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Research on PST, Salicylates & Sulfation

Home ||| Research Menu Page ||| Last update 10/14/2010

Listed in reverse date order:

Waring 2008 Phytoestrogens and xenoestrogens: the contribution of diet and environment to endocrine disruption.
Harris 2008 Sulfotransferase inhibition: potential impact of diet and environmental chemicals on steroid metabolism and drug detoxification.
Healy 2008  Control of salicylate intolerance with fish oils.
Horvath 2002 Autism and gastrointestinal symptoms.
Harris 2000 Activity of phenolsulfotransferases in the human gastrointestinal tract.
Najbauer 2000                   The aspirin metabolite sodium salicylate causes focal cerebral hemorrhage and cell death in rats with kainic acid-induced seizures.
Alberti 1999 Sulphation deficit in "low-functioning" autistic children: a pilot study.
Harris 1998 Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis.
Alam 1997 Platelet sulphotransferase activity, plasma sulphate levels and sulphation capacity in patients with migraine and tension headache.
Baranczyk-Kuzma 1997   Biotransformation in monkey brain: coupling of sulfation to glutathione conjugation.
Harris 1996 Dietary modulation of human platelet phenolsulphotransferase activity.
McFadden 1996 Phenotypic Variation in Xenobiotic Metabolism and Adverse Environmental Response: Focus on Sulfur-Dependent Detoxification Pathways.
Ochi 1996 Effects of salicylate on neural activity in cat primary auditory cortex.
Corder 1995 Aspirin, salicylate, sulfite and tartrazine induced bronchoconstriction. Safe doses and case definition in epidemiological studies.
Li 1995 Aspirin inhibits secretagogue-stimulated and postprandial pancreatic exocrine secretion in conscious rats.
Bamforth 1993 Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases.
Baranczyk-Kuzma 1992   Properties of phenol sulphotransferase from brain of the monkey Rhesus macaca.
Loblay 1992   The Role of Food Intolerance in Chronic Fatigue Syndrome.
Park 1991 Sodium salicylate sensitivity in an asthmatic patient with aspirin sensitivity.
Koga 1989 Effects of food preservatives and local anesthetics on synthesis of outer membrane proteins in Vibrio parahaemolyticus.
Van Bever 1989 Food and food additives in severe atopic dermatitis.
Williams 1989 Aspirin-like effects of selected food additives and industrial sensitizing agents.
Groppetti 1988 Effect of aspirin on serotonin and met-enkephalin in brain: correlation with the antinociceptive activity of the drug.
Ikonomidou 1988 Differential effects of non-steroidal anti-inflammatory drugs on seizures produced by pilocarpine in rats
Scadding 1988 Poor sulphoxidation ability in patients with food sensitivity
Uetrecht 1987 Salicylate potentiates valproate-induced hyperammonemia in the rat.
Chudwin 1986 Sensitivity to non-acetylated salicylates in a patient with asthma, nasal polyps, and rheumatoid arthritis.
Weinshilboum 1986 Phenol sulfotransferase in humans: properties, regulation, and function.
Howrie 1985 Candy flavoring as a source of salicylate poisoning.
Swain 1985 Salicylates in foods.
Buelke 1984 Sex and strain differences in the developmental activity profile of rats prenatally exposed to sodium salicylate.
Chen 1980 Potentiation of noise-induced audiogenic seizure risk by salicylate in mice as a function of salicylate-noise exposure interval.
Chen 1980 Potentiation of acoustic-trauma-induced audiogenic seizure susceptibility by salicylates in mice.
Fitzsimon 1978 Salicylate sensitivity in children reported to respond to salicylate exclusion.

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  1. Platelet sulphotransferase activity, plasma sulphate levels and sulphation capacity in patients with migraine and tension headache, Alam Z, Coombes N, Waring RH, Williams AC, Steventon GB, Cephalalgia 1997 Nov;17(7):761-4
    "Activity of both the M- and P-forms of sulphotransferase (ST) was measured in platelets from patients with migraine, tension headache and controls.... The results suggest that PST activity may be a factor in the aetiology of migraine."

