Component

Anandamide / arachidonylethanolamide

Anandamide / arachidonylethanolamide. Species, exposure and limitations are retained in each linked claim.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Anandamide interacted specifically with cannabinoid receptors and inhibited adenylate cyclase, reproducing the signature response of the plant cannabinoids.

    Anandamide / arachidonylethanolamide → Adenylyl cyclase catalytic activity, model specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/8515284.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36a5b1eec5097dbdfd0224629f4d8449f8688d0476820823ffcbe3b92d68c66d", "start_char": 0, "end_char": 1015, "text_sha256": "36a5b1eec5097dbdfd0224629f4d8449f8688d0476820823ffcbe3b92d68c66d"}
    experimental_model
    Receptor binding and adenylate cyclase assays with anandamide
    exposure
    Anandamide against cannabinoid receptors and cyclase
    limitations
    Confirms the endogenous ligand reproduces the receptor signature of the drug.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Rat brain preparations
    plain_language
    The natural ligand does the same thing to the same enzyme as the drug.
    primary_references
    [thc-p8515284] Anandamide, a brain endogenous compound, interacts specifically with cannabinoid receptors and inhibits adenylate cyclase. (1993). https://pubmed.ncbi.nlm.nih.gov/8515284/ DOI: 10.1111/j.1471-4159.1993.tb03576.x
    tissue_or_cell_type
    Brain membranes

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 257–268

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor binding and adenylate cyclase assays with anandamide · source_derived_draft · unverified_draft

    ### thc-anandamide-inhibits-cyclase Anandamide interacted specifically with cannabinoid receptors and inhibited adenylate cyclase, reproducing the signature response of the plant cannabinoids. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The natural ligand does the same thing to the same enzyme as the drug. organism: Rat brain preparations tissue_or_cell_type: Brain membranes experimental_model: Receptor binding and adenylate cyclase assays with anandamide limitations: Confirms the endogenous ligand reproduces the receptor signature of the drug. exposure: Anandamide against cannabinoid receptors and cyclase evidence_span: {"source_cache": "artifacts/thc-research/8515284.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36a5b1eec5097dbdfd0224629f4d8449f8688d0476820823ffcbe3b92d68c66d", "start_char": 0, "end_char": 1015, "text_sha256": "36a5b1eec5097dbdfd0224629f4d8449f8688d0476820823ffcbe3b92d68c66d"} [thc-p8515284] Anandamide, a brain endogenous compound, interacts specifically with cannabinoid receptors and inhibits adenylate cyclase. (1993). https://pubmed.ncbi.nlm.nih.gov/8515284/ DOI: 10.1111/j.1471-4159.1993.tb03576.x
    Complete structured claim and evidence

  2. Arachidonylethanolamide, an arachidonic acid derivative isolated from porcine brain, competitively inhibited binding of a radiolabelled cannabinoid probe to synaptosomal membranes and produced concentration-dependent inhibition of the electrically evoked twitch of the mouse vas deferens, a characteristic effect of psychotropic cannabinoids.

    Anandamide / arachidonylethanolamide → Human cannabinoid receptor 1 / CB1 / CNR1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/1470919.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "45d534b5ac88c3edf040431942aea2f8421399c88e3931e8bc28b4b5e438f2f2", "start_char": 0, "end_char": 757, "text_sha256": "45d534b5ac88c3edf040431942aea2f8421399c88e3931e8bc28b4b5e438f2f2"}
    experimental_model
    Isolation from porcine brain with mass spectrometry, NMR and synthetic confirmation
    exposure
    Screen for endogenous ligands of the cannabinoid receptor
    limitations
    The isolation of the first endogenous ligand. The bioassay is a peripheral tissue twitch, not a central behavioural effect.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Pig brain, with mouse bioassay
    plain_language
    The brain makes its own version of the drug, and it is built from a fatty acid.
    primary_references
    [thc-p1470919] Isolation and structure of a brain constituent that binds to the cannabinoid receptor. (1992). https://pubmed.ncbi.nlm.nih.gov/1470919/ DOI: 10.1126/science.1470919
    tissue_or_cell_type
    Brain and vas deferens

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 244–255

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolation from porcine brain with mass spectrometry, NMR and synthetic confirmation · source_derived_draft · unverified_draft

