I wanted to share the details of the results for my mother, based on Urine test . Hopefully, this will help a few on this forum.
I am only indicating the High/Low items in the report. The remaining ( of the total of 77 items) were within the Ref. Range. See attached sample report from their website for the list of all the 77 items.
static1.squarespace.com/sta...
The report also includes the probable cause for the High or Low numbers and in some instances name of the therapeutic drug or supplement to be taken that I have specified within square brackets [ ].
I am concerned only with a couple of fungal markers (item #6 and #7) and Neurotransmitter metabolites (# 34 through #38).
ANY INPUT REGARDING tackling or getting rid off ASPERGILLUS and CLOSTRIDIA is WELCOME !
Surprised to find Vitamin deficiency - that I hope to set right with supplementation.
LOOKING FORWARD TO INPUTS.
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The following were marked as High(H) / Low (L) compared to Reference Range(RR) in the OAT Results .
Intestinal Microbial Overgrowth :
#6 ) Tartaric (Aspergillus) : (H) 35 vs RR of <= 4.5
#7 ) Arabinose : (H) 44 vs RR of < = 29
[High yeast/fungal metabolites (1-8): Elevations of one or more metabolites indicate a yeast/fungal overgrowth of the gastrointestinal (GI) tract. Prescription or natural (botanical) anti-fungals, along with supplementation of high potencymulti-strain probiotics, may reduce yeast/fungal levels].
Glycolytic Cycle Metabolites :
#22 ) Lactic : (H) 247 vs RR of < = 48
[High lactic acid and/or high pyruvic acid (22,23) may be caused by many nonspecific factors, such as vigorous exercise, bacterial overgrowth of the GI tract, shock, poor perfusion, anemia, mitochondrial dysfunction or damage, and many other causes. Conversion of pyruvic acid to acetyl-CoA requires the cofactors coenzyme A (derived from pantothenic acid), lipoic acid, FAD derived from riboflavin, and thiamine. However, the possibility of an inborn error of metabolism increases as the value exceeds 300 mmol/mol creatinine. Values greater than 1000 mmol/mol creatinine indicate a much higher likelihood of an inborn error of metabolism. There are many inborn errors of metabolism that present elevated lactic acid, including disorders of sugar metabolism and pyruvate dehydrogenase deficiency.]
Mitochondrial Markers - Amino Acid Metabolites :
#31 ) 3-Hydroxyglutaric : (H) 6.5 vs RR of < = 6.2
[High 3-hydroxyglutaric is a metabolite associated with the genetic disease glutaric aciduria type I, which is due toa deficiency of glutaryl CoA dehydrogenase, an enzyme involved in the breakdown of lysine, hydroxylysine, and tryptophan. Other organic acids elevated include glutaric and glutaconic. This disease has been associated with clinical symptoms ranging from near normal to encephalopathy, cerebral palsy, and other neurological abnormalities. Some individuals with glutaric acidemia have developed bleeding in the brain or eyes that may be mistaken for the effects ofchild abuse. This abnormality should be confirmed by additional testing of enzyme deficiencies and/ or DNA at a major pediatric medical genetics center (Morton et al. Glutaric aciduria type I: a common cause of encephalopathy and spasticparalysis in the Amish of Lancaster County, Pennsylvania. American J. Med. Genetics 41: 89-95, 1991). Elevated values may also be found in hepatic carnitine palmitoyltransferase I deficiency, short-chain acyl dehydrogenase deficiency
(SCAD), and ketosis. Mitochondrial dysfunction induced by glutaric acid metabolites causes astrocytes to adopt a proliferative phenotype, which may underlie neuronal loss, white matter abnormalities and macrocephalia. Values in glutaric aciduria type I range from 60-3000 mmol/mol creatinine. Values higher than normal but less than 60 mmol/mol creatinine may be due to mild glutaric acidemia type I or to the other causes indicated above. Treatment of this disorder includes special diets low in lysine and supplementation with carnitine or acetyl-L-carnitine.]
