Component
Human plasma phenylalanine concentration
Context-specific entity; species, compartment and exposure are stated on each claim.
6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
PRISM studies in 261 adults with PAH deficiency found substantial phenylalanine reductions during induction, titration and maintenance pegvaliase treatment.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Adult phase-3 clinical program with long-term titrated exposure.
- limitations
- Immune-mediated adverse events matter: 17 events in 12 participants met acute systemic hypersensitivity/anaphylaxis criteria. This is not dietary enzyme use.
- nutrient_topic
- L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
- plain_language
- The bypass can lower blood phenylalanine, but has its own treatment risks.
- primary_references
- Pegvaliase for the treatment of phenylketonuria: Results of a long-term phase 3 clinical trial program (PRISM). · 2018 · https://pubmed.ncbi.nlm.nih.gov/29653686/ · DOI 10.1016/j.ymgme.2018.03.006
L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 246–252
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Adult phase-3 clinical program with long-term titrated exposure. · source_derived_draft · unverified_draft
## l-phenylalanine-pal-clinical The bypass can lower blood phenylalanine, but has its own treatment risks. PRISM studies in 261 adults with PAH deficiency found substantial phenylalanine reductions during induction, titration and maintenance pegvaliase treatment. Model: Adult phase-3 clinical program with long-term titrated exposure. Limitations: Immune-mediated adverse events matter: 17 events in 12 participants met acute systemic hypersensitivity/anaphylaxis criteria. This is not dietary enzyme use. Evidence access: Primary abstract Pegvaliase for the treatment of phenylketonuria: Results of a long-term phase 3 clinical trial program (PRISM). · 2018 · https://pubmed.ncbi.nlm.nih.gov/29653686/ · DOI 10.1016/j.ymgme.2018.03.006
Complete structured claim and evidenceIn an 89-participant six-week PKU trial, sapropterin 10 mg/kg/day lowered mean phenylalanine by 236 micromol/L versus a 3 micromol/L rise with placebo; 44% versus 9% had at least a 30% reduction.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Randomized human PKU study enriched through prior responsiveness assessment.
- limitations
- Not all PAH defects respond; trial dose is historical evidence, not individualized guidance.
- nutrient_topic
- L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
- plain_language
- Providing the pharmaceutical cofactor helped some patients, with substantial response variation.
- primary_references
- Efficacy of sapropterin dihydrochloride (tetrahydrobiopterin, 6R-BH4) for reduction of phenylalanine concentration in patients with phenylketonuria: a phase III randomised placebo-controlled study. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693179/ · DOI 10.1016/S0140-6736(07)61234-3
L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 222–228
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized human PKU study enriched through prior responsiveness assessment. · source_derived_draft · unverified_draft
## l-phenylalanine-sapropterin-response Providing the pharmaceutical cofactor helped some patients, with substantial response variation. In an 89-participant six-week PKU trial, sapropterin 10 mg/kg/day lowered mean phenylalanine by 236 micromol/L versus a 3 micromol/L rise with placebo; 44% versus 9% had at least a 30% reduction. Model: Randomized human PKU study enriched through prior responsiveness assessment. Limitations: Not all PAH defects respond; trial dose is historical evidence, not individualized guidance. Evidence access: Primary abstract Efficacy of sapropterin dihydrochloride (tetrahydrobiopterin, 6R-BH4) for reduction of phenylalanine concentration in patients with phenylketonuria: a phase III randomised placebo-controlled study. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693179/ · DOI 10.1016/S0140-6736(07)61234-3
Complete structured claim and evidenceIn ten adults given 3 g, solution produced an earlier, higher phenylalanine peak than capsules: 191 versus 117 micromol/L at 32 versus 123 minutes.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Balanced Latin-square comparison.
- limitations
- Acute high-dose kinetics, not brain or safety equivalence.
- nutrient_topic
- Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
- plain_language
- The same dose need not give the same exposure.
- primary_references
- Plasma amino acid concentrations in normal adults administered aspartame in capsules or solution: lack of bioequivalence. · 1987 · https://pubmed.ncbi.nlm.nih.gov/3574137/ · DOI 10.1016/0026-0495(87)90052-7
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 82–88
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Balanced Latin-square comparison. · source_derived_draft · unverified_draft
## aspartame-formulation-phe The same dose need not give the same exposure. In ten adults given 3 g, solution produced an earlier, higher phenylalanine peak than capsules: 191 versus 117 micromol/L at 32 versus 123 minutes. Model: Balanced Latin-square comparison. Limitations: Acute high-dose kinetics, not brain or safety equivalence. Evidence access: Primary abstract Plasma amino acid concentrations in normal adults administered aspartame in capsules or solution: lack of bioequivalence. · 1987 · https://pubmed.ncbi.nlm.nih.gov/3574137/ · DOI 10.1016/0026-0495(87)90052-7
Complete structured claim and evidenceIn 18 fasted adults across 100, 150 and 200 mg/kg cohorts, mean plasma phenylalanine peaks were 20.3, 35.1 and 48.7 micromol/dL.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Six people per dose; aspartame in orange juice.
