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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 23, 2026
Reviewed October 24, 2026
49 sources · Measured in µmol/L

System: Metabolism & Metabolomics

Plasma amino acidsAmino acid panel · Plasma amino acid analysis · Quantitative plasma amino acids · Branched-chain amino acids · BCAA

A plasma amino acid panel is the validated test for inborn errors of amino acid metabolism, phenylketonuria first among them, with guideline targets in µmol/L; in adults, cohorts of thousands have made a few patterns into real risk markers, chiefly high branched-chain and aromatic amino acids predicting type 2 diabetes (about 36 percent higher risk per standard deviation across eight cohorts) and higher glycine predicting less diabetes and coronary disease, with genetics suggesting that insulin resistance raises the branched-chain amino acids at least as much as they cause it. Low citrulline marks a reduced small-intestinal lining. No trial has treated adults to a plasma amino acid target, and a single low value is not evidence of a dietary deficiency to supplement.

The amino acid panel measures about twenty free amino acids in plasma. Its established use is diagnosing and monitoring inherited metabolic disorders. In adults, the branched-chain amino acids (leucine, isoleucine, valine) and the aromatic ones (phenylalanine, tyrosine) rise with insulin resistance and predict diabetes, glycine runs the other way, and citrulline tracks the mass of the gut lining. Plasma levels follow diet only loosely, and supplementing single amino acids to move a number has little support and, for arginine after a heart attack, a signal of harm.

01 · The scale

Where the laboratory range and the evidence sit.

Two uses are firm. For inherited disorders, the panel diagnoses and monitors disease against guideline targets, such as blood phenylalanine kept at 120 to 360 µmol/L in phenylketonuria; for the small intestine, a fasting citrulline below 20 µmol/L identified permanent intestinal failure in short-bowel syndrome with 92 percent sensitivity. In adult cohorts, high branched-chain and aromatic amino acids predict type 2 diabetes (pooled risk about 1.36 per standard deviation) and, in 27,041 women, cardiovascular disease (1.13 per standard deviation, gone after accounting for insulin resistance), while glycine predicts less diabetes and fewer heart attacks. Genetics points both ways: inherited slower branched-chain breakdown raised diabetes risk, and inherited insulin resistance raised branched-chain levels. No trial has treated adults to an amino acid number, and supplement trials range from no effect to harm.

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  1. Citrulline, one analyte of the panel: below 10 µmol/L was the threshold for intestinal failure in villous atrophy disease

    0 to 10 µmol/L · Crenn 2008

  2. Citrulline, one analyte of the panel: below 20 µmol/L identified permanent intestinal failure in short-bowel syndrome (92 percent sensitivity, 90 percent specificity)

    10 to 20 µmol/L · Crenn 2000; Crenn 2008

  3. Citrulline, one analyte of the panel: between the failure threshold and the healthy average; reduced kidney function can raise citrulline and hide a low gut signal

    20 to 30 µmol/L · Crenn 2008

  4. Citrulline, one analyte of the panel: healthy controls averaged 40 µmol/L, with a standard deviation of 10 (51 adults, fasting)

    30 to 50 µmol/L · Crenn 2000

  5. Citrulline, one analyte of the panel: above the control range; no study on this page assigns a meaning to a high value in a person with normal kidneys

    50 and above µmol/L · Crenn 2000; Crenn 2008

  • Laboratory range
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in µmol/L. Each amino acid is reported separately in µmol/L. Read the panel fasting: citrulline thresholds were set on postabsorptive samples, a whey meal raises plasma amino acids sharply within the hour and a casein meal holds them up for hours, and most plasma metabolites, amino acids among them, follow a daily rhythm. Ask for prompt separation: blood left on its cells at room temperature loses arginine and gains ornithine. Methods differ: mass-spectrometry and ion-exchange results agreed closely for only about half of 21 amino acids in one comparison, so compare a person's results on the same method. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Plasma amino acids measures.

Amino acids are the building blocks of protein and also fuels, nitrogen carriers and signals in their own right, and the plasma panel reports the free amino acids circulating at one moment, not the protein in the diet or in muscle. The test's settled role is in inherited metabolic disease: a 2020 laboratory comparison opens by calling plasma amino acid analysis key to the diagnosis and monitoring of inherited disorders of amino acid synthesis, breakdown and transport, and newborn screening programs measure amino acids with acylcarnitines in a dried blood spot by tandem mass spectrometry, one analysis for many metabolites and many diseases.1,2Grade A

Metabolomics brought the panel into adult risk research. In the Framingham Offspring Study, 201 of 2,422 people with normal glucose developed diabetes over 12 years; matched against controls for age, body mass index and fasting glucose, five amino acids (isoleucine, leucine, valine, tyrosine and phenylalanine) were strongly associated with future diabetes, a combination of three gave more than fivefold the risk in the top quarter, and the result was replicated in a second cohort. A 2016 meta-analysis of eight prospective studies (8,000 people, 1,940 with diabetes) put the risk per standard deviation at 1.36 for isoleucine, leucine and tyrosine, 1.35 for valine and 1.26 for phenylalanine, while glycine (0.89) and glutamine (0.85) were associated with lower risk.3,4Grade B

One analyte has a different meaning altogether. Citrulline is an amino acid not built into proteins and made mainly by the cells lining the small intestine, so its plasma level reads out the mass of that lining. In 57 adults with short-bowel syndrome, postabsorptive citrulline averaged 20 µmol/L against 40 in 51 controls, correlated with remaining small-bowel length (r 0.86), and a threshold of 20 identified permanent intestinal failure with 92 percent sensitivity and 90 percent specificity.5,6Grade B

03 · Origins

Where it came from, and where it sits in the network.