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  2. Sulphation deficit in "low-functioning" autistic children: a pilot study, Alberti A, Pirrone P, Elia M, Waring RH, Romano C, Biological Psychiatry 1999 Aug 1;46(3):420-4
    "The hypothesis that autistic behavior might be related to metabolic dysfunctions has led us to investigate in a group of "low functioning" autistic children and in an age-matched control group each made up of 20 subjects, the sulphation capacity available. ... RESULTS: The PS/PG ratio in the group of autistic subjects gave a significantly lower results than the control group ... CONCLUSIONS: The inability to effectively metabolize certain compounds particularly phenolic amines, toxic for the CNS, could exacerbate the wide spectrum of autistic behavior."

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    [See also HARRIS STUDY HERE for info about salicylate & the PST enzyme]

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  3. Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases. Bamforth KJ, Jones AL, Roberts RC, Coughtrie MW, Biochem Pharmacol 1993 Nov 17;46(10):1713-20
    "... dopamine sulphotransferase (ST) activity was inhibited strongly by (+/-)-catechin, (+)-catechin, octyl gallate, tartrazine [Yellow #5] and vanillin. Sulphation of the xenobiotic steroid 17 alpha-ethinyloestradiol (EE2) was inhibited by vanillin, erythrosin B and octyl gallate [anti-oxidant used in margarine]. ... Vanillin was found to inhibit 50% of liver EE2 ST activity ..."
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  4. Properties of phenol sulphotransferase from brain of the monkey Rhesus Macaca
    Baran'czyk-Kuz'ma A, Audus KL, Borchardt RT., Acta Biochim Pol. 1992;39(1):153-8.
    "Conjugation with sulphate catalysed by phenol sulphotransferase (PST, EC 2.8.2.1) plays a very important role in inactivation and removal of catecholamines [neurotransmitters like epinephrine, norepinephrine, and dopamine] as well as in inactivation of various exogenous [from outside the body] phenolic compounds. ... It can be concluded that brain cortex of the money Rh.macaca contains two different forms of phenol sulphotransferase; both are able to inactivate exogenous phenols, but only the main, anionic form shows an affinity towards catecholamines. ..."

