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Home , Hydroxyproline, Taurine, Tyrosine (data page)

Interpretive Guide for Amino Acids

Intervention Options LOW HIGH Essential Amino Acids (Arg) Arg Mn (His) , His (Ile) * B6, Check for insulin insensitivity (Leu) * B6, Check for insulin insensitivity (Lys) C, Niacin, B6, , a-KG (Met) * B6, á-KG, Mg, SAM (Phe) * Iron,VitaminC,Niacin,LowPhediet (Thr) * B6, Zn (Trp) Trpor5-HTP Niacin, B6 (Val) * B6, Check for insulin insensitivity Essential Derivatives Neuroendocrine Metabolism y-Aminobutyric Acid (GABA) a-KG,B6 (Gly) Gly Folate, B6,B2,B5 (Ser) B6, Mn, Folate * Taurine (Tau) Tau, B6 Vit. E, Vit. C, B-Carotene, CoQ10, Lipoate (Tyr) Iron,Tyr,VitaminC,Niacin Cu, Iron, , B6 Ammonia/Energy Metabolism a-Aminoadipic Acid B6, a-KG (Asn) Mg (Asp) a-KG,B6 Mg, Zn (Cit) Mg, Aspartic acid (Glu) B6, a-KG Niacin, B6 (Gln) a-KG,B6 (Orn) Arg Mg, a-KG,B6 Metabolism (Cys) NAC B2 B6

Homocystine (HCys) B6, Folate, B12, Betaine Additional Metabolites a-Amino-N-Butyric Acid a-KG,B6 B6, a-KG (Ala) * B6 Anserine Zn n-Alanine and Bifidobacteria, B6 n-Aminoisobutyric Acid B6 Carnosine Zn Mg (HLys) Vitamin C, Iron, a-KG Hydroxyproline (HPro) Vitamin C, Iron, a-KG

1-Methylhistidine , B12, Folate 3-Methylhistidine BCAAs, Vit. E, Vit. C, n-Carotene, CoQ10, Lipoate

Phosphoethanolamine (PE) SAM, B12, Folate, Betaine Phosphoserine Mg (Pro) a-KG Vitamin C, Niacin B2

* Use balanced or custom mixtures of essential amino acids Nordic Laboratiroes∙ Nygade 6, 3.sal ∙ 1164 Copenhagen K ∙ DenmarkTel: +45 33 75 1000 ∙ e-mail: [email protected] In association with ©Metametrix, Inc. All rights reserved Interpretive Guide for Amino Acids 2