Life builds its proteins from twenty amino acids, and the question of which ones a body must eat is an evolutionary one. Plants and fungi can make all twenty with pathways inherited from their bacterial ancestors; the ability to make nine (phenylalanine, tryptophan, isoleucine, leucine, valine, lysine, histidine, threonine and methionine) was lost in many eukaryotes that evolved to feed on other organisms, and whole-genome analysis shows the nine pathways were lost independently in animals and in several single-celled lineages. A comparative genomic study across phyla describes a broad loss of these pathways, followed in animals by an inability to assimilate inorganic nitrogen, and proposes that it followed relaxed selection once food supplied what the pathways had made. Those nine are the essential amino acids of human nutrition.7,8Grade C

The neat line between essential and nonessential blurs on inspection. A review of human requirements notes that, strictly by metabolism, only lysine, threonine and tryptophan are wholly indispensable and only glutamate and serine wholly dispensable, that a third class of conditionally essential amino acids can be made by the body but in amounts limited by precursors, maturity and illness, and that by function all of them are essential. Amino acids eaten beyond what is built into protein are burned, and their nitrogen must be disposed of through the urea cycle in the liver; inherited defects of that cycle, with an estimated incidence of 1 in 35,000, cause high blood ammonia that can lead to intellectual disability or death, about half of them presenting as newborns.9,10Grade C

The amino acid pool is also a signaling system. Nutrient scarcity has shaped most cellular processes, and cells sense amino acids directly: when food is abundant, nutrient-sensing pathways drive building and storage, and scarcity triggers the release of internal stores through autophagy. Leucine switches on the growth controller mTORC1 by binding the protein Sestrin2, with a dissociation constant of 20 micromolar, the leucine concentration that half-maximally activates mTORC1 in cells; the opposite sensor, the kinase GCN2, detects the absence of one or more amino acids by binding uncharged transfer RNAs. Both pathways answer deprivation by slowing general protein synthesis while increasing the translation of specific messages that restore balance, and both are candidate links between dietary amino acid restriction and longevity in animals.11,12,13Grade C

On the panel, each amino acid sits at a junction of the network. Muscle is the main reservoir of amino acids for the rest of the body when nothing is being absorbed and supplies the liver's raw material for making glucose; in obese volunteers fasting five to six weeks, the branched-chain amino acids rose transiently in the first week, glycine, threonine and serine rose after the fifth day, and alanine fell furthest and fastest, taken up by the liver in larger amounts than all other amino acids combined. Serine, glycine and methionine feed the folate-dependent one-carbon network that makes purines and thymidine, maintains methylation and supports antioxidant defense, which is where homocysteine comes from. Tryptophan and tyrosine compete with the branched-chain amino acids for one transporter into the brain, where they become serotonin and the catecholamines. And gut bacteria make amino acids too: in 277 Danish adults without diabetes, the high branched-chain amino acids of insulin resistance tracked a gut microbiome rich in genes for making them.14,15,16,17,18Grade C

04 · The laboratory range

What a laboratory calls normal.

Laboratories print an interval for each of about twenty amino acids, set by age and method; in one study arginine plus ornithine ran 74 to 148 µmol/L, and fasting citrulline averaged about 40 µmol/L in healthy adults.

The reference intervals are a table, not a number, and they change with age. In 148 healthy children from birth to 18 years measured by ion-exchange chromatography, the 23 amino acids followed five different age patterns: nine fell in the first year of life and then rose through childhood, nine rose steadily from infancy to adolescence, and five followed neither pattern. An adult value read against a child's interval, or the reverse, can look abnormal without being so.19Grade C

Handling moves some analytes more than illness does. Blood left with its cells at room temperature loses arginine and gains ornithine, presumably through the arginase in red cells; their sum stayed constant over the first hour and defined a reference interval of 74 to 148 µmol/L in 20 promptly separated samples, and the ratio of the two suggested that 35 of 91 adult specimens sent to one laboratory (38 percent) had not been separated promptly.20Grade C

The method matters as well. Comparing two commercial tandem mass-spectrometry kits with ion-exchange chromatography for 21 common amino acids, close agreement (concordance above 0.95) held for 10 of the 21 with each kit, and a single-stage mass-spectrometry kit agreed for 6; the authors concluded that ion exchange should no longer be called the gold standard. In 22 healthy adults sampled over about nine weeks by mass spectrometry, within-person variation ran from 9.5 to 32.5 percent and between-person variation from 8.6 to 50.0 percent, with essential amino acids varying less within a person than nonessential ones. Two results from different laboratories, or a single result near a limit, carry less information than they appear to.1,21Grade C

05 · The evidence

What the studies support.

The panel's established use is inherited disease, and phenylketonuria is the model. Phenylalanine hydroxylase deficiency raises blood phenylalanine and was the first inborn error of metabolism found through population screening; the American guideline asks for lifelong treatment with a goal of 120 to 360 µmol/L. The European guideline needs no treatment below 360 µmol/L untreated, treats to age 12 between 360 and 600 and for life above 600, and sets targets of 120 to 360 to age 12 and in pregnancy and 120 to 600 after 12. Newborn screening by tandem mass spectrometry now reads amino acids and acylcarnitines from one blood spot for many disorders at once, and the urea cycle guideline grades its evidence formally for a group of disorders that under-recognition still delays.22,23,2,10Grade A

The adult signal began as an observation about obesity and became a prediction about diabetes. Felig, Marliss and Cahill reported on plasma amino acid levels and insulin secretion in obesity in 1969 (PubMed carries no abstract, so this page cites only the title). Forty years later, metabolomic profiling found a branched-chain amino acid signature that separated obese from lean people and correlated with insulin resistance; in rats, adding branched-chain amino acids to a high-fat diet caused insulin resistance without the weight gain, reversed by the mTOR inhibitor rapamycin, while adding them to standard chow did not. In 1,680 young Finnish adults aged about 32, branched-chain and aromatic amino acids predicted insulin resistance six years later (odds ratio 2.09 for their sum in men) but did not improve prediction beyond established risk factors, and the authors read the diabetes link as at least partly running through insulin resistance.24,25,26Grade B

The prospective cohorts agree with one another. Beyond Framingham, the EPIC-Potsdam study (27,548 adults, 800 incident cases, 163 metabolites) found phenylalanine associated with more diabetes and glycine with less, and the eight-cohort meta-analysis found 26 to 36 percent higher risk per standard deviation for each branched-chain and aromatic amino acid with little heterogeneity for isoleucine. In 27,041 women of the Women's Health Study followed 18.6 years, total branched-chain amino acids carried a hazard ratio of 1.13 per standard deviation for cardiovascular disease, about the same as LDL cholesterol (1.12), stronger in women who developed diabetes first; adjusting for HbA1c and insulin resistance eliminated it.27,4,28Grade B

Mendelian randomization points both ways on causation. Genome-wide study of 16,596 people found variants that slow the main branched-chain breakdown enzyme, and in up to 47,877 cases and 267,694 controls a genetically higher level per standard deviation carried odds ratios for type 2 diabetes of 1.44 for isoleucine, 1.85 for leucine and 1.54 for valine, consistent with a causal role for branched-chain metabolism. In 1,321 Danes with the larger consortium data beside them, a genetic score for higher branched-chain levels was not associated with fasting insulin or insulin resistance, while a genetic score for insulin resistance raised branched-chain levels; those authors concluded that insulin resistance drives the level. Both can be true: impaired breakdown may add risk, and insulin resistance itself raises the number.29,30Grade B