    ### thc-anandamide-isolated Arachidonylethanolamide, an arachidonic acid derivative isolated from porcine brain, competitively inhibited binding of a radiolabelled cannabinoid probe to synaptosomal membranes and produced concentration-dependent inhibition of the electrically evoked twitch of the mouse vas deferens, a characteristic effect of psychotropic cannabinoids. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The brain makes its own version of the drug, and it is built from a fatty acid. organism: Pig brain, with mouse bioassay tissue_or_cell_type: Brain and vas deferens experimental_model: Isolation from porcine brain with mass spectrometry, NMR and synthetic confirmation limitations: The isolation of the first endogenous ligand. The bioassay is a peripheral tissue twitch, not a central behavioural effect. exposure: Screen for endogenous ligands of the cannabinoid receptor evidence_span: {"source_cache": "artifacts/thc-research/1470919.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "45d534b5ac88c3edf040431942aea2f8421399c88e3931e8bc28b4b5e438f2f2", "start_char": 0, "end_char": 757, "text_sha256": "45d534b5ac88c3edf040431942aea2f8421399c88e3931e8bc28b4b5e438f2f2"} [thc-p1470919] Isolation and structure of a brain constituent that binds to the cannabinoid receptor. (1992). https://pubmed.ncbi.nlm.nih.gov/1470919/ DOI: 10.1126/science.1470919
    Complete structured claim and evidence

What acts on it

  1. The olive oil diet increased brain anandamide and oleoylethanolamide without changing tissue fatty acid composition and without changing 2-arachidonoylglycerol, while the safflower oil diet increased linoleoylethanolamide and linoleic acid in brain, jejunum and liver.

    Dietary olive oil → Anandamide / arachidonylethanolamide source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/18316044.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3", "start_char": 0, "end_char": 1668, "text_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3"}
    experimental_model
    Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement
    exposure
    Short-term feeding of palm, olive, safflower, fish or arachidonic acid enriched diets
    limitations
    A five-arm dietary comparison measuring the mediators directly. Short-term feeding, and some changes occurred without any change in tissue fatty acid composition.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Rat
    plain_language
    Which fat is eaten changes which of these messengers the brain has, sometimes without changing the tissue fat itself.
    primary_references
    [thc-p18316044] Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine. (2008). https://pubmed.ncbi.nlm.nih.gov/18316044/ DOI: 10.1016/j.bbalip.2008.01.006
    tissue_or_cell_type
    Brain, liver and small intestine

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 660–671

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement · source_derived_draft · unverified_draft

    ### thc-diet-shapes-endocannabinoids The olive oil diet increased brain anandamide and oleoylethanolamide without changing tissue fatty acid composition and without changing 2-arachidonoylglycerol, while the safflower oil diet increased linoleoylethanolamide and linoleic acid in brain, jejunum and liver. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Which fat is eaten changes which of these messengers the brain has, sometimes without changing the tissue fat itself. organism: Rat tissue_or_cell_type: Brain, liver and small intestine experimental_model: Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement limitations: A five-arm dietary comparison measuring the mediators directly. Short-term feeding, and some changes occurred without any change in tissue fatty acid composition. exposure: Short-term feeding of palm, olive, safflower, fish or arachidonic acid enriched diets evidence_span: {"source_cache": "artifacts/thc-research/18316044.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3", "start_char": 0, "end_char": 1668, "text_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3"} [thc-p18316044] Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine. (2008). https://pubmed.ncbi.nlm.nih.gov/18316044/ DOI: 10.1016/j.bbalip.2008.01.006
    Complete structured claim and evidence

  2. Fatty acid amide hydrolase is the principal enzyme hydrolysing fatty acid amides including anandamide, terminating their signalling.

    Fatty acid amide hydrolase / FAAH → Anandamide / arachidonylethanolamide source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/15952893.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3213ef73e4fe6ef00bd2a0f1c09319ebc1e000f9cfd200ce3c1852f1e045c62c", "start_char": 0, "end_char": 724, "text_sha256": "3213ef73e4fe6ef00bd2a0f1c09319ebc1e000f9cfd200ce3c1852f1e045c62c"}
    experimental_model
    Review of fatty acid amide hydrolase structure and function
    exposure
    Hydrolysis of fatty acid amides including anandamide
    limitations
    A review, labelled as such, used for the enzymology. The structural claim is recorded from the crystal structure paper separately.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Mammalian enzyme
    plain_language
    One enzyme destroys the natural ligand within seconds of it being made.
    primary_references
    [thc-p15952893] Structure and function of fatty acid amide hydrolase. (2005). https://pubmed.ncbi.nlm.nih.gov/15952893/ DOI: 10.1146/annurev.biochem.74.082803.133450
    tissue_or_cell_type
    Membrane-bound enzyme

