- Diet has a significant impact on citric acid levels:
» Increased acid load due to diets high in animal-based proteins, carbonated drinks, and in severe carbohydrate restriction can lead to mild metabolic acidosis, hypercalciuria, and reduced citric-acid excretion.
» Plant-based diets are associated with increased citric acid. Alkalinization of urine through consumption of citrus foods, alkaline mineral water, fruits and vegetables, or citrate supplements (such as mag-citrate) increase citric acid levels.
- Low urine citric acid has been associated with insulin resistance, metabolic acidosis, bone-density, hypokalemia, the development of kidney stones, kidney disease, and chronic kidney disease, and immune-mediated inflammatory diseases, including rheumatoid arthritis, psoriasis, psoriatic arthritis, systemic lupus erythematosus, Crohn’s disease, and ulcerative colitis.
Low urine citric acid has been associated with insulin resistance, metabolic acidosis, bone-density, hypokalemia, the development of kidney stones, kidney disease, and chronic kidney disease, and immune-mediated inflammatory diseases, including rheumatoid arthritis, psoriasis, psoriatic arthritis, systemic lupus erythematosus, Crohn’s disease, and ulcerative colitis.
Nutritional Considerations: Low levels can be suggestive of insufficiency of one or more of these nutrients: Essential fatty acids, essential amino acids, B1, B2, B3, B6, Lipoic Acid. Secondary considerations as correlates to individual biochemistry, clinical presentation and nutritional needs include glutathione, manganese, l-arginine. Clinical consideration is also to augment the use of citrate chelated minerals, such as calcium citrate, as a non-specific example of such a mineral chelate.
Possible Interfering Factors: Inadequate pyruvate or cis-aconitate levels as precursors.
Clinical Considerations: Low levels of citrate can result in altered levels of other citric acid cycle (CAC) levels (Kreb’s cycle). Looking at precursor metabolites and overall dietary balance to help ensure proper fueling of the CAC pathway is essential. A diet low in either fat, protein or carbohydrate can ultimately lead to overburden and overdependence for substrates to optimally fuel this pivotal step in energy and metabolic biochemistry. If after other changes citrate does not improve glutathione must be considered for testing and support.
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Nutritional Considerations: A high level of citrate often points to insufficient co-factors to ensure proper downstream metabolism of citrate into cis-aconitate. Common nutrients used include: Essential Amino Acids, Aspartate, Arginine, Magnesium, Manganese, Lipoic Acid. When cis-aconitate is also high consider n-acetylcysteine (NAC), Iron, Glutathione (GSH).
Possible Interfering Factors: Poor protein digestion or assimilation or protein insufficient diet. Theoretically high intake of citrate rich supplements (ex. calcium citrate).
Clinical Considerations: May be due to poor protein or carbohydrate metabolism. Also excess citric acid in dietary foods, particularly processed foods and supplements can artificially throw off the balance of this metabolite.
Must also rule out heavy metal toxicity such as arsenic, mercury, cadmium, fluoride, bromide, perchlorate and antimony.
Metabolic acidosis and insufficient antioxidant status can be contributory, along with inadequate pancreatic and/or kidney function.
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1-Methylhistidine, 1-Methylhistidine (Plasma), 2-,3-, and 4-Methylhippuric acid, 2-Methylhippuric Acid, 2-Methylsuccinic Acid, 3,4-Dihydroxyhydrocinnamic Acid, 3,5-Dihydroxybenzoic Acid, 3-Methylhistidine (Plasma), 3-Phenylpropionylglycine, 4-Hydroxybenzoic Acid, 4-Hydroxyphenylacetic Acid, 4-Hydroxyphenylpyruvic Acid, 5-Hydroxyindoleacetic Acid, 8-Hydroxy-2'-deoxyguanosine, a-Hydroxybutyric Acid, a-Keto-b-methylvaleric Acid, a-Ketobutyric Acid, a-Ketoglutaric Acid, a-Ketoisocaproic Acid, a-Ketoisovaleric Acid, a-Aminoadipic Acid (Plasma), Adipic Acid, Alanine, Alanine (Plasma), Aldosterone, Anserine (Plasma), Anthranilic Acid, Arabinitol, Arginine (Plasma), Arginosuccinic Acid, Arginosuccinic Acid (Plasma), Asparagine (Plasma), Aspartic Acid (Plasma), b-Hydroxybutyric Acid, b-Hydroxyisovaleric Acid, b-Alanine (Plasma), Benzoic Acid, Benzoylform, Branched Chain Alpha-Keto Organic Acids, Carnosine, Carnosine (Plasma), cis-Aconitic Acid, Citric Acid, Citrulline (Plasma), Cortisol, Cortisone, Creatinine, Cystathionine (Plasma), Cystine (Plasma), D-Lactic Acid, Equol, Ethanolamine (Plasma), Ethylmalonic Acid, Formiminoglutamic Acid, Fructose, Fumaric Acid, g-Aminobutyric Acid (Plasma), Glucaric Acid, Glucose, Glutamic Acid (Plasma), Glutamine (Plasma), Glutamine / Glutamate Ratio (Plasma), Glutaric Acid, Glycine (Plasma), Glycylproline (Plasma), Hexanoylglycine, Hippuric Acid, Histidine (Plasma), Homocitrulline (Plasma), Homocystine (Plasma), Homogentisic Acid, Homovanillic Acid, Hydroxykynurenine, Hydroxyproline, Hydroxyproline (Plasma), Indoleacetic Acid, Isocitric Acid, Isoleucine/allo-Isoleucine (Plasma), KT Ratio, KT Ratio (Plasma), Kynurenic Acid, Kynurenine, Kynurenine (Plasma), Lactic Acid, Leucine (Plasma), Lysine (Plasma), Malic Acid, Mandelic Acid, Methionine (Plasma), Methylmalonic Acid, Microalbumin, Ornithine, Ornithine (Plasma), Orotic Acid, Oxalic Acid, pH, Phenylacetic Acid, Phenylalanine (Plasma), Phosphate, Phosphoethanolamine (Plasma), Picolinic Acid, Pimelic Acid, Proline (Plasma), Pyridoxic Acid, Pyroglutamic Acid, Pyruvic Acid, Quercetin, Quinolinic Acid, Sarcosine (Plasma), Sebacic Acid, Serine (Plasma), Suberic Acid, Suberylglycine, Succinic Acid, Sulfocysteine (Plasma), Tartaric Acid, Taurine (Plasma), Threonine (Plasma), Total Branched Chain Amino Acids (Plasma), Tryptophan, Tryptophan (Plasma), Tyrosine, Tyrosine (Plasma), Valine (Plasma), Vannilylmandelic Acid, Xanthurenic Acid