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Prevention with gestational niacin was demonstrated in mice, not as an established prenatal treatment in humans.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Niacin research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"niacin","display_name":"Niacin (vitamin B3)","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"An inherited break in the tryptophan pathway can leave NAD low even when the problem is not simply food intake.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[nia-clin-shi2017] NAD Deficiency, Congenital Malformations, and Niacin Supplementation. 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Prevention with gestational niacin was demonstrated in mice, not as an established prenatal treatment in humans.\nexposure: Biallelic HAAO or KYNU loss-of-function variants\ncross_nutrient: Human 3-hydroxyanthranilate 3,4-dioxygenase / HAAO (affected_enzyme); L-Tryptophan (upstream_precursor); Nicotinamide adenine dinucleotide, oxidized (measured_coenzyme)\nevidence_span: {\"source_cache\": \"artifacts/niacin-clinical-sources/shi2017.abstract.txt\", \"locator\": \"Indexed primary abstract\", \"file_sha256\": \"2c5dcc72d338ac41bd47e4363a149abc503859e2760398fed030f02d5891e2bb\", \"start_char\": 0, \"end_char\": 1874, \"text_sha256\": \"2c5dcc72d338ac41bd47e4363a149abc503859e2760398fed030f02d5891e2bb\"}\n[nia-clin-shi2017] NAD Deficiency, Congenital Malformations, and Niacin Supplementation. 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