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 361–372

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of fatty acid amide hydrolase structure and function · source_derived_draft · unverified_draft

    ### thc-faah-degrades-anandamide Fatty acid amide hydrolase is the principal enzyme hydrolysing fatty acid amides including anandamide, terminating their signalling. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: One enzyme destroys the natural ligand within seconds of it being made. organism: Mammalian enzyme tissue_or_cell_type: Membrane-bound enzyme experimental_model: Review of fatty acid amide hydrolase structure and function limitations: A review, labelled as such, used for the enzymology. The structural claim is recorded from the crystal structure paper separately. exposure: Hydrolysis of fatty acid amides including anandamide evidence_span: {"source_cache": "artifacts/thc-research/15952893.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3213ef73e4fe6ef00bd2a0f1c09319ebc1e000f9cfd200ce3c1852f1e045c62c", "start_char": 0, "end_char": 724, "text_sha256": "3213ef73e4fe6ef00bd2a0f1c09319ebc1e000f9cfd200ce3c1852f1e045c62c"} [thc-p15952893] Structure and function of fatty acid amide hydrolase. (2005). https://pubmed.ncbi.nlm.nih.gov/15952893/ DOI: 10.1146/annurev.biochem.74.082803.133450
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others.

    Human cannabinoid receptor 1 / CB1 / CNR1 → Cellular cyclic AMP accumulation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"}
    experimental_model
    Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1
    exposure
    A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin
    limitations
    Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Human receptor in CHO cells
    plain_language
    The same receptor can push cAMP up as well as down, and which way depends on which drug is bound.
    primary_references
    [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
    tissue_or_cell_type
    Transfected cells

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 179–190

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 · source_derived_draft · unverified_draft

    ### thc-agonist-specific-trafficking Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The same receptor can push cAMP up as well as down, and which way depends on which drug is bound. organism: Human receptor in CHO cells tissue_or_cell_type: Transfected cells experimental_model: Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 limitations: Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed. exposure: A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin evidence_span: {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"} [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
    Complete structured claim and evidence

  2. The CB1 antagonist SR141716A attenuated the memory impairment produced by THC or by anandamide.

    SR141716A / rimonabant, a CB1 receptor antagonist → Spatial memory performance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/thc-research/9862397.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59e00778f9e8b2a2aba64063224de431ef098aaffcf26dca95fd9ddb36981a1f", "start_char": 0, "end_char": 1576, "text_sha256": "59e00778f9e8b2a2aba64063224de431ef098aaffcf26dca95fd9ddb36981a1f"}
    experimental_model
    Memory impairment by THC or anandamide with SR141716A pretreatment
    exposure
    THC or anandamide with a CB1 antagonist
    limitations
    Shows the antagonist rescues the impairment for both the drug and the natural ligand.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Rat
    plain_language
    Blocking the receptor protects the memory, whichever agonist caused the problem.
    primary_references
    [thc-p9862397] The cannabinoid CB1 receptor antagonist SR141716A attenuates the memory impairment produced by delta9-tetrahydrocannabinol or anandamide. (1998). https://pubmed.ncbi.nlm.nih.gov/9862397/ DOI: 10.1007/s002130050733
    tissue_or_cell_type
    Behaviour
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 452–463

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Memory impairment by THC or anandamide with SR141716A pretreatment · source_derived_draft · unverified_draft

    ### thc-antagonist-rescues-memory The CB1 antagonist SR141716A attenuated the memory impairment produced by THC or by anandamide. Condition category: machinery_impairment nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Blocking the receptor protects the memory, whichever agonist caused the problem. organism: Rat tissue_or_cell_type: Behaviour experimental_model: Memory impairment by THC or anandamide with SR141716A pretreatment limitations: Shows the antagonist rescues the impairment for both the drug and the natural ligand. exposure: THC or anandamide with a CB1 antagonist evidence_span: {"source_cache": "artifacts/thc-research/9862397.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59e00778f9e8b2a2aba64063224de431ef098aaffcf26dca95fd9ddb36981a1f", "start_char": 0, "end_char": 1576, "text_sha256": "59e00778f9e8b2a2aba64063224de431ef098aaffcf26dca95fd9ddb36981a1f"} [thc-p9862397] The cannabinoid CB1 receptor antagonist SR141716A attenuates the memory impairment produced by delta9-tetrahydrocannabinol or anandamide. (1998). https://pubmed.ncbi.nlm.nih.gov/9862397/ DOI: 10.1007/s002130050733
    Complete structured claim and evidence

  3. The arachidonic acid diet increased anandamide and 2-arachidonoylglycerol in jejunum without effect on liver, and the fish oil diet decreased liver levels of most N-acylethanolamines with similar changes in their precursors.

