amino acids - long

[Guest guest]

We have often discussed the fact that some of us have low amino acids

and have been told that they are not significant. I found the

following on-line and thought it might be of interest to these folks.

laurie

Alanine 
Low - may point to hypoglycemic conditions because of its

role in gluconeogenesis. Supplement with alanine and the branched

chain amino acids leucine, isoleucine, and valine. 
High - possible

inadequate cellular energy substrates. Check for hypoglycemia or for

exercise prior to blood draw. Chronic use of alanine for energy can

lead to muscle wasting. Supplement the branched-chain amino acids.

Vitamin B6 helps to drive metabolism.

Anserine 
High - high dietary intake of poultry can contribute to

elevated anserine. Zinc is required for the normal conversion to

ß-alanine or 1-methylhistidine - see ß-Amino Acids Pathways Diagram

Arginine 
Low - often reflects a diet poor in high quality protein,

causing arginine to be poorly absorbed. Because arginine is required

for nitric oxide production, deficiencies have wide-ranging effects on

cardiovascular and other systems. 
High - may indicate a functional

block in the urea cycle. Manganese activates an arginase enzyme, so

supplementing with manganese may help.

Asparagine 
Low - can reflect functional need for magnesium in the

conversion from aspartic acid. Supplement magnesium. 
High - can

indicate problems with purine (protein) synthesis.

Aspartic Acid 
Low - inhibits ammonia detoxification in the urea

cycle. Can be converted to oxaloactetate using vitamin B6 and a-KG and

thus enter the Krebs cycle. Low levels can reflect decreased cellular

energy generation, often resulting in fatigue. Citric and aspartic

acids can drive the Krebs (citric acid) cycle when combined with

vitamin B6 and a-KG. 
High - sometimes seen in epilepsy and stroke.

Magnesium and zinc may counteract high aspartic acid levels.

Carnosine 
High - deficiency of carnosinase enzyme or its cofactor

zinc. This analyte is a ß-alanyl dipeptide of histidine. Inherited

carnosinase enzyme deficits lead to neurological development problems

and sensory polyneuropathy.

Citrulline 
High - can indicate a functional enzyme block in the urea

cycle, leading to an ammonia buildup. Supplement magnesium and

aspartic acid to drive the cycle. Lower protein intake is suggested in

ammonia toxicities.

Cystathionine 
High - possible vitamin B6 functional deficit as

vitamin B6 or P-5-P is required for the conversion of cystathionine to

cysteine. Hence, low cysteine can result.

Cystine 
Low - possible dietary deficiency of sulfur-containing amino

acids. Low cystine can impair taurine synthesis. 
High - excessive

dietary intake or impaired cystine metabolism. Converted to cysteine

(reduced cystine) via a vitamin B2 and dependent step. Cystine is a

major component of tissue antioxidant mechanisms.

Ethanolamine 
High - sluggish conversion of this serine derivative to

phosphoethanolamine, possibly reducing acetylcholine synthesis.

Supplement magnesium, a main cofactor for this conversion.

(GABA) Gamma-aminobutyric acid 
High - may reflect decreased ability

to convert to succinate for use in the Krebs (citric acid) cycle for

energy generation. Cofactors here are a-KG and vitamin B6.

Glutamic Acid 
Low - can suggest mild hyperammonemia, especially if

high glutamine. Low protein, high complex carbohydrate in the diet and

supplementation with vitamin B6, a-KG, and Branched Chain Amino Acids

(BCAAs) can correct ammonia toxicity. 
High - possible underconversion

to a-KG in liver for use in citric acid cycle. Supplement niacin and

vitamin B6.

Glutamine 
Low - chronic deficient intake or absorption of essential

amino acids or protein catabolic condition. Check overall amino acid

level of diet. 
High - marker of vitamin B6 deficiency. Ammonia

accumulation suspected if low or low normal glutamic acid. Extra a-KG

needed to combine with ammonia and to make up for energy deficit

caused by overutilization of a-KG to deal with toxic ammonia levels.