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  5. Biotransformation in monkey brain: coupling of sulfation to glutathione conjugation. Baranczyk-Kuzma A, Sawicki J, Life Sci 1997;61(18):1829-41
    "... The effect of PST substrates ... and PST products ... on GST activity was investigated ... The greatest inhibitory effect was observed with neurotoxic compounds such as 6-OHDA and manganese. The commonly used analgesic drugs inhibit both GST forms. These enzymes are also inhibited by phenacetin, the precursor of paracetamol, and prototype salicylates such as sodium salicylate and acetylsalicylic acid. ... The obtained results point to a possible interaction between sulfation and glutathione conjugation in vivo since many physiologically, therapeutically and toxicologically active compounds which are sulfated by brain phenol sulfotransferases may be bound by brain glutathione-S-transferases. These compounds may lose their activity (on being bound to GST) and expose the brain to the toxic electrophiles (by decreasing GST activity).
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  6. Sex and strain differences in the developmental activity profile of rats prenatally exposed to sodium salicylate. Buelke-Sam J, Kimmel CA, Nelson CJ, Sullivan PA, Neurobehav Toxicol Teratol 1984 Mar-Apr;6(2):171-5
    "... Prenatal exposure [of rats] ... to the doses of sodium salicylate used here resulted in subtle alterations in developmental locomotor activity, the pattern of which was dependent on sex, strain and bedding condition during testing. ... All significant dose-related differences in CD rats were increased activity levels in treated animals relative to controls. Male rats showed more dose-related changes in activity than did females, ... These results suggest a behavioral teratogenic effect of sodium salicylate. In addition, they point out the subtle nature of many behavioral effects in the absence of more overt toxicity ..."
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  7. Potentiation of noise-induced audiogenic seizure risk by salicylate in mice as a function of salicylate-noise exposure interval, Chen CS, Aberdeen GC, Acta Otolaryngol 1980;90(1-2):61-5
    " Audiogenic seizure risk can be induced in genetically seizure-resistant BALB/c mice by exposure to an intense noise. . . . the greatest potentiation effect was obtained when animals were exposed to the noise 6 hr after the intake of salicylate. The findings were taken as indirect evidence suggesting that the ototoxic action of sodium salicylate could potentiate vulnerability of the mouse cochlea to noise damage."
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  8. Potentiation of acoustic-trauma-induced audiogenic seizure susceptibility by salicylates in mice. Chen CS, Aberdeen GC, Experientia 1980 Mar 15;36(3):330-1
    " Combined exposure to noise and salicylates was found to produce greater acoustic trauma induced audiogenic seizure risk than exposure to the noise alone. The result suggests that salicylates could make the mouse cochlea more vulnerable to the traumatic action of noise."
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  9. Sensitivity to non-acetylated salicylates in a patient with asthma, nasal polyps, and rheumatoid arthritis. Chudwin DS, Strub M, Golden HE, Frey C, Richmond GW, Luskin AT, Ann Allergy 1986 Aug;57(2):133-4
    " A woman experienced exacerbations of bronchial asthma after taking aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) for rheumatoid arthritis. On oral challenges, she developed an urticarial reaction after tartrazine; urticarial and bronchospastic reactions after salicylsalicylic acid; and urticarial and bronchospastic reactions after choline magnesium trisalicylate. . . . The results of sensitivity studies of our patient indicates that such patients may also be sensitive to non-acetylated salicylates."
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  10. "Aspirin, salicylate, sulfite and tartrazine induced bronchoconstriction. Safe doses and case definition in epidemiological studies. Corder EH, Buckley CE 3rd, J Clin Epidemiol 1995 Oct;48(10):1269-75
    Allergic-like reactions to chemical components of foods and medicines may be common. ... A 15% decrease in the amount of air expired in one second was defined a positive response. ... Doses to which the most sensitive (5%) and practically all (95%) susceptible persons might respectively respond are: metabisulfite 4.6 mg, 255.8 mg; tartrazine 3.4 mg, 885.6 mg; aspirin 0.8 mg, 332.3 mg; and salicylate 2.6 mg, 89.9 mg. Doses within these ranges can be used in epidemiological studies."
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  11. Salicylate sensitivity in children reported to respond to salicylate exclusion. Fitzsimon M, Holborow P, Berry P, Latham S, Medical Journal of Australia 1978 Dec 2;2(12):570-2
    Twelve children, aged six to 13 years, whose parents reported an improvement in behavioural problems with use of the Feingold (K-P) diet for an average period of 12 months, were challenge-tested with 40 mg of acetylsalicylic acid in a double-blind, cross-over trial with ascorbic acid as a placebo. ... significance was reached in tests of general cognitive capacity, line walking and the "finger-to-nose" tests, as well as increased disturbance in sleep patterns in these children.
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  12. Effect of aspirin on serotonin and met-enkephalin in brain: correlation with the antinociceptive activity of the drug. Groppetti A, Braga PC, Biella G, Parenti M, Rusconi L, Mantegazza P, Neuropharmacology. 1988 May;27(5):499-505.
    "Intravenous administration of acetyl salicylate of lysine, a soluble salt of aspirin, reduced in rats the firing discharge of thalamic neurones, evoked by noxious stimuli. Concomitantly, concentrations of 5-hydroxyindole acetic acid increased, while those of met-enkephalin-like immuno-reactive derivatives were decreased in several areas of the brain. Similar electrophysiological and biochemical responses were obtained by administering tryptophan or 5-hydroxytryptophan plus carbidopa. The effect of aspirin on the evoked firing of the thalamic neurones was counteracted by pretreating the animals with metergoline. On the other hand, naloxone did not antagonize the inhibitory effect of aspirin and 5-hydroxytryptophan on pain-induced neuronal excitation. These data indicate that a serotonin-, but not a naloxone-sensitive opiate mechanism, may be relevant for aspirin-mediated antinociception [pain tolerance]."

    Translation: salicylate affects serotonin, one of the major brain neurotransmitters.

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  13. Sulfotransferase inhibition: potential impact of diet and environmental chemicals on steroid metabolism and drug detoxification. Harris RM, Waring RH. Current Drug Metabolism, 2008 May;9(4):269-75.
    " . . . As these environmental contaminants and dietary components all act at the same site, their effects would be expected to be additive and could potentially therefore reduce sulfonation of drugs and lead to altered pharmacological responses."

    Note: This would include altered sulfonation of food additives and neurotransmitters.

