciuria are risk factors for calcium stone formation in kidneys. The high dietary acid load can cause diabetes, hypertension, and cardiovascular diseases.
A kidney patient is advised to avoid acidic foods because metabolic acidosis can make them more prone to osteoporosis, endocrine disorders, and muscle loss. In kidney patients, parathyroid hormone is produced in large quantities which builds too much phosphate in the body. Now to cover the excessive phosphate, their body binds it to calcium that no longer remains available for bones and causes the bones to weaken progressively.
Environmental toxins and kidney-metabolic diseases.
There is a strong connection between environmental toxins and metabolic diseases such as chronic kidney failure, respiratory diseases, cancer, and heart diseases. But being responsible for waste management and homeostasis, our kidneys are the primary target of these hazards and thus are highly vulnerable to the harmful effects of the toxins. We can get exposed to these environmental toxins, unintentionally through oral, inhalational, or transdermal routes.
The greatest vulnerability of kidneys can be due to their certain physiological features such as highest blood flow per 100g tissues, highly active enzymatic metabolizing system, largest endothelial surface by weight, high concentration of filtered chemicals in tubular fluids adjacent to tubular cells, protein unbinding of chemical compounds in tubules and intrarenal biotransformation of chemicals.
The quicker progression of chronic kidney diseases to dialysis induced by renal toxicity has two major mechanisms backing up the damage. First is proximal tubular cells damage due to excessive uptake of toxins by the cells. It occurs through both apical and basolateral transport systems. Second is, there can be extensive tubular crystal formation due to the kidney’s concentrating ability.
Aristolochic acid, melamine, and heavy metals are different types of toxins contributing to kidney failure. Out of these, heavy metals such as cadmium, lead, zinc, and Mercury are widespread occupational and environmental chemical risks.
The study of St. Louis VA Medical Centre found that, for every increase in pollution of 10 microorganisms per cubic meter of air, there was a 25 to 37% increase in veterans with new kidney diseases, 36% increase in rapid kidney function loss, and a 31% increase in the risk of kidney failure followed by dialysis. This data was compiled in 8.5 years of careful study on around 2.5 million veterans’ cases with zero renal or any metabolic disease, initially.
These environmental toxins act as fuel on the fire when a person is already suffering from metabolic acidosis. Mycotoxins are a diverse group of chemicals produced by fungi and are the most notorious fungal toxins of modern times. One of the common types is aflatoxins which not only produce acute toxic syndromes but also are carcinogenic. Some other fungal metabolites are nephrotoxic like cytotoxin. They inhibit, damage, or destroy the cells of the kidneys due to which kidney function deteriorates rapidly.
Metal toxicity can occur as a result of air pollution, industry exposure, food, medicines, or drugs. Some heavy metals stay in the blood for almost ninety days. These metals exist in an ionized state in plasma that leads to acute toxicity and abounds. This bound is an inert form of metal when it conjugates with metallothionein and is then delivered to the liver possibly causing the kidney chronic disease.
Glyphosate is a non-selective systemic herbicide and is carcinogenic for humans. Recent medical studies have shown that exposure to low doses of it in roundup can cause organ damage, primarily liver and kidneys.
Microplastics can contaminate our food chain and accumulate in the liver, kidneys, gut, and muscles. Their long-term exposure can damage kidney cells. Polystyrene is a popular plastic used worldwide. It induces renal failure, oxidative stress, and mitochondrial dysfunction.
These toxins can damage the tissue of kidneys because they take time to excrete, and their accumulation exerts pressure on kidney cells. Damaged kidney cells become unable to filter these carcinogenic heavy metals and other toxins, promoting acidic pH.
How to reduce excessive reabsorption due to acidic pH?
One of the major drawbacks of acidic urine is that water-soluble toxic metabolites can be reabsorbed back into the kidneys and blood. Usually, doctors prescribe avoiding acid-inducing diets. However, to prevent the body from the harm of these toxins and optimize the normal body clearance process, renal and hepatic recycling should be reduced to a minimum. Otherwise, excessive reabsorption can lead to serious health conditions such as kidneys dysfunction, cognitive heart diseases, liver failure, etc. Due to the buildup of these toxic heavy metals and the burden of environmental pollutants, the normal excretory process declines in function and structure.
Reduced renal recycling.
Renal recycling can be reduced through excessive ionization. The compounds of urine are dissociated based on their dissociation constant (ka) and urine pH. A small change in urine pH can have a major effect on the reabsorption of a compound because pka is an algorithmic function. So, the more the compounds of urine are ionized, the lesser are the chances of their diffusion by tubules. The compounds that are less prone to ionization are more likely to get reabsorbed. Like xenobiotics conjugated with glycine, taurine, or glutathione in phase 2 of liver pathways. These are weak acids and are hard to ionize which promotes their renal reuptake
On the other hand, alkaline urine enhances waste and toxic removal from the body. The best example is dimercaptosuccinic acid also called DMSA. It has a greater affinity for cadmium than for Lead and Mercury. At acidic urine pH of 5.5, DMSA releases all the cadmium. On the contrary, at basic pH like 7.4, the cadmium remains firmly attached to DMSA. Forced alkalinization facilitates the excretion of fatal poisons like herbicide 2,4-D. It is performed through intravenous administration of sodium bicarbonate.
Excessive eating of whole foods and reducing the intake of proteins that possess sulfur-containing amino acids to promote alkalinization. Some alkalinizing agents such as citrates, low sulfur, and high bicarbonates containing beverages support alkalinization in our body.
Are you ready for your personalized pH Balanced Ketogenic Diet therapy?
American Academy of Family Physicians: "Diabetic Ketoacidosis."
American Diabetes Association: "DKA (Ketoacidosis) & Ketones."
Crinnion, Walter J.; Pizzorno, Joseph E. Clinical Environmental Medicine (Kindle Locations 34626-34627). Elsevier Health Sciences. Kindle Edition.
Gennari, F. Clinical Journal of the American Society of Nephrology, November 2008.
Medscape: "Metabolic Acidosis Clinical Presentation," "Metabolic Acidosis Workup,"
"Metabolic Acidosis: Pathophysiology, Diagnosis and Management: Adverse Effects of Metabolic Acidosis," "Metabolic Acidosis Medication."
National Kidney and Urologic Diseases Information Clearinghouse: "Renal Tubular Acidosis."
Palmer BF. Metabolic acidosis. In: Feehally J, Floege J, Tonelli M, Johnson RJ, eds. Comprehensive Clinical Nephrology. 6th ed. Philadelphia, PA: Elsevier; 2019: chap 12.
Scott & White Healthcare: "Metabolic Acidosis."
Seifter JL. Acid-base disorders. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. Philadelphia, PA: Elsevier; 2020: chap 110.
UCSF School of Medicine: "Metabolic Acidosis -- Anion Gap."