Glycine 
Low - possible generalized tissue loss, glycine being part of

the nitrogen pool and important in gluconeogenesis. Supplement

glycine. 
High - supplement vitamin B5, folic acid, and vitamins B6,

and B2 for the efficient metabolism of glycine to pyruvic acid for

oxidation and for glutathione synthesis or gluconeogenesis.

Histidine 
Low - check dietary protein, or malabsorption if other

essential AAs are low. Low histidine is associated with rheumatoid

arthritis and folate deficiency. 
High - may indicate excessive

protein intake. If high 3-methyl-histidine, muscle protein breakdown

is indicated.

Homocystine 
High - increased risk for atherosclerosis and

abnormalities in the ocular, neurological, and musculo-skeletal

systems. The enzyme that converts homocysteine (reduced homocystine)

to cystathionine is B6 dependent; remethylation of homocysteine to

methionine requires B12, folate, and betaine. Supplementation of these

nutrients is effective for the proper metabolism of homocystine.

Hydroxylysine 
High - indicative of connective and bone tissue

breakdown. Collagen synthesis requires iron and vitamin C.

Supplementation of these plus chondroitin sulfate, a-KG, and manganese

are extremely helpful.

Hydroxyproline 
High - another indicator of bone resorption via

collagen breakdown. Supplement as in the case of high hydroxylysine

above.

Isoleucine 
Low - a chronic deficiency of this AA can cause

hypoglycemia and related problems and loss of muscle mass or inability

to build muscle. 
High - large intake of this AA or incomplete

metabolism of it. If other BCAAs are high, add vitamin B6 to aid

metabolism.

Leucine 
Low - potential catabolism of skeletal muscle. Check

3-methyl-histidine to confirm this. 
High - large intake of this AA or

incomplete metabolism of it. If other BCAAs are high, add vitamin B6

to aid metabolism.

Lysine 
Low - either poor dietary intake or too high intake of

arginine. Low levels can inhibit transamination of AA collagen

synthesis. If concurrent weakness or high triglycerides, add

carnitine. 
High - impaired metabolism of lysine. Add vitamin C,

niacin, vitamin B6, and iron to enhance utilization of lysine.

Methionine 
Low - possible poor-quality protein diet. Adverse effects

on sulfur metabolism. Improve dietary methionine intake or supplement.


High - excessive intake of methionine-rich protein or inefficient

metabolism. If other sulfur-containing AAs are low, then enhance

methionine utilization by adding the necessary cofactors, magnesium

and vitamin B6.

Ornithine 
Low - possibly due to low arginine, as ornithine is

synthesized from arginine. As a source of regulatory polyamines, low

loads can affect cellular metabolism. 
High - a possible metabolic

block in urea cycle, causing excess ammonia burden. Confirm by

checking for high glutamine or low glutamic acid. Consider

supplementation of vitamin B6 and a-KG.

Phenylalanine 
Low - can result in altered thyroid function and

catecholamine deficits including symptoms of depression, cognitive

disorders, memory loss, fatigue, and autonomic dysfunction. Reduce

lifestyle stressors and supplement phenylalanine. 
High - high protein

intake or a block in the conversion of phenylalanine to tyrosine.

Iron, vitamin C, and niacin are necessary for this enzymatic step.

Check tyrosine level and, if low, supplement tyrosine and iron.

Phosphoethanolamine 
High - possible inhibition of choline and

acetylcholine synthesis due to impaired methionine metabolism

involving methylation by S-adenosylmethionine (SAM). Supplement

vitamin B12, folate, and betaine or SAM.

Phosphoserine 
High - magnesium functional deficiency causing

incomplete conversion to serine. Supplement magnesium.

Proline 
Low - tissue levels probably low. As proline is a major

component of collagen, low plasma levels can mean defective connective

tissue synthesis. Proline is metabolized to a-KG. Check intake of high

quality protein. 
High - can demonstrate poor utilization. Supplement

vitamin C to aid collagen synthesis if symptoms present and niacin

(cofactor precursor), which helps oxidize proline to glutamate.

Sarcosine 
High - Metabolism requires B2. May indicate functional B2

deficiency.