Glycine runs the other way. Beside its inverse association with diabetes in the meta-analysis and in EPIC-Potsdam, plasma glycine in 4,109 Norwegians undergoing angiography for suspected stable angina predicted fewer heart attacks over 7.4 years (616 events; hazard ratio 0.89 per standard deviation after adjustment for standard risk factors). A genome-wide study of glycine in 80,003 people found 27 loci, a genetic association of higher glycine with lower coronary risk, partly through blood pressure, a weaker genetic link to diabetes, and a strong inverse effect of high insulin on glycine, which suggests that the diabetes association reflects insulin resistance lowering glycine.4,27,31,32Grade B

Other patterns are earlier in their evidence. In 1,015 Framingham and 746 Malmö participants, insulin resistance traits went with lower glutamine and higher glutamate; a high glutamine to glutamate ratio predicted less diabetes in Framingham (odds ratio 0.79) but not in Malmö, and glutamine given to mice improved glucose tolerance. Tryptophan is broken down mostly along the kynurenine pathway, which inflammation and exercised muscle both regulate; in 7,015 Norwegians followed 14 years with 1,496 deaths, a higher kynurenine to tryptophan ratio and several kynurenines predicted higher mortality, and tryptophan lower mortality, with hazard ratios of 1.19 to 1.60 and 0.73 to 0.87 between top and bottom quarters. These are markers of inflammation and metabolism in cohorts, not targets.33,34,35Grade C

Citrulline is the one adult analyte with a validated clinical threshold. Across more than 500 patients with short-bowel syndrome, villous atrophy, Crohn's disease, chemotherapy or radiation injury to the bowel and small-bowel transplantation, a lower citrulline tracked a reduced enterocyte mass regardless of nutritional and inflammatory status; the threshold for intestinal failure is 10 µmol/L in villous atrophy and 20 in short-bowel syndrome, and reduced kidney function can raise the value.6,5Grade B

What the cohorts do not support is reading a single low amino acid as a dietary deficiency. In 392 British men aged 30 to 49, vegans ate up to 47 percent less of most amino acids than meat-eaters, yet only 6 of 21 plasma amino acids differed by diet group, by minus 13 to plus 16 percent, glycine was highest in vegans, and the authors noted that plasma differences were less marked than and did not mirror intake. In 12 obese adults with prediabetes, 20 g a day of branched-chain amino acids for four weeks did not change their plasma levels. The plasma level is set by synthesis, breakdown, insulin, muscle and the gut as much as by the plate.36,37,9Grade C

The supplement trials with outcomes are small, mixed, and in one case harmful. In 153 people after a first ST-elevation heart attack, L-arginine 3 g three times a day for six months did not improve vascular stiffness or heart function, and 6 people on arginine (8.6 percent) died against none on placebo, so enrollment was closed. Taurine lowered blood pressure by about 3 mmHg in a meta-analysis of 7 studies with 103 participants. Tryptophan and 5-hydroxytryptophan beat placebo for depression in the two adequate trials (64 patients) out of 108 located, evidence the Cochrane reviewers called insufficient. Glycine with N-acetylcysteine for 16 weeks in 12 older adults against 12 on placebo improved glutathione and several measures of aging biology, as its authors report; it is a pilot-sized trial.38,39,40,41Grade C

The longevity claims rest on animals. Cutting dietary methionine from 0.86 to 0.17 percent of the diet lengthened the life of male rats by 30 percent while abolishing growth. In 26 obese adults with metabolic syndrome, 16 weeks of methionine restriction raised fat oxidation and lowered liver fat, while insulin sensitivity improved equally on both diets. Taurine falls with age in mice, monkeys and humans; supplementing it lengthened health span and life span in mice and health span in monkeys, and in humans lower taurine correlated with age-related diseases, which the authors say warrants trials. None of this tells a person what their plasma methionine or taurine should be.42,43,44Grade C

No trial has treated adults to a plasma amino acid target and measured an outcome. The trials that changed branched-chain intake moved insulin secretion or not, without a defined number to aim for, and the guideline targets that exist belong to inherited disorders. Any adult zone for an individual amino acid is a judgment, and this page offers none.45,37,22Grade D

06 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Insulin sensitivity and weight loss

    the branched-chain cluster falls as insulin resistance improves

    Genetics suggests insulin resistance drives the branched-chain level up, and the weight-loss data fit. In 500 adults who lost at least 4 kg in a weight-loss trial (mean 8.67 kg), a baseline cluster of branched-chain amino acids and their breakdown products correlated with insulin resistance (r 0.50) and predicted how much insulin resistance improved, independent of how much weight was lost, and the finding held in a separate group of 22. The number moves with the metabolism behind it.46,30Grade B

  • Resistance and aerobic training

    raises glycine; the fall in branched-chain amino acids tracked improved insulin sensitivity

    In nine overweight, untrained, insulin-resistant adults given six months of combined aerobic and resistance training, insulin sensitivity rose. Plasma branched-chain amino acids did not change on average, but within each person the fall in their sum was the best metabolic predictor of improvement, and glycine was higher after training and in lean controls. The authors propose more efficient clearance of branched-chain breakdown products through glycine conjugation as the link.47Grade C

  • Protein intake and source

    moves several amino acids modestly and less than intake suggests

    Diet moves the panel less than intuition says: vegans ate up to 47 percent less of most amino acids than meat-eaters but differed in only 6 of 21 plasma levels, by no more than about 16 percent. Protein type changes the after-meal curve, with whey producing a sharp, short rise in plasma amino acids and casein a prolonged moderate plateau. In people with type 2 diabetes, four weeks of a diet low in branched-chain amino acids lowered fasting levels by 17 percent and the after-meal rise by 62 percent, lowered meal-driven insulin secretion by 28 percent and raised an oral glucose sensitivity index by 24 percent, without changing insulin sensitivity under clamp. Protein dose, leucine and muscle are covered on the protein intake entry.36,48,45Grade C

  • Fasting state

    a meal raises it within the hour; prolonged fasting reshapes it

    The panel reads differently fed and fasted. A single protein meal raises plasma amino acids within the hour, and in prolonged fasting the pattern turns over: branched-chain amino acids rise transiently in the first week, glycine, threonine and serine climb after the fifth day, and alanine falls as the liver takes it up to make glucose. A draw after breakfast, or after several days of fasting, reports the meal or the fast.48,15Grade C

  • Sleep and time of day

    most metabolites follow a daily rhythm; a lost night raised tryptophan and taurine

    In 12 healthy young men sampled every two hours over 48 hours under controlled light, meals and posture, 109 of 171 plasma metabolites showed a daily rhythm, and during a night without sleep 27 rose compared with sleep, among them tryptophan, serotonin and taurine. The hour of the draw and the night before it are part of the result.49Grade C

  • The gut microbiome

    bacterial amino acid metabolism contributes to the branched-chain level

    In 277 Danish adults without diabetes, the high branched-chain amino acids of insulin resistance tracked a gut microbiome enriched in genes for making them and poor in genes for taking them up, driven mainly by two species; in mice, one of those species induced insulin resistance and raised circulating branched-chain amino acids. This is one population and a mouse experiment, and it is not yet a treatment.18Grade C

07 · Reading it well

Caveats, and what belongs with a physician.