Essential Amino Acids rich or inefficient metabolism. convert to succinate for use in the Krebs If other sulfur-containing AAs are low, (citric acid) cycle for energy generation. A r g i n i n e then enhance methionine utilization by Cofactors here are a-KG and vitamin B6. Low - often reflects a diet poor in high adding the necessary cofactors, quality protein, causing arginine to be and vitamin B6. G l y c i n e poorly absorbed. Because arginine is Low - possible generalized tissue loss, required for production, Phenylalanine glycine being part of the pool deficiencies have wide-ranging effects Low - can result in altered thyroid and important in gluconeogenesis. on cardiovascular and other systems. function and deficits Supplement glycine. High - may indicate a functional block including symptoms of depression, High - supplement vitamin B5, folic in the urea cycle. activates cognitive disorders, memory loss, acid, and B6, and B2 for the an arginase enzyme, so supplementing fatigue, and autonomic dysfunction. efficient metabolism of glycine to with manganese may help. Reduce lifestyle stressors and pyruvic acid for oxidation and for supplement phenylalanine. synthesis or H i s t i d i n e High - high protein intake or a block in gluconeogenesis. Low - check dietary protein, or malab- the conversion of phenylalanine to sorption if other essential AAs are low. tyrosine. Iron, vitamin C, and niacin are S e r i n e Low histidine is associated with necessary for this enzymatic step. Check Low - can lead to disordered rheumatoid arthritis, folate deficiency, tyrosine level and, if low, supplement methionine metabolism and deficits in and/or salicylate/steroid use. tyrosine and iron. synthesis. If simultaneous High - may indicate excessive protein high threonine or phosphoserine, then intake. If high 3-Methylhistidine, T h r e o n i n e need for vitamin B6, folate, and muscle protein breakdown is indicated. Low - can result in hypoglycemic manganese is indicated. symptoms, particularly if glycine High - when accompanied by low I s o l e u c i n e or serine is also low. Supplement threonine, indicates glucogenic Low - a chronic deficiency of this AA threonine/BCAAs. compensation and catabolism. can cause hypoglycemia and related High - excessive dietary intake or Supplement threonine and BCAAs. problems and loss of muscle mass or possible insufficient metabolism of inability to build muscle. threonine. The initial step here requires T a u r i n e High - large intake of this AA or (vitamin B6) and is needed to Low - may increase risk for oxidative incomplete metabolism of it. If other phosphorylate vitamin B6 to its active stress, fat maldigestion, high , BCAAs are high, add vitamin B6 to aid coenzyme form, so supplementation , angina, arrythmias, and metabolism. with vitamin B6 and zinc can be helpful. seizure disorders. Supplement taurine or and vitamin B6, even if fresh L e u c i n e T r y p t o p h a n fish or lean meat is eaten. Females do not Low - potential catabolism of skeletal Low - commonly correlated with synthesize taurine as easily as males. muscle. Check 3-Methylhistidine to depression, insomnia, and schizophrenia. High - may be due to excessive confirm this. Supplementation with 5- inflammation in the body or to High - large intake of this AA or Hydroxytryptophan (5-HTP) may help. 5- supplementation of other amino acids. incomplete metabolism of it. If other HTP is one enzymatic step away from BCAAs are high, add vitamin B6 to aid . T y r o s i n e metabolism. High - possibly inadequate metabolism of Low - implicated in depression, tryptophan. Required for this hypothyroidism, and blood pressure L y s i n e process include niacin and vitamin B6. disorders. If phenylalanine is normal or Low - either poor dietary intake or too high (barring PKU), iron, vitamin C, and high intake of arginine. Low levels can V a l i n e niacin supplementation might be inhibit transamination of AA Low - deficiency in this or other BCAAs indicated to help convert phenylalanine synthesis. If concurrent weakness or indicates potential muscle loss. If several to tyrosine. high triglycerides, add carnitine. High - essential AAs are low, check for adequate High - inadequate utilization of impaired metabolism of lysine. Add stomach acid. Supplement the BCAAs. tyrosine. Supplement the cofactors vitamin C, niacin, vitamin B6, a- High - excessive intake or vitamin B6 needed here including iron, , ketoglutarate and iron to enhance functional deficit. If other BCAAs are vitamin B6, and ascorbate. utilization of lysine. high, vitamin B6 should be given. Ammonia/Energy Metabolism M e t h i o n i n e Low - possible poor-quality protein diet. Derivatives Neuroendocrine a -Aminoadipic acid Adverse effects on sulfur metabolism. Metabolism High - possible inhibition of lysine Improve dietary methionine intake or metabolism and lowered amine group supplement. (GABA) Gamma-aminobutyric acid transfer in the tissues. Supplement High - excessive intake of methionine- High - may reflect decreased ability to vitamin B6 and a-KG to facilitate the Interpretive Guide for Amino Acids 3 transamination conversion of á- High - a possible metabolic block in for energy can lead to muscle wasting. aminoadipic to á-ketoadipic acid. urea cycle, causing excess ammonia Supplement the branched-chain amino burden. Confirm by checking for high acids. A s p a r a g i n e glutamine, low glutamic acid. Low - can reflect functional need for A n s e r i n e magnesium in the conversion from Sulfur Metabolism High - high dietary intake of poultry can aspartic acid. contribute to elevate anserine. Zinc is High - Can indicate problems with C y s t i n e required for the normal conversion to ß- purine (therefore protein) synthesis. Low - possible dietary deficiency of alanine plus 1-methylhistidine methionine and/or cystine. Low cystine Aspartic Acid can impair taurine synthesis. ß - A l a n i n e Low - inhibits ammonia detoxification in High - excessive dietary intake or High - possible bowel toxicity due to ß- the urea cycle. Can be converted to impaired cystine metabolism. Converted to alanine production by intestinal bacteria oxaloactetate using B6 and á-KG and thus cysteine (reduced cystine) via a B2 and and/or Candida albicans. Possible cause enter the Krebs cycle. Low levels can copper-dependent step. Cystine is a major for food sensitivity reactions when reflect decreased cellular energy component of tissue combined with low taurine and high 3- generation, seen as fatigue. Citric and mechanisms. methylhistidine, carnosine and/or aspartic acids can drive the Krebs (citric anserine, due to impaired renal tubular acid) cycle, when combined with B6 and á- Cystathionine resorption. Supplement B6 (to facilitate KG. High - possible B6 functional deficit as B6 amine group transfer). Bowel detox or High - sometimes seen in epilepsy and or P-5-P is required for the conversion of high potency Lactobacillus acidophilus stroke. Magnesium and zinc may cystathionine to cysteine. Hence low and Bifidobacteria can help with gut counteract high aspartic add levels. cysteine can result. dysbiosis.