Neurotransmitter Metabolites :
Phenylalanine and Tyrosine Metabolites
#33) Homovanillic (HVA) : (H) 35 vs RR of 0.8 to 3.6
[High HVA (33) : High HVA is usually associated with Clostridia colonization or excess fusaric acid from fungus of the gastrointestinal tract and/or deficiencies of dopamine-beta-hydroxylase (DBH) activity due to single nucleotide polymorphisms (SNPs) or genetic deletions that code for enzymes with low activity. The Great Plains Laboratory now offers a test for the activity of the DBH enzyme on blood serum. The genetic deficiencies of DBH can be treated with the drug Droxidopa (L-threo-dihydroxyphenylserine). Droxidopa has the ability to cross the blood brain barrier and be converted to norepinephrine by an alternate biochemical pathway that bypasses the DBH genetic block. Individuals with genetic deficiencies of DBH may have orthostatic hypertension and hypoglycemia and may be more susceptible to attention deficit disorder, Alzheimer’s disease, and Parkinson’s disease, depression, and bipolar depression. The severity of ADHD symptoms is related to decreased DBH enzyme activity. Cocaine abusers with low-activity DBH SNPs have increased sensitivity to cocaine-induced paranoia and euphoria. The drugs disulfiram and Etamicastat inhibit DBH and the inhibition of alcohol, drug, and gambling addictions by disulfiram may be mediated by DBH inhibition. If HVA is elevated and VMA is normal and the patient has elevated Clostridia markers , avoid supplementation with L-DOPA, phenylalanine or tyrosine until Clostridia is treated. Homovanillic acid (HVA), a dopamine metabolite, is often elevated due to stress-induced catecholamine output from the adrenal gland which depletes vitamin C. Supplementation with vitamin C (ascorbate) may be helpful in such cases.* Elevated HVA can result from the intake of L-DOPA, dopamine, phenylalanine, or tyrosine. Elevated HVA may also result from ingestion of aspartame (Nutrasweet®), salicylates (aspirin), and dietary salicylates. For more information about salicylates in foods go to <feingold.org/salicylate.php>. Elevated HVA may also result from toxic metal exposure (including lead, aluminum, manganese,arsenic, and mercury), presumably due to DBH inhibition. Heavy metal testing (blood or hair) might be useful to determine if such exposure is significant. If values are more than double the upper limit of normal, toxoplasmosis and tumors such as neuroblastoma, or other catecholamine-secreting tumors should be ruled out. Catecholamine-secreting tumors can be ruled out by 24- hour VMA and/or HVA testing in urine. Even in this subgroup, the incidence of tumors is extremely rare. ]
#35) HVA / VMA Ratio (H) 11 vs RR of .16 to 1.8
[High HVA/VMA ratio (35) the HVA/VMA ratio reflects the balance between dopamine and norepinephrine/epinephrine production by catecholamine producing neurons in the central nervous system, sympathetic nervous system, and adrenal gland. The most common reason for an elevation of the HVA/VMA ratio is a decreased conversion of dopamine to norepinephrine. The enzyme responsible for this conversion, dopamine beta-hydroxylase (DBH), is copper and vitamin C dependent so an elevated ratio could be due to deficiencies of these cofactors . The most common reason for this elevated ratio is inhibition of this enzyme by Clostridia byproducts including HPHPA, 4-cresol, or 4-hydroxyphenylacetic acid. Other causes of an increased ratio include inhibition of DBH by the mold metabolite fusaric acid, pharmaceuticals such as disulfiram, or food additives like aspartame. Another cause for an elevated ratio is a genetic variation (single nucleotide polymorphism or SNP) of the DBH enzyme. Alternatively, the activity of the DBH enzyme can be measured on blood serum. Individuals with low DBH activity can be treated with the drug Droxidopa™, which provides adequate norepinephrine by an alternate biochemical pathway. This DBH test on blood serum is now available at The Great Plains Laboratory. High ratios are common in a large number of neuropsychiatric diseases regardless of the reason for DBH deficiency.]
#36) Dihydroxyphenylacetic (DOPAC) : (H) 17 vs RR of 0.8 to 3.5
[ High 3,4-dihydroxyphenylacetic acid (DOPAC) (36) 3,4-dihydroxyphenylacetic acid (DOPAC) is an intermediate in the metabolism of dopamine. Values may be elevated due to increased intake of amino acid precursors of DOPAC such as phenylalanine, tyrosine, or DOPA. Values may be elevated due to factors that inhibit dopamine beta hydroxylase (DBH) like Clostridia metabolites, the mold metabolite fusaric acid, pharmaceuticals such as disulfiram, or food additives like aspartame, or to deficiencies of the DBH enzyme due to copper deficiency, vitamin C deficiency, or malic acid deficiency. Single nucleotide polymorphisms (SNPs) of DBH or catechol-O-methyltransferase (COMT) that result in reduced enzyme activities also result in increased amounts of DOPAC. SNPs of COMT are available on The Great Plains Laboratory DNA methylation pathway test which can be performed on a cheek swab. Deficiencies of S-adenosylmethionine (S-ame) also are associated with high amounts of DOPAC. DOPAC may also be increased when bananas are ingested the day before urine collection].