A panel is twenty-odd tests at once, and twenty-odd chances for one value to fall outside its interval by chance. Within-person variation of 9.5 to 32.5 percent means a repeat sample can differ meaningfully from the first, and agreement between methods held closely for only about half the amino acids in one comparison. A single result outside the interval, on its own, is a reason to repeat the test on the same method, not a finding.21,1Grade C

Preanalytical errors look like biology. Delayed separation lowers arginine and raises ornithine, and in one laboratory over a third of adult specimens showed that signature. Fasting, the time of day and a recent protein meal all change the panel. A result drawn after a meal, separated late, or measured by a different method than the last one is not comparable with it.20,49,48Grade C

The cohort associations are with standardized units, not with a number on a report. The diabetes and cardiovascular figures above are per standard deviation, or between the top and bottom of the cohort's own distribution, measured on research platforms, and the young Finnish cohort found that adding amino acids did not improve risk prediction beyond established factors. A branched-chain value at the top of a laboratory interval does not carry a known hazard ratio.4,26,28Grade B

Kidney function and age change the meaning. Reduced kidney function can raise citrulline and mask a reduced gut lining, and children's amino acids follow several age patterns that differ from adults'. Nothing on this page interprets a child's panel, which belongs with a pediatric metabolic specialist.6,19Grade C

Supplements change the number without telling you anything about the person, and some carry risk. Arginine after a heart attack went with excess deaths in the one trial that tested it, and the Cochrane review of tryptophan and 5-hydroxytryptophan noted that their possible link to eosinophilia-myalgia syndrome had not been resolved. Anyone taking a single amino acid should say so before the panel is read.38,40Grade C

See a physician

  • A markedly abnormal amino acid at any age, especially with developmental delay, seizures, recurrent vomiting or confusion after protein meals, or a family history of a metabolic disorder, which calls for a metabolic specialist rather than a diet change.
  • Confusion, unusual drowsiness or vomiting after a high-protein meal or during an illness, which can be a sign of high blood ammonia and is urgent.
  • A woman with phenylketonuria, or with a history of it, who is planning a pregnancy, since the guidelines set lower phenylalanine targets before conception and during pregnancy.
  • A low citrulline together with chronic diarrhea, weight loss or known bowel disease, which belongs with a gastroenterologist.
  • Anyone who has had a heart attack and is considering arginine, or anyone taking tryptophan or 5-hydroxytryptophan alongside an antidepressant, which should be reviewed with the prescribing physician first.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

08 · Open questions

What the literature does not settle.

  • No trial has treated adults to a plasma amino acid target and measured an outcome; whether lowering the branched-chain cluster by any means other than improving insulin sensitivity reduces diabetes or heart disease is untested.
  • The two Mendelian randomization studies point in opposite directions, impaired branched-chain breakdown raising diabetes risk in one and insulin resistance raising branched-chain levels in the other; how much of the association runs each way is unresolved.
  • The glycine and coronary disease link has genetic support, partly through blood pressure, but no trial has tested whether raising glycine prevents heart disease, and the glycine with N-acetylcysteine trial in older adults was pilot-sized.
  • Whether the gut microbiome's contribution to branched-chain amino acids is large enough in people to be a lever, beyond one Danish population and a mouse experiment, is unknown.
  • Taurine's role in aging rests on animal lifespan studies and human correlations; whether a lower taurine in an older person is a cause, a marker of less activity and illness, or neither has not been tested.
  • Adult reference intervals by mass spectrometry, with fasting and handling standardized, are not established in the way pediatric ones are; laboratories still differ by method.

09 · In practice

How Dr. Tagge reads it in his own practice.

I read an amino acid panel as a pattern, not as twenty separate deficiencies. One marker is a clue, three are a story, and the story I see most often is metabolic: a high branched-chain and aromatic cluster sitting beside a high fasting insulin and a high triglyceride is insulin resistance written in a different alphabet, and the genetics suggest that the insulin resistance is pushing the number, so I treat the insulin resistance and leave the protein that muscle needs alone. A low glycine or serine makes me ask about the one-carbon network, folate, B12 and homocysteine, and about sleep, before anyone reaches for a capsule. Citrulline tells me something about the lining of the gut, and I read it beside kidney function. I do not supplement single amino acids to move a number; the arginine trial after heart attack is the reason I am careful, and the other trials are small. I want the panel drawn fasting, separated promptly and run on the same method each time, and read beside protein intake, muscle, fasting insulin, homocysteine and B12. Where I am ahead of the evidence I will say so: the cohorts show these patterns predicting disease, and I use them as an early signal of metabolic drift, but no trial has shown that treating to an amino acid number prevents anything, so the panel informs what I do about the metabolism and never sets a target of its own.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

10

Questions

11 · Sources

49 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    Carling RS, McDonald BA, Austin D, Burden D, Correia J, Leung J, Mayers B, John C. Challenging the status quo: A comparison of ion exchange chromatography with liquid chromatography-mass spectrometry and liquid chromatography-tandem mass spectrometry methods for the measurement of amino acids in human plasma. Annals of Clinical Biochemistry. 2020. PMID 32438818. DOI 10.1177/0004563220933303.

    Laboratory method study · Plasma amino acid analysis is key to diagnosing and monitoring inherited disorders of amino acid synthesis, catabolism and transport; two LC-MS/MS kits agreed closely (concordance above 0.95) with ion-exchange chromatography for 10 of 21 amino acids, an LC-MS kit for 6; ion exchange should no longer be called the gold standard.

  2. 2.

