A build-up of histamine and salicylate can occur when the body doesn’t produce enough sulphate, which we use to detoxify the body of these substances. Excess undetoxified metabolites can cause symptoms, particularly excesses of salicylates and histamine.
How we use sulphate to detoxify histamines and salicylates
One of our detoxification pathways utilises sulphate. Sulphate attaches to phenols (salicylates and others) and amines (histamine and others) to assist detoxification1.
Our bodies must first make sulphate, which it does using protein, converting it to sulphite, then converting sulphite to sulphate2,3.
To make sulphate, we need:
- Protein
- Molybdenum
- Magnesium
- Zinc
- Omega-3 fatty acids
- Vitamin B1, B2, B5 and B6
Enzymes transport the sulphate to its final destination, attaching sulphate to phenols (salicylates) and amines (histamine).
Where it gets tricky
If you’re not a good sulphate producer, you’ll find you react to salicylates in food, medicines, aspirin, paracetamol (Tylenol), histamine-rich foods, histamine in the immune system, tyramine in mature cheese, and phenylethylamine in chocolate, for example4.
Fruits and vegetables slow down this transportation as they contain large amounts of salicylates. Epsom salts (magnesium sulphate) may improve sulphate levels since the sulphate passes through the skin and can be used to detoxify histamines and salicylates.
There is a limited capacity for us to make sulphate and get it around the body. It can only do what it can do at its own speed, particularly with high levels of phenols and amines.
Phenols have a failsafe system whereby we can add glucuronide, deactivating them. Salicylates have no such failsafe.
Gilbert’s syndrome and sulphate production and transport
If you have Gilbert’s syndrome, a liver function test will show raised bilirubin. Gilbert’s is a common inherited reduction in the enzyme (UGT1A1) the liver uses to glucuronidate bilirubin and other compounds5. Because glucuronidation and sulphation are the two competing routes for clearing phenols, reduced glucuronidation throws more of that load onto sulphation6 – so if your sulphation is already limited, phenols and salicylates are harder to clear.
Taking calcium D-glucarate can help, as this calcium salt inhibits beta-glucuronidase – a phase 2 liver detoxification enzyme7.
Detoxifying amines and histamine
Adding sulphate is one way to improve the detoxification of amines and phenols; however, there are more options.
Adding diamine oxidase (DAO) can help, alongside ensuring sufficient levels of copper. Low DAO can be genetic or due to a copper deficiency8.
We can also add what’s known as methyl groups to amines to process them efficiently8. You need sufficient magnesium, zinc, vitamins B1, B2, B6 and B12, and folate while also having sufficient methyl groups.
Beetroot is a good source of methyl groups, while if you want a supplement, you can take dimethylglycine (DMG) or trimethylglycine (TMG), or choline as a supplement. B12 and many other substances also provide methyls.
Reducing overall phenol and amine intake overall
Reducing dietary histamine and salicylate won’t be enough, as the detoxification pathway is still required to degrade all amines and phenols you ingest. However, it can help ease symptoms while you work on other areas.
The issue is compounded because quercetin, commonly used to degrade histamine, is a phenol. Vitamin C, also used to degrade histamine, often contains bioflavonoids and phenols.
Some foods cause the excretion of vitamin B2 (tomatoes, chilli, capsicum/peppers, soy, peanuts, broccoli, parsnips), which impedes your ability to make sulphate, produce energy, methylate and make some enzymes and hormones. B2 also recycles glutathione. Avoid supplements that contain boron (often in tablets).
It can be challenging to work out and treat, so see an experienced practitioner for support.
This article is general information and not a substitute for personalised medical advice. This is complex to work out and treat, so please see an experienced practitioner.
- Gamage N, Barnett A, Hempel N, et al. Human sulfotransferases and their role in chemical metabolism. Toxicological Sciences. 2006;90(1):5-22.
- Stipanuk MH. Sulfur amino acid metabolism: pathways for production and removal of homocysteine and cysteine. Annual Review of Nutrition. 2004;24:539-577.
- Mendel RR, Kruse T. Cell biology of molybdenum in plants and humans. Biochimica et Biophysica Acta. 2012;1823(9):1568-1579.
- Littlewood J, Glover V, Sandler M, Petty R, Peatfield R, Rose FC. Platelet phenolsulphotransferase deficiency in dietary migraine. The Lancet. 1982;319(8282):983-986.
- Bosma PJ, Chowdhury JR, Bakker C, et al. The genetic basis of the reduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert’s syndrome. New England Journal of Medicine. 1995;333(18):1171-1175.
- Prescott LF. Kinetics and metabolism of paracetamol and phenacetin. British Journal of Clinical Pharmacology. 1980;10(Suppl 2):291S-298S.
- Walaszek Z. Potential use of D-glucaric acid derivatives in cancer prevention. Cancer Letters. 1990;54(1-2):1-8.
- Maintz L, Novak N. Histamine and histamine intolerance. The American Journal of Clinical Nutrition. 2007;85(5):1185-1196.