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  14. Activity of phenolsulfotransferases in the human gastrointestinal tract. Harris RM, Picton R, Singh S, Waring RH, Life Sci 2000 Sep 15;67(17):2051-7
    " Sulfate conjugation by sulfotransferase enzymes is an important pathway for the detoxication of xenobiotics (things from outside the body) and endogenous (things made inside the body) compounds. . . . High concentrations of sulfotransferases in the reservoir areas of the right and left colon indicate possible importance in detoxication by sulfation and also perhaps in activating mutagens in the same areas. Nutritional factors, such as a high-fat diet may, however, alter sulfotransferase activity. "
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  15. Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis, Harris RM, Hawker RJ, Langman MJ, Singh S, Waring RH, Gut 1998 Feb;42(2):272-5
    "RESULTS: Salicylic acid consistently and selectively inhibited the P form of phenolsulphotransferase at subtherapeutic concentrations in both tissue samples. A 50% inhibition of sulphation by the P phenolsulphotransferase occurred at salicylic acid concentrations of about 40 and 130 microM in platelets and bowel mucosa respectively." [While this is a possible benefit in inhibiting cancer, it is also important in ADHD and Autism. See ALBERTI STUDY HERE]

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  16. Dietary modulation of human platelet phenolsulphotransferase activity, Harris RM, Waring RH, Xenobiotica 1996 Dec;26(12):1241-7
    "It is concluded that dietary factors have the potential to play a major role in modulating the sulphation detoxification pathway..."
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  17. Control of salicylate intolerance with fish oils. Healy E, Newell L, Howarth P, Friedmann PS., British Journal of Dermatology 2008 Dec;159(6):1368-9. Epub 2008 Sep 15.
    "We report three patients with disabling salicylate-induced intolerance who experienced abrogation of symptoms following dietary supplementation with omega-3 polyunsaturated fatty acids (PUFAs). All three patients experienced severe urticaria, asthma requiring systemic steroid therapy and anaphylactic reactions. After dietary supplementation with 10 g daily of fish oils rich in omega-3 PUFAs for 6-8 weeks all three experienced complete or virtually complete resolution of symptoms allowing discontinuation of systemic corticosteroid therapy. Symptoms relapsed after dose reduction. Fish oil appears a safe and effective treatment for this difficult and often serious condition."

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  18. Autism and gastrointestinal symptoms., Horvath K, Perman JA., Current Gastroenterology Reports 2002 Jun;4(3):251-8
    " . . . Recent clinical studies have revealed a high prevalence of gastrointestinal symptoms, inflammation, and dysfunction in children with autism. Mild to moderate degrees of inflammation were found in both the upper and lower intestinal tract. In addition, decreased sulfation capacity of the liver, pathologic intestinal permeability, increased secretory response to intravenous secretin injection, and decreased digestive enzyme activities were reported in many children with autism. Treatment of digestive problems appears to have positive effects on autistic behavior. These new observations represent only a piece of the unsolved autism "puzzle" and should stimulate more research into the brain-gut connection. "
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  19. Candy flavoring as a source of salicylate poisoning. Howrie DL, Moriarty R, Breit R. Pediatrics 1985 May;75(5):869-71
    " Methyl salicylate (oil of wintergreen) in the form of candy flavoring was ingested by a 21-month-old male infant who subsequently developed vomiting, lethargy, and hyperpnea. A "swallow" of the solution resulted in a serum salicylate concentration of 81 mg/dL six hours after ingestion. . . Hazards associated with salicylate use in this form include lack of parental awareness of the substance's toxic potential, the attractiveness of the candy-like odor, and the availability of the liquid in non-child-resistant packaging containing potentially lethal quantities."
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  20. Differential effects of non-steroidal anti-inflammatory drugs on seizures produced by pilocarpine in rats, Ikonomidou-Turski C, Cavalheiro EA, Turski L, Bortolotto ZA, Kleinrok Z, Calderazzo-Filho LS, Turski WA, Brain Res 1988 Oct 18;462(2):275-85
    " . . . Pretreatment of rats with sodium salicylate, ED50 103 mg/kg (60-174), and phenylbutazone, 59 mg/kg (50-70) converted the non-convulsant dose of pilocarpine, 200 mg/kg, to a convulsant one. . . ."
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  21. Effects of food preservatives and local anesthetics on synthesis of outer membrane proteins in Vibrio parahaemolyticus. Koga T, Kawata T, Tokushima J Exp Med 1989 Jun;36(1-2):41-5
    " The effects of seven food preservatives including salicylate, benzoate, . . . on the synthesis of major outer membrane proteins . . . were investigated. The synthesis of the outer membrane proteins a, b, c and e was remarkably inhibited by all the food preservatives except propionate and two additional outer membrane proteins with respective molecular weights of about 35,000 (protein b') and 32,000 (protein c') were induced . . ."
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  22. Aspirin inhibits secretagogue-stimulated and postprandial pancreatic exocrine secretion in conscious rats. Li P, Zhou L, Levine RA, Chey WY, Pancreas 1995 Jan;10(1):85-92
    " The effect of salicylate and nonsalicylate antiinflammatory drugs and prostaglandins (PGs) on pancreatic exocrine secretion are controversial. . . The data indicate that ASA [aspirin] inhibits both secretin- and CCK-stimulated pancreatic secretion by a mechanism independent of prostaglandin biosynthesis inhibition."
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  23. The Role of Food Intolerance in Chronic Fatigue Syndrome. Robert H. Loblay, Anne R. Swain, in The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome, B.M. Hyde, J. Goldstein, and P. Levine, Editors. 1992
    The Nightingale Research Foundation: Ottawa. p. 521-538
    " Although much attention has been paid in recent years to the adverse effects of food additives, naturally occurring food chemicals are a more insidious and more common cause of problems. Natural chemicals play a central role in the complex symbiotic relationship between animals and plants which has developed as a result of co-evolution. Plants are known to be capable of synthesizing an enormous range of substances important for their own survival and reproduction. Amongst these are a variety of anti-microbial and anti-parasitic agents, as well as chemicals which can modify the feeding behaviour of insects and higher animals. Not surprisingly, some of these substances can be toxic to humans if ingested in significant quantities."