    Chace DH, Kalas TA, Naylor EW. Use of tandem mass spectrometry for multianalyte screening of dried blood specimens from newborns. Clinical Chemistry. 2003. PMID 14578311. DOI 10.1373/clinchem.2003.022178.

    Review · Tandem mass spectrometry is replacing one-analysis, one-metabolite, one-disease newborn screening with a one-analysis, many-metabolites, many-diseases approach, measuring amino acids and acylcarnitines in dried blood spots.

  3. 3.

    Wang TJ, Larson MG, Vasan RS, Cheng S, Rhee EP, McCabe E, et al.. Metabolite profiles and the risk of developing diabetes. Nature Medicine. 2011. PMID 21423183. DOI 10.1038/nm.2307.

    Prospective cohort · Among 2,422 normoglycemic Framingham participants followed 12 years, 201 developed diabetes; isoleucine, leucine, valine, tyrosine and phenylalanine were strongly associated with future diabetes in cases matched for age, BMI and fasting glucose; a three-amino-acid combination gave more than fivefold risk in the top quartile; replicated in a second cohort.

  4. 4.

    Guasch-Ferré M, Hruby A, Toledo E, Clish CB, Martínez-González MA, Salas-Salvadó J, Hu FB. Metabolomics in Prediabetes and Diabetes: A Systematic Review and Meta-analysis. Diabetes Care. 2016. PMID 27208380. DOI 10.2337/dc15-2251.

    Systematic review and meta-analysis · Across eight prospective studies (8,000 people, 1,940 with type 2 diabetes), risk per SD was 1.36 for isoleucine, 1.36 leucine, 1.35 valine, 1.36 tyrosine and 1.26 phenylalanine; glycine (0.89) and glutamine (0.85) were inversely associated.

  5. 5.

    Crenn P, Coudray-Lucas C, Thuillier F, Cynober L, Messing B. Postabsorptive plasma citrulline concentration is a marker of absorptive enterocyte mass and intestinal failure in humans. Gastroenterology. 2000. PMID 11113071. DOI 10.1053/gast.2000.20227.

    Prospective cohort · In 57 adults with short-bowel syndrome, citrulline was 20 ± 13 against 40 ± 10 µmol/L in 51 controls, correlated with small-bowel length (r 0.86), and a 20 µmol/L threshold classified permanent intestinal failure with 92 percent sensitivity and 90 percent specificity.

  6. 6.

    Crenn P, Messing B, Cynober L. Citrulline as a biomarker of intestinal failure due to enterocyte mass reduction. Clinical Nutrition. 2008. PMID 18440672. DOI 10.1016/j.clnu.2008.02.005.

    Review · Citrulline (plasma about 40 µmol/L) is made mainly by small-bowel enterocytes; in more than 500 patients a lower level tracked reduced enterocyte mass independent of nutrition and inflammation; thresholds for intestinal failure are 10 µmol/L in villous atrophy and 20 in short-bowel syndrome; reduced renal function can raise it.

  7. 7.

    Payne SH, Loomis WF. Retention and loss of amino acid biosynthetic pathways based on analysis of whole-genome sequences. Eukaryotic Cell. 2006. PMID 16467468. DOI 10.1128/EC.5.2.272-276.2006.

    Review · Plants and fungi make all 20 amino acids using pathways inherited from bacteria; the ability to make nine (Phe, Trp, Ile, Leu, Val, Lys, His, Thr, Met) was lost independently in animals and several protists that feed on other organisms.

  8. 8.

    Guedes RL, Prosdocimi F, Fernandes GR, Moura LK, Ribeiro HA, Ortega JM. Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution. BMC Genomics. 2011. PMID 22369087. DOI 10.1186/1471-2164-12-S4-S2.

    Review · Comparative genomics shows a broad loss of essential amino acid biosynthesis in eukaryotes followed in derived metazoans by loss of nitrogen assimilation, a Great Deletion probably linked to relaxed selection under heterotrophy.

  9. 9.

    Reeds PJ. Dispensable and indispensable amino acids for humans. Journal of Nutrition. 2000. PMID 10867060. DOI 10.1093/jn/130.7.1835S.

    Review · Metabolically only lysine, threonine and tryptophan are wholly indispensable and only glutamate and serine wholly dispensable; a conditionally essential class depends on precursors, maturity and health; functionally all amino acids are essential.

  10. 10.

    Häberle J, Burlina A, Chakrapani A, Dixon M, Karall D, Lindner M, et al.. Suggested guidelines for the diagnosis and management of urea cycle disorders: First revision. Journal of Inherited Metabolic Disease. 2019. PMID 30982989. DOI 10.1002/jimd.12100.

    Guideline · Urea cycle disorders, estimated incidence 1 in 35,000, cause hyperammonemia of neonatal (about 50 percent) or late onset that can lead to intellectual disability or death; under-recognition and delayed diagnosis remain widespread; GRADE-scored European consensus.

  11. 11.

    Efeyan A, Comb WC, Sabatini DM. Nutrient-sensing mechanisms and pathways. Nature. 2015. PMID 25592535. DOI 10.1038/nature14190.

    Review · Nutrient scarcity has shaped the evolution of most cellular processes; amino acid and other nutrient sensors engage anabolism and storage in abundance and autophagy in scarcity, and are commonly deregulated in metabolic disease.

  12. 12.

    Wolfson RL, Chantranupong L, Saxton RA, Shen K, Scaria SM, Cantor JR, Sabatini DM. Sestrin2 is a leucine sensor for the mTORC1 pathway. Science. 2016. PMID 26449471. DOI 10.1126/science.aab2674.

    Laboratory method study · Leucine, but not arginine, binds Sestrin2 with a dissociation constant of 20 micromolar, the concentration that half-maximally activates mTORC1, and that binding is required for leucine to activate mTORC1 in cells.

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    Gallinetti J, Harputlugil E, Mitchell JR. Amino acid sensing in dietary-restriction-mediated longevity: roles of signal-transducing kinases GCN2 and TOR. Biochemical Journal. 2013. PMID 23216249. DOI 10.1042/BJ20121098.

    Review · GCN2 senses the absence of amino acids by binding uncharged tRNAs and TOR is activated by amino acids such as leucine; both respond to deprivation by inhibiting general translation while increasing translation of specific mRNAs, and may link amino acid restriction to longevity.

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    Wolfe RR. The underappreciated role of muscle in health and disease. American Journal of Clinical Nutrition. 2006. PMID 16960159. DOI 10.1093/ajcn/84.3.475.