#37) HVA / DOPAC Ratio : (H) 2.1 vs RR of .1 to 1.8
[High HVA/DOPAC ratio (37) HVA and DOPAC are the major metabolites of dopamine. An increase in the conversion of DOPAC to HVA might be due to excessive supplementation of S-adenosyl methionine (S-ame) and/or supplements suchas methyltetrahydrofolate or methylcobalamin that increase endogenous Sam-e].
Tryptophan Metabolites
#38) 5 Hydroxyindoleacetic (5-HIAA): (L) .63 vs RR of < = 0.63 ( .63 is
[5-hydroxyindoleacetic acid (5HIAA) (38) levels below the mean may indicate lower production and/or decreased metabolism of the neurotransmitter serotonin. 5-hydroxy-indoleacetic acid is a metabolite of serotonin. Low values have been correlated with symptoms of depression. Low production of 5HIAA can be due to decreased intake or absorption of serotonin’s precursor amino acid tryptophan, decreased quantities of cofactors needed for biosynthesis of serotonin such as tetrahydrobiopterin and vitamin B6 coenzyme. In addition, a number of genetic variations such as single nucleotide polymorphisms (SNPs) or mutations can cause reduced production of 5HIAA. Such SNPs are available on The Great Plains DNA methylation pathway test which can be performed on a cheek swab. Values may be decreased in patients on monoamine oxidase (MAO) inhibitors that are drugs or foods that contain tyramine such such as Chianti wine and vermouth, fermented foods such as cheeses, fish, bean curd, sausage, bologna, pepperoni, sauerkraut, and salami.]
Ketone and Fatty Acid Oxidation :
# 45) Ethylmalonic : (H) 8.0 vs RR of .44 to 2.8
#46) Methylsuccinic : (H) 3.9 vs RR of .1 to 2.2
[High ethylmalonic, methylsuccinic, adipic, suberic, or sebacic acids (45,46,47,48,49) may be due to fatty acid oxidation disorders, carnitine deficiency, fasting, or to increased intake of the medium-chain triglycerides found in coconut oil, MCT oil, and some infant formulas. The fatty acid oxidation defects are associated with hypoglycemia, apnea episodes, lethargy, and coma. [An acyl carnitine profile (Duke University Biochemical Genetics Laboratory,
medgenetics.pediatrics.duke... can rule out fatty acid oxidation defects.] Regardless of cause, supplementationwith L-carnitine or acetyl-L-carnitine may be beneficial.]
Nutritional Markers :
#51) Vitamin B6 (Pyridoxic) : (L) 2.5 vs RR of < =34 ( 2.5 is below the lower limit - not specified, while the upper limit is 34)
#52) Vitamin B5 (Panthothenic) : (L) 1.8 vs RR of < =10 (1.8 is below the lower limit - not specified, while upper limit is 10)
#54 ) Vitamin C (Ascorbic) : (L) 20 vs RR of 10 -200 ( 20 is really close to the lower limit of 20)
[Pyridoxic acid (B6) levels below the mean (51) may be associated with less than optimum health conditions (low intake, malabsorption, or dysbiosis). Supplementation with B6 or a multivitamin may be beneficial.
Pantothenic acid (B5) levels below the mean (52) may be associated with less than optimum health conditions.Supplementation with B5 or a multivitamin may be beneficial.
Ascorbic acid (vitamin C) levels below the mean (54) may indicate a less than optimum level of the antioxidant vitamin C. Individuals who consume large amounts of vitamin C can still have low values if the sample is taken 12 or more hours after intake. Supplementation with buffered vitamin C taken 2 or 3 times a day is suggested.]
Amino Acid Metabolites:
#72) 4- Hydroxyphenyllactic (H) 2.4 vs RR of < = 2.0
[High 4-hydroxyphenyllactic acid (72) is associated with tyrosinemia, which can be due to immature development of enzymes in infants or to genetic deficiencies. Even a mild case would have levels of at least 100 mmol/mol creatinine. Values between the upper limit of normal and 100 mmol creatinine may be due to the heterozygous genetic carrier state, or mild disease or unknown physiological conditions.]
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