Methionine Unit Converter

Convert methionine between mg/dL and µmol/L — and see why the direction matters more than the size, since a raised homocysteine with a high methionine and one with a low methionine are two different disorders with two different treatments.

Last updated 12 Sep 2026

Methionine converter

mg/dL ⇄ µmol/L

Methionine

Multiply mg/dL by 67.02 to get µmol/L. Methionine is always read beside the total homocysteine from the same sample — that pair, not the methionine alone, is what identifies a disorder of sulphur amino acid metabolism.

Reference groupPublished intervals assume a fasting sample separated promptly — Mayo states its values are for fasting patients, and amino acids shift with feeding and again in the tube if the blood is left to stand. In an infant, the sample is taken immediately before a feed or at the interval the metabolic service specifies. The first three groups are the Mayo fasting intervals and the last is the Labcorp neonatal band. Note how much wider the youngest bands are — a methionine of 50 µmol/L is raised in an adult and unremarkable in a newborn.

27µmol/LExample

Methionine 0.4 mg/dL on a fasting profile, read against the adult reference interval

Formula and conversion factor

µmol/L = mg/dL × 67.0196
mg/dL = µmol/L ÷ 67.0196

67.0196: derived from the molecular weight of L-methionine, 149.21 Da. Methionine is the sulphur-containing essential amino acid and the precursor of S-adenosylmethionine, the body's main methyl donor
direction discriminates: raised homocysteine with a HIGH methionine is cystathionine beta-synthase deficiency; raised homocysteine with a LOW or normal methionine is a remethylation defect. Same homocysteine, different disorder, different treatment
13–40 µmol/L: the adult reference interval used here. Classical homocystinuria in childhood has been reported at 200–1,500 µmol/L, and adult-onset disease above 50
the screening blind spot: newborn screening for homocystinuria is done on methionine, so remethylation defects, which lower it, may not be detected at all — and pyridoxine-responsive cases can screen negative too

Worked example

Methionine 0.4 mg/dL on a fasting profile, read against the adult reference interval
0.4 × 67.0196 = 26.81 µmol/L, reported as 27 µmol/L
Within the Mayo adult interval of 13–40 µmol/L used here, and within Labcorp's 12.7–41.1 µmol/L
The same 27 µmol/L in a two-week-old sits low-to-middle in a neonatal band that reaches 69 µmol/L — the number has not changed, the interval has
And on its own it settles nothing either way. With a total homocysteine of 180 µmol/L, a methionine of 27 µmol/L is not classical homocystinuria — it is the pattern of a remethylation defect, and the treatment is different
That is the whole point of the page: the methionine tells you which disorder the raised homocysteine belongs to, and 27 µmol/L is an answer, not a blank

Same raised homocysteine, opposite methionine, different disorder

The first two rows are the reason this page exists. The homocysteine is the same finding in both; the methionine is what says which disorder it is, and the two treatments point in opposite directions — restricting methionine in a remethylation defect would worsen the very deficiency that causes it. Neither the pattern nor this page makes the diagnosis: a metabolic service does, with enzyme and molecular confirmation.
	Total homocysteine	Methionine	Treatment direction
Cystathionine beta-synthase deficiency — classical homocystinuria	Often > 100 µmol/L	High — 200–1,500 µmol/L in childhood-onset, > 50 in adult-onset	Pyridoxine trial, methionine-restricted diet, betaine, cysteine supplementation
Remethylation defects — MTHFR deficiency, cblC and related	Raised	Low or normal	Hydroxocobalamin, betaine, folate. Methionine restriction would be actively wrong
Liver disease	Variable	Raised, with the aromatic amino acids	Directed at the liver; the Fischer ratio falls
Methionine adenosyltransferase I/III deficiency	Normal	Raised, sometimes markedly	Usually benign, and importantly not homocystinuria
Recent high-protein meal or a non-fasting sample	Normal	Mildly raised	Repeat fasting before anything else

Published intervals, and what newborn screening on methionine misses

Adult intervals for methionine agree closely, which is unusual among the amino acids — the disagreement here is in the neonatal band, where Labcorp's upper limit is 12 µmol/L above Mayo's. The last row is the important one: because newborn screening for homocystinuria is done on methionine, the disorders that lower methionine are not what it is designed to find, and pyridoxine-responsive cystathionine beta-synthase deficiency can screen negative as well.
Source	Adult (µmol/L)	Children (µmol/L)	Youngest band (µmol/L)
Mayo Clinic Laboratories — fasting	13 – 40 (≥18 y)	13 – 41 (2–17 y)	12 – 57 (<24 months)
Labcorp	12.7 – 41.1 (>15 y)	12.5 – 40.2 (2–15 y)	13.9 – 68.7 (0–30 days)
GeneReviews, quoted as normal	10 – 40	—	—
Screening blind spot — remethylation defects	methionine LOW or normal	—	may not be detected by screening on methionine at all