    Review · Muscle is the principal reservoir of amino acids for protein synthesis in vital organs when none are being absorbed, and supplies the liver's gluconeogenic precursors.

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    Felig P, Owen OE, Wahren J, Cahill GF Jr. Amino acid metabolism during prolonged starvation. Journal of Clinical Investigation. 1969. PMID 5773094. DOI 10.1172/JCI106017.

    Laboratory method study · In obese subjects fasting 5 to 6 weeks, valine, leucine, isoleucine and methionine rose transiently in week one, glycine, threonine and serine rose after day five, and alanine fell most and fastest, extracted by the splanchnic bed more than all other amino acids combined.

  16. 16.

    Ducker GS, Rabinowitz JD. One-Carbon Metabolism in Health and Disease. Cell Metabolism. 2017. PMID 27641100. DOI 10.1016/j.cmet.2016.08.009.

    Review · Folate-mediated one-carbon metabolism supports purine and thymidine synthesis, amino acid balance of glycine, serine and methionine, epigenetic maintenance and redox defense, with mitochondrial reactions producing glycine and NADPH.

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    Fernstrom JD. Large neutral amino acids: dietary effects on brain neurochemistry and function. Amino Acids. 2013. PMID 22677921. DOI 10.1007/s00726-012-1330-y.

    Review · Tryptophan, tyrosine and the branched-chain amino acids compete for one blood-brain barrier transporter; raising blood BCAA lowers brain tryptophan and tyrosine uptake and serotonin and catecholamine synthesis.

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    Pedersen HK, Gudmundsdottir V, Nielsen HB, Hyotylainen T, Nielsen T, Jensen BA, et al.. Human gut microbes impact host serum metabolome and insulin sensitivity. Nature. 2016. PMID 27409811. DOI 10.1038/nature18646.

    Cross-sectional study · In 277 non-diabetic Danes, raised serum BCAA in insulin resistance correlated with a gut microbiome enriched in BCAA biosynthesis genes and poor in BCAA transporters, driven by Prevotella copri and Bacteroides vulgatus; P. copri induced insulin resistance and raised BCAA in mice.

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    Lepage N, McDonald N, Dallaire L, Lambert M. Age-specific distribution of plasma amino acid concentrations in a healthy pediatric population. Clinical Chemistry. 1997. PMID 9439460.

    Laboratory method study · In 148 healthy children aged 0 to 18 measured by ion-exchange chromatography, 23 amino acids followed five age profiles: nine fell in the first year then rose, nine rose steadily, five followed neither.

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    Nuttall KL, Chen M, Komaromy-Hiller G. Delayed separation and the plasma amino acids arginine and ornithine. Annals of Clinical and Laboratory Science. 1998. PMID 9846202.

    Laboratory method study · Plasma left on cells at room temperature loses arginine and gains ornithine; their sum is stable over the first hour with a reference interval of 74 to 148 µmol/L (n = 20); 35 of 91 adult specimens (38 percent) showed a ratio suggesting delayed processing.

  21. 21.

    Ercan M, Akbulut ED, Caniklioğlu A, Fırat Oğuz E, Dülgeroğlu Y, Avcı E, Ercan Ş. Sex-based estimation of biological variation in plasma-free amino acid concentrations among healthy adults. Journal of Mass Spectrometry and Advances in the Clinical Lab. 2025. PMID 40433056. DOI 10.1016/j.jmsacl.2025.04.010.

    Laboratory method study · In 22 healthy adults sampled over about nine weeks by LC-MS/MS, within-subject variation ranged from 9.5 to 32.5 percent and between-subject variation from 8.6 to 50.0 percent, lower within subjects for essential than nonessential amino acids.

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    Vockley J, Andersson HC, Antshel KM, Braverman NE, Burton BK, Frazier DM, et al.; ACMG Therapeutics Committee. Phenylalanine hydroxylase deficiency: diagnosis and management guideline. Genetics in Medicine. 2014. PMID 24385074. DOI 10.1038/gim.2013.157.

    Guideline · Phenylalanine hydroxylase deficiency was the first inborn error identified through population screening; treatment must be lifelong with a goal of blood phenylalanine 120 to 360 µmol/L.

  23. 23.

    van Spronsen FJ, van Wegberg AM, Ahring K, Bélanger-Quintana A, Blau N, Bosch AM, et al.. Key European guidelines for the diagnosis and management of patients with phenylketonuria. Lancet Diabetes and Endocrinology. 2017. PMID 28082082. DOI 10.1016/S2213-8587(16)30320-5.

    Guideline · No treatment if untreated phenylalanine is below 360 µmol/L; treat to age 12 between 360 and 600 and for life above 600; targets 120 to 360 µmol/L to age 12 and in maternal PKU, 120 to 600 after 12.

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    Felig P, Marliss E, Cahill GF Jr. Plasma amino acid levels and insulin secretion in obesity. New England Journal of Medicine. 1969. PMID 5809519. DOI 10.1056/NEJM196910092811503.

    Cross-sectional study · The early report relating plasma amino acid levels to insulin secretion in obesity; PubMed carries no abstract, and the entry cites it by title only.

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    Newgard CB, An J, Bain JR, Muehlbauer MJ, Stevens RD, Lien LF, et al.. A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance. Cell Metabolism. 2009. PMID 19356713. DOI 10.1016/j.cmet.2009.02.002.

    Laboratory method study · A BCAA-related metabolite signature separated obese from lean humans and correlated with insulin resistance; in rats, BCAA added to a high-fat diet caused insulin resistance despite low weight gain, reversed by rapamycin, while BCAA added to chow did not.

  26. 26.

    Würtz P, Soininen P, Kangas AJ, Rönnemaa T, Lehtimäki T, Kähönen M, Viikari JS, Raitakari OT, Ala-Korpela M. Branched-chain and aromatic amino acids are predictors of insulin resistance in young adults. Diabetes Care. 2013. PMID 23129134. DOI 10.2337/dc12-0895.

    Prospective cohort · In 1,680 Young Finns aged about 32, branched-chain and aromatic amino acids predicted 6-year insulin resistance (sum OR 2.09, 1.38 to 3.17, in men) but did not improve risk discrimination; the diabetes link is at least partly mediated through insulin resistance.

  27. 27.

    Floegel A, Stefan N, Yu Z, Mühlenbruch K, Drogan D, Joost HG, et al.. Identification of serum metabolites associated with risk of type 2 diabetes using a targeted metabolomic approach. Diabetes. 2013. PMID 23043162. DOI 10.2337/db12-0495.