- limitations
- Healthy subjects, not PKU; no direct neurotransmitter assay.
- nutrient_topic
- Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
- plain_language
- Large loads produce larger amino-acid excursions.
- primary_references
- Plasma and erythrocyte concentrations of free amino acids in adult humans administered abuse doses of aspartame. · 1981 · https://pubmed.ncbi.nlm.nih.gov/7230277/ · DOI 10.1080/15287398109529980
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 138–144
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Six people per dose; aspartame in orange juice. · source_derived_draft · unverified_draft
## aspartame-high-dose-phe Large loads produce larger amino-acid excursions. In 18 fasted adults across 100, 150 and 200 mg/kg cohorts, mean plasma phenylalanine peaks were 20.3, 35.1 and 48.7 micromol/dL. Model: Six people per dose; aspartame in orange juice. Limitations: Healthy subjects, not PKU; no direct neurotransmitter assay. Evidence access: Primary abstract Plasma and erythrocyte concentrations of free amino acids in adult humans administered abuse doses of aspartame. · 1981 · https://pubmed.ncbi.nlm.nih.gov/7230277/ · DOI 10.1080/15287398109529980
Complete structured claim and evidenceAfter 34 mg/kg, twelve female PKU heterozygotes had higher peak phenylalanine than ten noncarrier females, 15.1 versus 8.95 micromol/dL.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human carrier comparison, also including twelve noncarrier men.
- limitations
- Heterozygotes do not represent patients with biallelic PAH deficiency; the damaged male-baseline sentence in indexed abstract is not reconstructed.
- nutrient_topic
- Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
- plain_language
- Reduced metabolic reserve can change the response to a precursor source.
- primary_references
- Plasma phenylalanine levels in phenylketonuric heterozygous and normal adults administered aspartame at 34 mg/kg body weight. · 1981 · https://pubmed.ncbi.nlm.nih.gov/7268794/ · DOI 10.1016/0300-483x(81)90108-6
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 146–152
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human carrier comparison, also including twelve noncarrier men. · source_derived_draft · unverified_draft
## aspartame-pku-carrier-kinetics Reduced metabolic reserve can change the response to a precursor source. After 34 mg/kg, twelve female PKU heterozygotes had higher peak phenylalanine than ten noncarrier females, 15.1 versus 8.95 micromol/dL. Model: Human carrier comparison, also including twelve noncarrier men. Limitations: Heterozygotes do not represent patients with biallelic PAH deficiency; the damaged male-baseline sentence in indexed abstract is not reconstructed. Evidence access: Primary abstract Plasma phenylalanine levels in phenylketonuric heterozygous and normal adults administered aspartame at 34 mg/kg body weight. · 1981 · https://pubmed.ncbi.nlm.nih.gov/7268794/ · DOI 10.1016/0300-483x(81)90108-6
Complete structured claim and evidenceSix adults consumed eight hourly 600 mg servings; phenylalanine rose modestly and plateaued after four to five servings within the reported normal postprandial range.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human beverage crossover; 4.8 g total over eight servings.
- limitations
- Small healthy-adult study; not a PKU population or a long-term trial.
- nutrient_topic
- Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
- plain_language
- Repeated exposure did not produce unlimited accumulation in this protocol.
- primary_references
- Effect of repeated ingestion of aspartame-sweetened beverage on plasma amino acid, blood methanol, and blood formate concentrations in normal adults. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2566887/ · DOI 10.1016/0026-0495(89)90125-x
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 106–112
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human beverage crossover; 4.8 g total over eight servings. · source_derived_draft · unverified_draft
## aspartame-repeated-phenylalanine Repeated exposure did not produce unlimited accumulation in this protocol. Six adults consumed eight hourly 600 mg servings; phenylalanine rose modestly and plateaued after four to five servings within the reported normal postprandial range. Model: Human beverage crossover; 4.8 g total over eight servings. Limitations: Small healthy-adult study; not a PKU population or a long-term trial. Evidence access: Primary abstract Effect of repeated ingestion of aspartame-sweetened beverage on plasma amino acid, blood methanol, and blood formate concentrations in normal adults. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2566887/ · DOI 10.1016/0026-0495(89)90125-x
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.