    Dietary arachidonic acid → 2-Arachidonoylglycerol / 2-AG source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/18316044.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3", "start_char": 0, "end_char": 1668, "text_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3"}
    experimental_model
    Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement
    exposure
    Short-term feeding of palm, olive, safflower, fish or arachidonic acid enriched diets
    limitations
    A five-arm dietary comparison measuring the mediators directly. Short-term feeding, and some changes occurred without any change in tissue fatty acid composition.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Rat
    plain_language
    Feeding the precursor raises the messengers, and feeding fish oil lowers them.
    primary_references
    [thc-p18316044] Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine. (2008). https://pubmed.ncbi.nlm.nih.gov/18316044/ DOI: 10.1016/j.bbalip.2008.01.006
    tissue_or_cell_type
    Brain, liver and small intestine

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 673–684

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement · source_derived_draft · unverified_draft

    ### thc-arachidonic-diet-raises-both The arachidonic acid diet increased anandamide and 2-arachidonoylglycerol in jejunum without effect on liver, and the fish oil diet decreased liver levels of most N-acylethanolamines with similar changes in their precursors. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Feeding the precursor raises the messengers, and feeding fish oil lowers them. organism: Rat tissue_or_cell_type: Brain, liver and small intestine experimental_model: Rats fed five different dietary fats with tissue endocannabinoid and fatty acid measurement limitations: A five-arm dietary comparison measuring the mediators directly. Short-term feeding, and some changes occurred without any change in tissue fatty acid composition. exposure: Short-term feeding of palm, olive, safflower, fish or arachidonic acid enriched diets evidence_span: {"source_cache": "artifacts/thc-research/18316044.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3", "start_char": 0, "end_char": 1668, "text_sha256": "fa2ad40ef984af77cc4c50a6126ce53354a2fd56fe6fada84871e2382cef07b3"} [thc-p18316044] Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine. (2008). https://pubmed.ncbi.nlm.nih.gov/18316044/ DOI: 10.1016/j.bbalip.2008.01.006
    Complete structured claim and evidence

  4. The time-dependent reduction in potency of anandamide toward inhibition of cannabinoid agonist binding in rat cerebellar membranes was blocked by ibuprofen but not by acetylsalicylic acid, sulindac, acetaminophen or to any significant extent by ketoprofen and naproxen, a direct assay of anandamide amidase gave a half-maximal inhibitory concentration for ibuprofen of approximately 400 micromolar, and that potency was of the same order as required for inhibition of cyclooxygenase-2 in cell-free systems and as the peak plasma concentrations following a two times 200 milligram dose regimen, so following therapeutic doses the metabolism of anandamide may be affected.

    Ibuprofen → Metabolism of anandamide by amidohydrolase source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"}
    experimental_model
    Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay
    exposure
    Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen
    limitations
    The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Rat
    plain_language
    Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal.
    primary_references
    [ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.x
    tissue_or_cell_type
    Cerebellar membranes

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 448–459

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay · source_derived_draft · unverified_draft

    ### ibu-blocks-anandamide-breakdown The time-dependent reduction in potency of anandamide toward inhibition of cannabinoid agonist binding in rat cerebellar membranes was blocked by ibuprofen but not by acetylsalicylic acid, sulindac, acetaminophen or to any significant extent by ketoprofen and naproxen, a direct assay of anandamide amidase gave a half-maximal inhibitory concentration for ibuprofen of approximately 400 micromolar, and that potency was of the same order as required for inhibition of cyclooxygenase-2 in cell-free systems and as the peak plasma concentrations following a two times 200 milligram dose regimen, so following therapeutic doses the metabolism of anandamide may be affected. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal. organism: Rat tissue_or_cell_type: Cerebellar membranes experimental_model: Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay limitations: The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them. exposure: Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen evidence_span: {"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"} [ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.x
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