    Prospective cohort · In EPIC-Potsdam (27,548 adults; 800 incident cases; subcohort 2,282; 163 metabolites), phenylalanine was associated with higher and glycine with lower risk of type 2 diabetes.

  28. 28.

    Tobias DK, Lawler PR, Harada PH, Demler OV, Ridker PM, Manson JE, Cheng S, Mora S. Circulating Branched-Chain Amino Acids and Incident Cardiovascular Disease in a Prospective Cohort of US Women. Circulation: Genomic and Precision Medicine. 2018. PMID 29572205. DOI 10.1161/CIRCGEN.118.002157.

    Prospective cohort · In 27,041 women followed a mean 18.6 years (2,207 events), total BCAA carried HR 1.13 (1.08 to 1.18) per SD for CVD, comparable to LDL-C (1.12), greater in women who developed diabetes first; adjustment for HbA1c and insulin resistance eliminated the association.

  29. 29.

    Lotta LA, Scott RA, Sharp SJ, Burgess S, Luan J, Tillin T, et al.. Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis. PLoS Medicine. 2016. PMID 27898682. DOI 10.1371/journal.pmed.1002179.

    Mendelian randomization · With GWAS in 16,596 people (strongest signal near PPM1K) and up to 47,877 cases and 267,694 controls, a genetically higher level per SD gave type 2 diabetes ORs of 1.44 for isoleucine, 1.85 leucine and 1.54 valine, consistent with a causal role of BCAA metabolism.

  30. 30.

    Mahendran Y, Jonsson A, Have CT, Allin KH, Witte DR, Jørgensen ME, et al.. Genetic evidence of a causal effect of insulin resistance on branched-chain amino acid levels. Diabetologia. 2017. PMID 28184960. DOI 10.1007/s00125-017-4222-6.

    Mendelian randomization · In 1,321 ADDITION-PRO participants with consortium GWAS data, a BCAA-raising genetic score was not associated with fasting insulin or HOMA-IR, while an insulin-resistance genetic score raised BCAA levels; insulin resistance drives higher fasting BCAA.

  31. 31.

    Ding Y, Svingen GF, Pedersen ER, Gregory JF, Ueland PM, Tell GS, Nygård OK. Plasma Glycine and Risk of Acute Myocardial Infarction in Patients With Suspected Stable Angina Pectoris. Journal of the American Heart Association. 2015. PMID 26722126. DOI 10.1161/JAHA.115.002621.

    Prospective cohort · In 4,109 patients undergoing angiography for suspected stable angina, followed a median 7.4 years with 616 myocardial infarctions, plasma glycine carried HR 0.89 (0.82 to 0.98) per SD after adjustment for standard risk factors.

  32. 32.

    Wittemans LBL, Lotta LA, Oliver-Williams C, Stewart ID, Surendran P, Karthikeyan S, et al.. Assessing the causal association of glycine with risk of cardio-metabolic diseases. Nature Communications. 2019. PMID 30837465. DOI 10.1038/s41467-019-08936-1.

    Mendelian randomization · A glycine GWAS in 80,003 people found 27 loci; glycine was genetically associated with lower coronary heart disease risk, partly through blood pressure; genetic evidence for diabetes was weaker, with a strong inverse genetic effect of hyperinsulinemia on glycine.

  33. 33.

    Cheng S, Rhee EP, Larson MG, Lewis GD, McCabe EL, Shen D, et al.. Metabolite profiling identifies pathways associated with metabolic risk in humans. Circulation. 2012. PMID 22496159. DOI 10.1161/CIRCULATIONAHA.111.067827.

    Prospective cohort · In Framingham (1,015) and Malmö (746), insulin resistance traits went with lower glutamine and higher glutamate; a high glutamine to glutamate ratio predicted lower incident diabetes in Framingham (OR 0.79) but not Malmö; glutamine improved glucose tolerance in mice.

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    Cervenka I, Agudelo LZ, Ruas JL. Kynurenines: Tryptophan's metabolites in exercise, inflammation, and mental health. Science. 2017. PMID 28751584. DOI 10.1126/science.aaf9794.

    Review · Kynurenines from tryptophan breakdown regulate host-microbiome signaling, immunity and neuronal excitability; peripheral inflammation can raise brain kynurenine, and exercised skeletal muscle clears kynurenine.

  35. 35.

    Zuo H, Ueland PM, Ulvik A, Eussen SJ, Vollset SE, Nygård O, et al.. Plasma Biomarkers of Inflammation, the Kynurenine Pathway, and Risks of All-Cause, Cancer, and Cardiovascular Disease Mortality: The Hordaland Health Study. American Journal of Epidemiology. 2016. PMID 26823439. DOI 10.1093/aje/kwv242.

    Prospective cohort · In 7,015 Norwegians with 1,496 deaths over a median 14 years, the kynurenine to tryptophan ratio and several kynurenines predicted higher mortality and tryptophan lower, with top versus bottom quartile HRs of 1.19 to 1.60 and 0.73 to 0.87.

  36. 36.

    Schmidt JA, Rinaldi S, Scalbert A, Ferrari P, Achaintre D, Gunter MJ, Appleby PN, Key TJ, Travis RC. Plasma concentrations and intakes of amino acids in male meat-eaters, fish-eaters, vegetarians and vegans: a cross-sectional analysis in the EPIC-Oxford cohort. European Journal of Clinical Nutrition. 2016. PMID 26395436. DOI 10.1038/ejcn.2015.144.

    Cross-sectional study · In 392 men aged 30 to 49, intakes of all 18 dietary amino acids differed by diet (up to 47 percent lower in vegans), but only 6 of 21 plasma amino acids differed, by minus 13 to plus 16 percent; glycine was highest in vegans; plasma differences did not mirror intake.

  37. 37.

    Woo SL, Yang J, Hsu M, Yang A, Zhang L, Lee RP, et al.. Effects of branched-chain amino acids on glucose metabolism in obese, prediabetic men and women: a randomized, crossover study. American Journal of Clinical Nutrition. 2019. PMID 31005973. DOI 10.1093/ajcn/nqz024.

    Randomized trial · In 12 obese adults with prediabetes, 20 g BCAA daily for 4 weeks against low-BCAA protein did not impair glucose metabolism and did not change circulating leucine, valine or isoleucine.

  38. 38.

    Schulman SP, Becker LC, Kass DA, Champion HC, Terrin ML, Forman S, et al.. L-arginine therapy in acute myocardial infarction: the Vascular Interaction With Age in Myocardial Infarction (VINTAGE MI) randomized clinical trial. JAMA. 2006. PMID 16391217. DOI 10.1001/jama.295.1.58.

