Salicylic acid is an odourless organic compound found naturally in plants. Composed of a phenol group and a carboxylic acid group, salicylic acid is both a carboxylic acid and a non-flavonoid phenol.

The body has evolved incredible systems for processing chemicals, some of which kick in only when another system becomes overwhelmed. Much like how the adaptive immune system takes over when the innate immune system is no longer able to destroy germs on its own, the body also has more than one way of expelling phenols from the body; handy as a build-up of salicylates can be detrimental to health (7).

The first way the body attempts to transform unwanted phenols for safe elimination is by adding oxygen to the molecule to form a reactive site. The second phase involves a process of adding a hydrophilic (water-soluble) group to this now reactive site. Examples include sulfation (the transfer of a sulfate group to a compound) and glucuronidation (the transfer of glucuronic acid to a compound). The increased solubility of the altered phenol can in theory lead to enhanced excretion in the bile and urine (6).

Now, sulfation is great for relatively small quantities of phenols (8), however, its capacity to work is limited by the amount of sulfate in the body, the enzymes required for reactions to take place and the level of amines in the body – sulfation is involved in processing amines too. If too many phenols and amines build up, glucuronidation, a reaction of low affinity and high capacity kicks in. While it isn’t as efficient as sulfation, it deals much better with larger quantities of phenols (8).

Phenol metabolism can also be influenced by factors such as gender, age, gut microbial activity and genetic traits (1). If a person has a poor ability to transform phenols via one or both systems, it is thought that they can build up, becoming a problem for those who have a low chemical threshold.

So what does all this mean for those with salicylate sensitivity? Salicylates are a subgroup of phenols found in a multitude of foods, drinks, and other products. If a person has a limited capacity to remove them from the body, perhaps due to low plasma sulfate levels and/or altered enzyme activity, the chemical could, in theory, build up. For those who are salicylate sensitive, it may not take much for their chemical threshold to become overrun, leading to undesirable symptoms due to the chemical’s ability to irritate nerve endings in different parts of the body (2).

Interestingly, it has been observed that salicylates can significantly worsen symptoms in autistic children (4). Another study found that autistic patients tend to be deficient in the enzyme Phenol Sulphur Transferase, a biological catalyst involved in the elimination of phenols and amines (5). These two studies together point to salicylates possibly contributing to adverse symptoms due to a decreased ability to eliminate phenols.

If a reduction in phenol processing is indeed a contributor to symptoms experienced by salicylate-sensitive individuals, then it may make sense to strive for ways to reduce the total phenol and amine load on the body. This could be achieved by limiting the intake of foods high in the chemical and/or increasing the amount of sulfate in the body.

Certain nutrients such as Omega 3 fatty acids, vitamin B (3), sulfur-containing amino acids, and sun exposure to the skin (9), can help in the body’s ability to make sulphate. Another way to acquire sulfate is via an Epsom salt (magnesium sluphate) bath, the sulphate of which can be absorbed through the skin. It should be noted that adverse effects have been experienced by ingesting high levels of inorganic sulfate, and as of yet, there is limited information available to set a tolerable upper intake level for sulfate (10).

But what is it specifically about salicylates that make them a problem compared to other phenols? As far as science is concerned, the mechanism(s) of salicylate side effects are not well understood. While there is research showing that conditions such as asthma, migraine, IBS, and behavioural problems may be associated with salicylates (12)(13)(14), further research is required to fully understand salicylate’s link to symptoms and disease.

It’s important to understand that the above information is speculation rather than an explanation for why symptoms of salicylate sensitivity occur. It’s hoped that with continued research into the effects of dietary salicylates on sensitive individuals, more will be understood about this life-impacting condition.

Brigid xx

References

(1) Zamora-Ros, Raul et al. “Urinary excretions of 34 dietary polyphenols and their associations with lifestyle factors in the EPIC cohort study.” Scientific reports vol. 6 26905. 7 Jun. 2016, doi:10.1038/srep26905

(2) Swain, A., Soutter, V, & Loblay, R. (2011). RPAH Elimination Diet Handbook with food and shopping guide. Australia: Allergy Unit, Royal Prince Alfred Hospital.

(3) Margaret Moss & Rosemary H. Waring (2003) The Plasma Cysteine/Sulphate Ratio: A Possible Clinical Biomarker, Journal of Nutritional & Environmental Medicine, 13:4, 215-229, DOI: 10.1080/13590840310001642003

(4) Alberti, A., Pirrone, P., Elia, M., Waring, R.H. & Romano, C. (1999): Sulphation deficit in “low-functioning” autistic children: a pilot study. Biol. Psychiat., 46, 420–424.

(5) Waring, R.H. & Klovrza, L.V. (2000): Sulphur metabolism in autism. J. Nutr. Environ. Med., 10, 25–32

(6) Hodges, Romilly E, and Deanna M Minich. “Modulation of Metabolic Detoxification Pathways Using Foods and Food-Derived Components: A Scientific Review with Clinical Application.” Journal of nutrition and metabolism vol. 2015 (2015): 760689. doi:10.1155/2015/760689

(7) Baenkler, Hanns-Wolf. “Salicylate intolerance: pathophysiology, clinical spectrum, diagnosis and treatment.” Deutsches Arzteblatt international vol. 105,8 (2008): 137-42. doi:10.3238/arztebl.2008.0137

(8) Chapter 24 – Biotransformation Reactions and their Enzymes, Editor(s): Camille Georges Wermuth, David Aldous, Pierre Raboisson, Didier Rognan, The Practice of Medicinal Chemistry (Fourth Edition), Academic Press, 2015, Pages 561-584, ISBN 9780124172050, https://doi.org/10.1016/B978-0-12-417205-0.00024-9.

(9) Seneff, Stephanie et al. “A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome.” Theoretical biology & medical modelling vol. 12 9. 27 May. 2015, doi:10.1186/s12976-015-0006-1

(10) Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. https://doi.org/10.17226/10925.

(11) Hallstrand, Teal S, and William R Henderson Jr. “An update on the role of leukotrienes in asthma.” Current opinion in allergy and clinical immunology vol. 10,1 (2010): 60-6. doi:10.1097/ACI.0b013e32833489c3

(12) Jenkins C, Costello J, Hodge L. Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice. BMJ. 2004 Feb 21;328(7437):434. doi: 10.1136/bmj.328.7437.434. PMID: 14976098; PMCID: PMC344260.

(13) Loblay RH, Swain AR. ‘Food intolerance’. In Wahlqvist ML, Truswell AS, Recent Advances in Clinical Nutrition. London: John Libbey, 1986, pages 169-177.

(14) Swain A, Soutter V, Loblay R, Truswell AS. Salicylates, oligoantigenic diets, and behaviour. Lancet 1985;2(8445):41-2.