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  24. Phenotypic Variation in Xenobiotic Metabolism and Adverse Environmental Response: Focus on Sulfur-Dependent Detoxification Pathways, S.A. McFadden, Toxicology, July 1996, Vol. 111(1-3), pp. 43-65
    "...a significant number of individuals with environmental intolerance or chronic disease have impaired sulfation of phenolic xenobiotics. This impairment is demonstrated with the probe drug acetaminophen and is presumably due to starvation of the sulfotransferases for sulfate substrate... In addition, impaired sulfation may be relevant to intolerance of phenol, tyramine, and phenylic food constituents, and it may be a factor in the success of the Feingold diet."
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  25. The aspirin metabolite sodium salicylate causes focal cerebral hemorrhage and cell death in rats with kainic acid-induced seizures, Najbauer J, Schuman EM, Mamelak AN, Neuroscience 2000;99(1):107-17
    " Aspirin (acetylsalicylic acid), and its main metabolite sodium salicylate, have been shown to protect neurons from excitotoxic cell death in vitro. . . . We report that sodium salicylate did not protect neurons from seizure-induced cell death, and to the contrary, it caused focal hemorrhage and cell death in the hippocampal formation and the entorhinal/piriform cortex of rats with kainic acid-induced seizures. . . .These initial observations may have important clinical implications for patients with epilepsy who take aspirin while affected by these conditions, and should promote further investigation of this relationship."
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  26. Effects of salicylate on neural activity in cat primary auditory cortex. Ochi K, Eggermont JJ, Hear Res 1996 May;95(1-2):63-76
    "The effect of systemically applied salicylate on single-unit firing activity in primary auditory cortex was investigated in six cats. ... All animals showed 20-30 dB of threshold shift about 2 h after administration and showed no recovery during the following 4 h..."
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  27. Sodium salicylate sensitivity in an asthmatic patient with aspirin sensitivity. Park HS et al., J Korean Med Sci 1991 Jun;6(2):113-7
    " ...The result of this study suggests that sodium salicylate may cross-react with aspirin in aspirin-and tartrazine-sensitive patients."
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  28. Poor sulphoxidation ability in patients with food sensitivity, Scadding GK et al., British Medical Journal 1988 Jul 9;297(6641):105-7
    "Patients with well defined reactions to foods were examined for their ability to carry out both sulphur and carbon oxidation reactions ... The proportion of poor sulphoxidisers (58 of 74) was significantly greater than that of a previously determined normal control population (67 of 200; p less than 0.005)... Metabolic defects may play a part in the pathogenesis of adverse reactions to foods."
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  29. Salicylates in foods. Swain AR, Dutton SP, Truswell AS, J Am Diet Assoc 1985 Aug;85(8):950-60
    " To determine salicylate content, 333 food items were analyzed. . . Salicylic acid was separated by high performance liquid chromatography and quantified by reading at 235 nm. . . This is the most comprehensive set of data on food salicylates yet published; . . . Most fruits, especially berry fruits and dried fruits, contain salicylate. Vegetables show a wide range from 0 to 6 mg salicylate per 100 gm food (for gherkins). Some herbs and spices were found to contain very high amounts per 100 gm, e.g., curry powder, paprika, thyme, garam masala, and rosemary. [Curry powder & paprika are avoided on Stage One, but the others are normally used in very small amounts and usually are not a problem on Stage One.] Among beverages, tea provides substantial amounts of salicylate. Licorice and peppermint candies and some honeys contain salicylates. Cereals, meat, fish, and dairy products contain none or negligible amounts."