    Randomized trial · In 153 patients after a first ST-elevation MI, L-arginine 3 g three times daily for 6 months did not improve vascular stiffness or ejection fraction; 6 (8.6 percent) died on arginine against none on placebo, and enrollment was closed.

  39. 39.

    Waldron M, Patterson SD, Tallent J, Jeffries O. The Effects of Oral Taurine on Resting Blood Pressure in Humans: a Meta-Analysis. Current Hypertension Reports. 2018. PMID 30006901. DOI 10.1007/s11906-018-0881-z.

    Systematic review and meta-analysis · Across seven studies with 103 participants, oral taurine at 1 to 6 g a day lowered systolic and diastolic blood pressure by a mean of about 3 mmHg, with no adverse events reported.

  40. 40.

    Shaw K, Turner J, Del Mar C. Tryptophan and 5-hydroxytryptophan for depression. Cochrane Database of Systematic Reviews. 2002. PMID 11869656. DOI 10.1002/14651858.CD003198.

    Systematic review and meta-analysis · Of 108 trials located, two with 64 patients were of adequate quality; they favored tryptophan or 5-HTP over placebo (Peto OR 4.10) but the evidence was insufficient to be conclusive, and a possible link to eosinophilia-myalgia syndrome was unresolved.

  41. 41.

    Kumar P, Liu C, Suliburk J, Hsu JW, Muthupillai R, Jahoor F, Minard CG, Taffet GE, Sekhar RV. Supplementing Glycine and N-Acetylcysteine (GlyNAC) in Older Adults Improves Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Physical Function, and Aging Hallmarks: A Randomized Clinical Trial. Journals of Gerontology Series A. 2023. PMID 35975308. DOI 10.1093/gerona/glac135.

    Randomized trial · Twenty-four older adults were randomized to glycine with N-acetylcysteine or alanine placebo (12 each) for 16 weeks; the authors report that the combination, not placebo, improved glutathione, oxidative stress, mitochondrial function, inflammation and physical function.

  42. 42.

    Orentreich N, Matias JR, DeFelice A, Zimmerman JA. Low methionine ingestion by rats extends life span. Journal of Nutrition. 1993. PMID 8429371. DOI 10.1093/jn/123.2.269.

    Laboratory method study · Lifelong reduction of dietary methionine from 0.86 to 0.17 percent gave male Fischer 344 rats a 30 percent longer life span and abolished growth, independent of food restriction.

  43. 43.

    Plaisance EP, Greenway FL, Boudreau A, Hill KL, Johnson WD, Krajcik RA, et al.. Dietary methionine restriction increases fat oxidation in obese adults with metabolic syndrome. Journal of Clinical Endocrinology and Metabolism. 2011. PMID 21346062. DOI 10.1210/jc.2010-2493.

    Randomized trial · In 26 obese adults with metabolic syndrome on a methionine-restricted diet with placebo (12) or methionine capsules (14) for 16 weeks, insulin sensitivity improved comparably in both groups, while restriction raised fat oxidation and reduced liver fat.

  44. 44.

    Singh P, Gollapalli K, Mangiola S, Schranner D, Yusuf MA, Chamoli M, et al.. Taurine deficiency as a driver of aging. Science. 2023. PMID 37289866. DOI 10.1126/science.abn9257.

    Laboratory method study · Circulating taurine declines with age in mice, monkeys and humans; supplementation increased health span and life span in mice and health span in monkeys; in humans lower taurine correlated with age-related diseases; the authors call for human trials.

  45. 45.

    Karusheva Y, Koessler T, Strassburger K, Markgraf D, Mastrototaro L, Jelenik T, et al.. Short-term dietary reduction of branched-chain amino acids reduces meal-induced insulin secretion and modifies microbiome composition in type 2 diabetes: a randomized controlled crossover trial. American Journal of Clinical Nutrition. 2019. PMID 31667519. DOI 10.1093/ajcn/nqz191.

    Randomized trial · In well-controlled type 2 diabetes, 4 weeks of a BCAA-reduced diet lowered fasting BCAA 17 percent and meal-test BCAA 62 percent, lowered meal-derived insulin secretion 28 percent and raised the oral glucose sensitivity index 24 percent, with no change in clamp insulin sensitivity.

  46. 46.

    Shah SH, Crosslin DR, Haynes CS, Nelson S, Turer CB, Stevens RD, et al.. Branched-chain amino acid levels are associated with improvement in insulin resistance with weight loss. Diabetologia. 2012. PMID 22065088. DOI 10.1007/s00125-011-2356-5.

    Prospective cohort · In 500 trial participants who lost at least 4 kg (mean 8.67), a baseline BCAA factor correlated with HOMA-IR (r 0.50) and predicted improvement in HOMA-IR independent of weight lost, validated in 22 others.

  47. 47.

    Glynn EL, Piner LW, Huffman KM, Slentz CA, Elliot-Penry L, AbouAssi H, et al.. Impact of combined resistance and aerobic exercise training on branched-chain amino acid turnover, glycine metabolism and insulin sensitivity in overweight humans. Diabetologia. 2015. PMID 26254576. DOI 10.1007/s00125-015-3705-6.

    Prospective cohort · In nine overweight insulin-resistant adults, six months of aerobic and resistance training raised insulin sensitivity; plasma BCAA did not change on average, but the individual fall in BCAA sum best predicted improvement, and glycine was higher after training.

  48. 48.

    Boirie Y, Dangin M, Gachon P, Vasson MP, Maubois JL, Beaufrère B. Slow and fast dietary proteins differently modulate postprandial protein accretion. Proceedings of the National Academy of Sciences of the United States of America. 1997. PMID 9405716. DOI 10.1073/pnas.94.26.14930.

    Laboratory method study · In healthy adults, a whey meal produced a dramatic but short rise in plasma amino acids and a casein meal a prolonged plateau of moderate hyperaminoacidemia.

  49. 49.

    Davies SK, Ang JE, Revell VL, Holmes B, Mann A, Robertson FP, et al.. Effect of sleep deprivation on the human metabolome. Proceedings of the National Academy of Sciences of the United States of America. 2014. PMID 25002497. DOI 10.1073/pnas.1402663111.

    Laboratory method study · In 12 healthy young men sampled two-hourly over 48 hours, 109 of 171 plasma metabolites showed daily rhythms, and during sleep deprivation 27 rose, including tryptophan, serotonin and taurine.

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