C i t r u l l i n e Homocystine ß-Aminoisobutyric acid High - can indicate a functional enzyme High - increased risk for atherosclerosis High - indicates lack of a transaminase block in the urea cycle, leading to an and abnormalities in the ocular, enzyme needed to metabolize this ammonia buildup. Supplement neurological and musculo-skeletal substance in the presence of á-KG, an magnesium and aspartic add to drive the systems. The enzyme that converts apparently benign phenomenon, seen in cycle. Lower protein intake is suggested (reduced homocystine) to kwashiorkor (chronic protein in ammonia toxicities. cystathionine is B6 dependent; deficiency). remethylation of homocysteine to Glutamic Acid methionine requires B12, folate and C a r n o s i n e Low - can suggest mild hyper- betaine. Supplementation of these High - deficiency of enzyme carnosinase ammonemia, especially if high nutrients plus magnesium is effective for or its cofactor, zinc. This analyte is a ß- glutamine. Low protein, high complex the proper metabolism of homocystine. alanyl dipeptide of histidine. Inherited carbohydrate and B6, á-KG and BCAA’s carnosinase enzyme deficits lead to suggested to correct ammonia toxicity. Additional Metabolites neurological development problems and High - possible underconversion to á- sensory polyneuropathy. KG in liver for use in citric add cycle. α -Amino-N-butyric acid Supplement niacin and B6. Low - possible increased need for the Ethanolamine nutrients which aid in threonine High - sluggish conversion of this serine G l u t a m i n e metabolism from which this AA is derivative to phosphoethanolamine, Low - deficient intake or absorption of derived. These include á-KG and B6. possibly reducing acetylcholine essential amino acids (glutamine is High - inadequate utilization of this AA synthesis. Supplement magnesium, a derived fiom histidine). Check overall for cellular energy generation. Alpha- main cofactor for this conversion. amino acid level of diet. ABA is converted to succinyl Co-A for High - marker of vitamin B6 deficiency. use in the via Hydroxylysine Ammonia accumulation suspected, if low mechanisms requiring biotin and B12. High - indicative of connective and or low normal glutamic acid. Extra á-KG bone tissue breakdown. Collagen needed to combine with ammonia and to A l a n i n e synthesis requires iron, á-KG and make up for energy deficit caused by Low - may point to hypoglycemic vitamin C. Supplementation of these overutilization of á-KG to deal with toxic conditions because of its role in plus and manganese ammonia levels. gluconeogenesis. Supplement with are extremely helpful. alanine and the branched chain amino O r n i t h i n e acids leucine, isoleucine and valine. Hydroxyproline Low - possibly due to low arginine, as High - possible inadequate cellular High - another indicator of bone it is synthesized from arginine. As a energy substrates. Check for resorption via collagen breakdown. source of regulatory polyamines, a hypoglycemia or for exercise prior to Supplement as in the case of high low can affect cellular metabolism. blood draw. Chronic use of alanine hydroxylysine above. Interpretive Guide for Amino Acids 4