The direction is the diagnosis

Methionine is the sulphur-containing essential amino acid and the precursor of S-adenosylmethionine, the body’s principal methyl donor. Its breakdown runs two ways. In transsulphuration, methionine becomes homocysteine and then, through cystathionine beta-synthase, cystathionine and cysteine. In remethylation, homocysteine is converted back to methionine using a methyl group supplied by folate and vitamin B12. A block in either pathway raises homocysteine — and the methionine is what says which block it was. The conversion itself is simple: 1 mg/dL is 67.02 µmol/L, from a molecular weight of 149.21 Da.

When cystathionine beta-synthase is deficient, homocysteine cannot go forward, so both homocysteine and the methionine behind it accumulate. This is classical homocystinuria, with reported plasma methionine of 200 to 1,500 µmol/L in childhood-onset disease and above 50 µmol/L in adult-onset disease, against a normal 10 to 40. Untreated it causes lens dislocation, marfanoid habitus, skeletal disease, thromboembolism and intellectual disability, and treatment turns on whether the person responds to pyridoxine.

When remethylation fails instead — MTHFR deficiency, or a cobalamin disorder such as cblC — homocysteine still rises, but methionine is low or normal, because homocysteine can no longer be converted back into it. The homocysteine looks the same on the report; the disorder and the treatment do not. Classical homocystinuria is managed with a methionine-restricted diet among other things, while a remethylation defect is treated with hydroxocobalamin, betaine and folate, and restricting methionine there would deepen the deficiency that causes it. This is also why newborn screening on methionine misses remethylation defects: they lower the very analyte the screen looks for, and pyridoxine-responsive cystathionine beta-synthase deficiency can screen negative too.

Other things move methionine. Liver disease raises it alongside the aromatic amino acids, methionine adenosyltransferase I/III deficiency raises it without raising homocysteine at all, and a non-fasting sample or a recent high-protein meal raises it mildly. Reference intervals for methionine agree unusually closely between laboratories in adults, but they remain age-dependent and differ most in the neonatal band, where the published upper limits are 12 µmol/L apart. Convert the number, read it beside the total homocysteine from the same fasting, promptly separated sample, and take the pair to the metabolic service — neither value decides anything alone.

Frequently asked questions

How do I convert methionine from mg/dL to µmol/L?

Multiply by 67.0196, derived from the molecular weight of methionine, 149.21 Da. A methionine of 0.4 mg/dL is 27 µmol/L. To go the other way, divide the µmol/L figure by 67.0196.

What is a normal methionine level?

Roughly 13–40 µmol/L in a fasting adult; Labcorp gives 12.7–41.1 µmol/L and GeneReviews quotes 10–40. Adult intervals agree closely for this amino acid. The neonatal band is much wider, reaching 57–69 µmol/L depending on the laboratory, so a newborn value needs a newborn interval.

What does a raised methionine mean?

With a markedly raised total homocysteine, it is the pattern of classical homocystinuria from cystathionine beta-synthase deficiency, where methionine has been reported from above 50 µmol/L in adult-onset disease to 200–1,500 µmol/L in childhood-onset disease. Liver disease, methionine adenosyltransferase deficiency and a non-fasting sample also raise it.

Why does a low methionine matter if the homocysteine is high?

Because it changes the diagnosis. A raised homocysteine with a low or normal methionine is a remethylation defect — MTHFR deficiency or a cobalamin disorder such as cblC — rather than classical homocystinuria, and it is treated with hydroxocobalamin, betaine and folate. Restricting methionine, which is right in the first disorder, would be wrong in the second.

Can newborn screening miss homocystinuria?

Yes, in two ways. Screening is done on methionine, so remethylation defects, which lower methionine, may not be detected at all. And pyridoxine-responsive cystathionine beta-synthase deficiency can present with a methionine that is not raised at the time the screening sample is taken. A total homocysteine is what answers the question.

Related calculators

References

Sacharow SJ, Picker JD, Levy HL. Homocystinuria Caused by Cystathionine Beta-Synthase Deficiency. In: GeneReviews. Seattle: University of Washington; 2004, updated 2017.
Morris AAM, Kožich V, Santra S, et al. Guidelines for the diagnosis and management of cystathionine beta-synthase deficiency. J Inherit Metab Dis. 2017;40(1):49–74.
Huemer M, Diodato D, Schwahn B, et al. Guidelines for diagnosis and management of the cobalamin-related remethylation disorders cblC, cblD, cblE, cblF, cblG, cblJ and MTHFR deficiency. J Inherit Metab Dis. 2017;40(1):21–48.

Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.