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  30. Salicylate potentiates valproate-induced hyperammonemia in the rat. Uetrecht JP, Pharmacology 1987;34(5):279-85
    " Valproic acid is known to cause an increase in blood ammonia levels in humans at the usual clinical dose. In most patients, this increase is small and asymptomatic, but in some patients the increase is larger and is associated with encephalopathy. . . Salicylate potentiated this increase in blood ammonia . . . consistent with the apparent association between salicylates and Reye's syndrome which is also characterized by hyperammonemia. "
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  31. Food and food additives in severe atopic dermatitis. Van Bever HP, Docx M, Stevens WJ, Allergy 1989 Nov;44(8):588-94
    "In this study the role of food additives, tyramine and acetylsalicylic acid, was investigated by double-blind placebo-controlled challenges (DBPCC) in 25 children with severe atopic dermatitis (AD). All children challenged with foods (n = 24), except one, showed one or more positive reactions to the DBPCC with foods. Positive reactions presented as different combinations of flares of skin symptoms, intestinal symptoms and respiratory symptoms... Six children underwent DBPCC with food additives, tyramine and acetylsalicylic acid. All were found to demonstrate positive skin and/or intestinal reactions to at least one of the food additives. Two children reacted to tartrazine, three to sodium benzoate, two to sodium glutamate, two to sodium metabisulfite, four to acetylsalicylic acid and one to tyramine. It is concluded that some foods, food additives, tyramine and acetylsalicylic acid, can cause positive DBPCC in children with severe AD."
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  32. Phytoestrogens and xenoestrogens: the contribution of diet and environment to endocrine disruption. Waring RH, Ayers S, Gescher AJ, Glatt HR, Meinl W, Jarratt P, Kirk CJ, Pettitt T, Rea D, Harris RM., Journal of Steroid Biochemistry and Molecular Biology, 2008 Feb;108(3-5):213-20. Epub 2007 Sep 7.
    "... A range of environmental phenolic contaminants and dietary flavonoids was tested ... Endocrine disrupting effects in man may be multifactorial when components from both the diet and the environment act at the same point in steroid metabolism."
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  33. Phenol sulfotransferase in humans: properties, regulation, and function. Weinshilboum RM, Fed Proc 1986 Jul;45(8):2223-8
    Phenol sulfotransferase (PST) catalyzes the sulfate conjugation of phenolic and catechol drugs and neurotransmitters. ... The biochemical properties of platelet PST are very similar to those of PST in human brain, liver, and small intestine. ... observations are compatible with the conclusions that platelet PST activity may reflect the activity of the enzyme at sites of drug metabolism, and that variation in PST activity is one factor responsible for individual differences in the sulfate conjugation of orally administered drugs."
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  34. Aspirin-like effects of selected food additives and industrial sensitizing agents. Williams WR, Pawlowicz A, Davies BH, Clin Exp Allergy 1989 Sep;19(5):533-7
    " A number of food additives and industrial chemicals, responsible for inducing symptoms of intolerance in some individuals, have been studied in tests measuring platelet activation by noradrenaline. . . Suboptimal inhibitory concentrations of the agents studied had additive inhibitory effects on platelet aggregation when they were tested in pairs, or when tested with salicylate or aspirin. The results support the theory that some food additives and industrial chemicals induce intolerance because of their aspirin-like properties."

    NOTE: These results also support the hypothesis that single "challenges" of food coloring alone are not sufficient when testing the relationship of diet and behavior.

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