1-Methylhistidine Phosphoserine S a r c o s i n e High - can mean impaired methionine High - functional magnesium deficiency High - Metabolism requires B2. May metabolism. Supplement B12, folate or causing incomplete conversion to serine. indicate functional B2 deficiency. DMG. Can also inhibit carnosinase; give zinc. P r o l i n e Low - tissue levels probably low. As 3-Methylhistidine proline is a major component of High - indicates active catabolism of collagen, low plasma level can mean muscle protein which may be due to defective connective tissue synthesis. poor antioxidant . Proline metabolized to á-KG. Check intake of high quality protein. High - Phosphoethanolamine can demonstrate poor utilization. Add High - possible inhibition of vitamin C to aid collagen synthesis if and acetylcholine synthesis due to symptoms present. Niacin (cofactor impaired methionine metabolism precursor) helps oxidize proline to involving methylation by S-adenosyl- glutamate. methionine (SAM). Supplement B12, folate and betaine or SAM.

Sources: 1. Tucker DM, et al. Iron status and brain function: Am. J. Fitness, Sept. 1985, 54-60. Clin. Nutr, 39:105-113(1984). 15. Wurtman and Wurtman. Nutrition and the Brain, Vol 1-4, 2. Shinnar, DL Cobalamin C mutation in adolescence: N. Eng. Raven Press, NY(1977-83). J. Med. 311:451(1984). 16. Adams, PW et al. Effect of pyridoxine upon depression 3. Harper et al. Review of Physiological Chemistry, 17th associated with oral contraceptives. Lancet, 1:897(1973). Ed. Lange Medical Publications (1979). 17. Gelenberg, AJ et al. Tyrosine treatment of depression. Am 4. Cherrington, AD et al. Amino acids in gluconeogenesis. J Psychiat. 137:622(1980). In Amino Acids: Metabolism and Medical Applications, pp. 18. Thomson, J et al. The treatment of depression in general 63- 76. (Ed.) Blackburn et al., Wright PSG, Boston, 1983. practice: A comparison of L-tryptophan, amitryptyline and 5. Pangborn, JB. Nutritional and anti-inflammatory aspects of combination with placebo. Psychol. Med. 12:741(1982). amino acids. In Yearbook of Nutritional Medicine, 1984-85, 19. Youdin MBH et al. Putative biological mechanisms of the pp. 153-178. (Ed.) Bland, JS, Keats, New Canaan, 1985. effect of iron deficiency on brain chemistry and 6. Huxtable, RJ and Pasanter-Moralies, H. Taurine in Nutrition behavior. Am. J. Clin Nutr. 50:607-17(1989). and Neurology, Plenum, New York, 1982. 20. Hayes, KC et al. Taurine modulates platelet aggregation in 7. Azuma, J. et al. Taurine for treatment of congestive cats and humans. Am. J. Clin. Nutr. 49:1211-16(1989). heart failure. Int. J. Cardiol. 2:303(1982). 21. Rudman, D et al. Fasting plasma amino acids in elderly men. 8. McCully, KS and Wilson, RB. Homocysteine theory of Am J Clin Nutr. 49:559-66(1989). athero- sclerosis. Atherosclerosis, 22:2(1975). 22. Braverman, ER with Carl Pfeiffer. The Healing Nutrients 9. Wikken, DEL Homocysteinuria: The effects of betaine in Within. Keats Publishing, New Canaan, CT, 1987. treatment of patients not responsive to pyridoxine. N.Eng. J. Med., 309:448(1983). 10. Gerber, DA Low free serum histidine concentration in rheu- matoid arthritis. A measure of disease activity. J. Clin. Invest. 55:1164-73(1975). 11. Scriver, CD et al. Disorders of B-alanine, carnosine and homocarnosine metabolism. In The Metabolic Basis of Inher ited Disease, 5th Ed. (Ed.) Stanbury et al, Chap. 28, McGraw- Hill, NY, 1983. 12. Finkelstein, DA. Regulation of methionine metabolism in mammals. Arch. Biochem. Biophys.159:160(1973). 13. Hoffman, RM Altered methionine metabolism, DNA methylation and oncogene expression in carcinogenesis, Biochem. Biophys. Acta. 738:49-87(1984). 14. Bralley, JA, Murray, M. Research suggests amino acid supplements can be as potent as anabolic steroids. Sports Interpretive Guide for Amino Acids 5

