Pyruvic acid, also known as pyruvate, is a key intermediate in several metabolic pathways throughout the body. Its presence in urine can provide valuable insights into a person's metabolic health and energy production processes. Pyruvic acid is a product of glycolysis, the process by which glucose is broken down to produce energy. After glycolysis, pyruvate can follow several pathways: it can be converted into acetyl-CoA and enter the Krebs cycle for further energy production, or it can be transformed into lactate under anaerobic conditions. Elevated levels of pyruvic acid in urine might indicate issues with carbohydrate metabolism, potential enzyme deficiencies, or problems in the Krebs cycle.

Pyruvic Acid feeds into the citric acid cycle & converts into acetyl CoA. Pyruvate is formed from carbohydrate via glucose or glycogen & secondarily from fats (glycerol) & glycogenic amino acids. Pyruvic acid is also formed from lactic acid with O2 and zinc.

Pyruvic Acid feeds into the citric acid cycle & converts into acetyl CoA. Pyruvate is formed from carbohydrate via glucose or glycogen & secondarily from fats (glycerol) & glycogenic amino acids.

Pyruvic Acid feeds into the citric acid cycle & converts into acetyl CoA. Pyruvate is formed from carbohydrate via glucose or glycogen & secondarily from fats (glycerol) & glycogenic amino acids.

Lactic Acid and Pyruvic Acid are byproducts of glycolysis. Carbohydrates, which contain glucose, are broken down through glycolysis to form pyruvate and two ATP molecules. Pyruvate can also be generated through the catabolism of various amino acids, including alanine, serine, cysteine, glycine, tryptophan and threonine. Magnesium is an important cofactor for a number of glycolytic enzymes necessary to produce pyruvate. Optimally, pyruvic acid is oxidized to form Acetyl-CoA to be used aerobically via the Citric Acid Cycle to produce energy. In an anaerobic state, lactic acid is formed instead.

Pyruvic acid is an intermediate compound in the metabolism of carbohydrates, proteins, and fats. Pyruvic acid is found to be associated with Fumarase deficiency, which is an inborn error of metabolism. It is also a metabolite of Corynebacterium. Elevated levels of pyruvic acid are associated with vigorous exercise, bacterial overgrowth of the GI tract, shock, poor perfusion, B-vitamin deficiency, mitochondrial dysfunction or damage, and anemia, among others. High pyruvic acid indicates the possibility of an inborn error of metabolism when the value exceeds 100 mmol/mol creatinine.

Pyruvic acid, an intermediate metabolite, plays an important role in linking carbohydrate and amino acid metabolism to the tricarboxylic acid cycle, the fatty acid beta-oxidation pathway, and the mitochondrial respiratory chain complex. Though isolated elevated pyruvate is not diagnostic of any inborn error of metabolism, analysis with lactate may suggest an inborn error of metabolism as some present with lactic acidosis or a high lactate-to-pyruvate (L:P) ratio.

The QUANTIFERON®-TB Gold Plus (QFT-Plus) test is a blood test used to check for latent tuberculosis (TB) infection. It’s often recommended for people who may have been around someone with TB or who are at higher risk of exposure, such as healthcare workers or people with weakened immune systems. This test helps detect TB bacteria that may be inactive in the body but could still cause health issues if they become active later on.

Research has noted antidiabetic, anti-inflammatory, antioxidant, antimicrobial, anti-Alzheimer's, antiarthritic, cardiovascular, and wound-healing effects.

People who are new to the GFD encounter new foods and/or over-consume old favorites to compensate for the lack of wheat in the diet. Gluten-free cookies, crackers, breads and cakes often contain copious amounts of rice, amaranth, sorghum and other substitutes. Some of these new-to-the-patient foods may illicit an adverse reaction. Other foods that are often introduced to the patient on the GFD are quinoa, buckwheat and hemp. Some People may turn to the “ancient” grains (Polish wheat, spelt, barley, rye), not knowing that these contain gluten. Another problem patients often face on the GFD is the over-consumption of another starch to make up for the loss of wheat. They turn to potato, rice or corn as a substitute. This can lead to the development of a new sensitivity or the enhancement of old sensitivities.

The presence of antibodies to Quinoa is an indication of food immune reactivity. The offending food and its known cross-reactive foods should be eliminated from the diet. Quinoa is considered a beneficial food, especially for celiac patients and vegetarians. Quinoa is labeled by the scientific community as a nonallergenic food, however, severe allergic reaction to Quinoa has been reported. If a recently diagnosed gluten-reactive patient exhibits high levels of antibodies to Quinoa, it may be due to the late introduction of Quinoa into the diet.

Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Tryptophan and its different pathways:

The management of tryptophan converting to serotonin within the brain has some complex moving parts. Tryptophan gets converted into serotonin. High levels of stress of any type and acute/chronic infections can change this process by provoking an immune system response. Instead of serotonin being made from tryptophan in this process, two other compounds are eventually made: They are kynurenic acid which is neuroprotective and quinolinic acid which is neurodegenerative.The quinolinic acid is a NMDA-agonist, i.e. quinolinic acid, NMDA, and inflammation are best friends and like to wreak havoc when kynurenic acid is lacking. Recent research showed that patients suffering from severe depression and suicidality were found to have very high levels of inflammation and elevated NMDA activity as a result of long-term dysregulation of this pathway. The researchers’ recommended goal was to find ways to dampen the NMDA receptors and quinolinic acid in the brain.

Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.