Serine 
Low - can lead to disordered methionine metabolism and

deficits in acetylcholine synthesis. If simultaneous high threonine or

phosphoserine, then need for vitamin B6, folate, and manganese is

indicated. 
High - when accompanied by low threonine, indicates

glucogenic compensation and catabolism. Supplement threonine and

BCAAs.

Taurine 
Low - may increase risk for oxidative stress, fat

maldigestion, high cholesterol, atherosclerosis, angina, arrythmias,

and seizure disorders. Supplement taurine or cysteine and vitamin B6,

even if fresh fish or lean meat is eaten. Females do not synthesize

taurine as easily as males. 
High - may be due to excessive

inflammation in the body or to supplementation of other amino acids.

Threonine 
Low - can result in hypoglycemic symptoms, particularly if

glycine or serine is also low. Supplement threonine/BCAAs. 
High -

excessive dietary intake or possible insufficient metabolism of

threonine. The initial step here requires (vitamin B6) and zinc is

needed to phosphorylate vitamin B6 to its active coenzyme form, so

supplementation with vitamin B6 and zinc can be helpful.

Tryptophan 
Low - commonly correlated with depression, insomnia, and

schizophrenia. Supplementation with 5-hydroxy-tryptophan (5-HTP) may

help. 5-HTP is one enzymatic step away from serotonin. 
High -

possibly inadequate metabolism of tryptophan. Required nutrients for

this process include niacin and vitamin B6.

Tyrosine 
Low - implicated in depression, hypothyroidism, and blood

pressure disorders. If phenylalanine is normal or high (barring PKU),

iron, vitamin C, and niacin supplemen-tation might be indicated to

help convert phenylalanine to tyrosine. 
High - inadequate utilization

of tyrosine. Supplement the cofactors needed here including iron,

copper, vitamin B6, and ascorbate.

Valine 
Low - deficiency in this or other BCAAs indicates potential

muscle loss. If several essential Amino Acids (AAs) are low, check for

adequate stomach acid. Supplement the BCAAs. 
High - excessive intake

or vitamin B6 functional deficit. If other BCAAs are high, vitamin B6

should be given.

1-Methylhistidine 
Low - can signify inadequate methyl group transfer

leading to low histidine levels. Vitamin B12 and folate are needed to

catalyze the methyl-transferase enzymes. 
High - can mean impaired

methionine metabolism. Supplement vitamin B12 or folate. Can also

inhibit carnosinase; give zinc if carnosine is high.

3-Methylhistidine 
High - indicates active catabolism of muscle

protein, which may be due to poor antioxidant nutrition.

Supplementation of anti-oxidants and BCAAs may help.

a-Amino-N-butyric acid 
Low - possible increased need for the

nutrients that aid in threonine metabolism from which this AA is

derived. These include a-KG and vitamin B6. 
High - inadequate

utilization of this AA for cellular energy generation. Alpha-ABA is

converted to succinyl 
Co-A for use in the citric acid cycle 
via

mechanisms requiring biotin and vitamin B12.

a-Aminoadipic acid 
High - possible inhibition of lysine metabolism

and lowered amine group transfer in the tissues. Supplement vitamin B6

and a-KG to facilitate the transamination conversion of a-aminoadipic

to a-ketoadipic acid

ß-Alanine 
High - possible bowel toxicity due to ß-alanine production

by intestinal bacteria and/or Candida albicans. Possible cause for

food sensitivity reactions when combined with low taurine and high

3-methylhistidine, carnosine, and/or anserine, due to impaired renal

tubular resorption. Supplement B6 (to facilitate amine group

transfer). Bowel detox or high potency Lactobacillus acidolphilus and

Bifidobacteria can help with gut dysbiosis.

ß-Aminoisobutyric acid 
High - indicates lack of a transaminase enzyme

needed to metabolize this substance in the presence of a-KG, an

apparently benign phenomenon, seen in kwashiorkor (chronic protein

deficiency). Excessive folate can elevate this marker, also.

Neurotransmitters from Amino Acids

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