MetabolismofTryptophan NeurotransmittersfromAminoAcids

B i o p t e r i n Biopterin Tryptophan 5-Hydroxytryptophan Biopterin ++ Fe+++ Fe+++ Fe Phenylalanine __ Tyrosine ______DOPA P 5 P

O Pyridoxal-5-phosphate O2 2 H2OH2O

5-Hydroxytryptamine Cu++ CO 2 (Serotonin) I 2

Dopamine Monoamine Oxidase O 2 FAD (B2) Thyramine Melanin ++ Cu Ascorbate Cu++

H 2 O Dehydrogenase SAH + 3 NAD (B )

Epinephrine 5-Hydroxyindoleacetate SAM (excreted in urine)

Relevant Ammonia Metabolism Pathways

NH4 + α-Ketoglutaric Acid______Glutamic Acid B3 Most Tissues NH4 + especially the brain Glutamic Acid Glutamine B 6

NH3 + H2O UREA CYCLE CO2 + ATP (Kreb's Cycle) Mg++ Oxaloacetic Acid M g+ 1. Citrulline Carbamoyl Aspartic Acid Phosphate

3. 2. Liver (Kidney) Hepatic Ornithin Argininosuccinic Acid Mitochondriae Cytosol 4. 5. Mn++ Urea

Arginine Fumaric Acid H 2 O

HYPERAMMONEMIA AND: FAULTY ENZYME: 1. Low Urinary Orotate Carbamoyl Phosphate Synthetase 2. Oroticaciduria Ornithine Carbamoyl Transferase 3. Citrullinemia Argininosuccinate Synthetase 4. Argininosuccinic Aciduria Argininosuccinate Arginine Lyase 5. Hyperagininemia Arginase Interpretive Guide for Amino Acids 6

Metabolism of Glycine & Serine Relevant Sulfur-Containing AA Pathways

Methionine Sulfoxide

Enzyme Structure

THF ATP Methionine (Remethylation) B ADP 12 5M-THF Phosphocreatine DMGB r a i n (Muscle) Purines DNA, RNA Threonine Betaine SAM B Porphyrins Homocysteine 6 Serine Glutathione Precursors Glycocholate SAHt h a n Cystathionine Hippurate and Choline Creatine other hepatic Epinephrine Glutamate Glycine phase II conjugates Creatine C u + + Glutathione Cysteine GR(B2 )

B 6 SAM = S-Adenosylmethionine SAH = S-Adenoslyhomocysteine THF = Tetrahydrofolate 5M-THF = 5 Methylterahydrofolate Taurine Pyruvate GR = Glutathione Reductase DMG = Dimethyl Glycine

R e l e v a n t â -Amino Acid Pathways

DNA Cytosine ++ Zn Enzyme Liver Carnosine β-ALANINE (plasma) (plasma) Strenuous Dietary Sources of â-Alanine exercise Carnosine (red meat) β-Alanine Carnosine β-Alanylhistine (muscle) (muscle) or Histidine Anserine (poultry) or 1MH Activate myosin ATPase β-Alanyl-1-methylhistidine α -KG Gut microbes P-5-P Malonate Acetate CO2 + H20

Aspartic acid Glutamate C O 2 AND ______

CH3 OH O O ATP HO CH2 C C C NH CH2 CH2 C OH Coenzyme A

CH3

Pantoic acid â-Alanine

Pantothenic acid