Last update Oct. 4, 2020

Infant G6PD deficiency

Low Risk

Possibly safe. Probably compatible. Mild risk possible. Follow up recommended. Read the Comment.

Glucose-6-phosphate dehydrogenase (G6FD) deficiency is an X-linked genetic disease that causes fragility of red blood cells, causing anemia due to hemolysis (destruction of red blood cells), although most of the time it is asymptomatic (AEHH 2012). It is transmitted by women and is more common in men.
It is the most prevalent enzyme deficiency in the world, exceeding 5% of the population in many countries (Nkhoma 2009).

Oxidative stress in the face of infections, excessive exercise or certain oxidizing substances can precipitate hemolytic crises, the substances most frequently implicated being certain medications such as Ascorbic Acid, Nalidixic Acid, Aspirin and Salicylates, Methylene Blue, Ciprofloxacin, Dapsone, Dimercaprol, Phenazone, Phenazopyridine, Phenylhydrazine, Glibenclamide, Glipizide, Menadione, Niridazole, Nitrofurantoin, Nitrofurazone, Primaquine, Probenecid, Quinine, Salsalate, Sulfamethoxazole, Sulfasalazine, Sulfisoxazole, Tafenoquine, Trimethoprim, or exposure to camphor or henna. Please consult for more information.

Fava beans (Belsey 1973), which contain vicin and convicin, and which are metabolized to products with a powerful oxidizing action, can trigger hemolytic anemia crises when ingested by people with a certain type of G6FD deficiency, which is why this disease is also known as favism.

Numerous cases of severe hemolytic crisis have been reported in G6FD-deficient breastfed infants after their mothers had eaten fava beans (Kaplan 1998, Schiliro 1979, Kattamis 1971, Taj-Eldin 1971, Emanuel 1961, Casper 1956), one case after the mother took aspirin (Harley 1962), and several cases after tonic water containing quinine was consumed (Bichali 2017).

Breastfeeding mothers with a personal or family history of G6FD deficiency or with infants diagnosed with this disease should not take the medications described and should not eat fava beans or drink tonic water containing quinine, or use camphor or henna.

Given the high global prevalence of G6FD deficiency (Nkhoma 2009), which is higher in certain ethnicities, it may be prudent to generally recommend that breastfeeding mothers avoid ingesting or coming into contact with these oxidizing substances (Wennberg 2017).

See below the information of these related products:

  • Aspirin (Possibly safe. Probably compatible. Mild risk possible. Follow up recommended. Read the Comment.)
  • Fava beans (Possibly safe. Probably compatible. Mild risk possible. Follow up recommended. Read the Comment.)
  • Tonic water ( Safe. Compatible. Minimal risk for breastfeeding and infant.)

Suggestions made at e-lactancia are done by APILAM team of health professionals, and are based on updated scientific publications. It is not intended to replace the relationship you have with your doctor but to compound it. The pharmaceutical industry contraindicates breastfeeding, mistakenly and without scientific reasons, in most of the drug data sheets.

Jose Maria Paricio, Founder & President of APILAM/e-Lactancia

Your contribution is essential for this service to continue to exist. We need the generosity of people like you who believe in the benefits of breastfeeding.

Thank you for helping to protect and promote breastfeeding.

José María Paricio, founder of e-lactancia.

Other names

Infant G6PD deficiency is also known as Glucose-6-phosphate dehydrogenase deficiency in infants. Here it is a list of alternative known names::


Infant G6PD deficiency belongs to this group or family:


  1. Wennberg RP, Watchko JF, Shapiro SM. Maternal Empowerment - An Underutilized Strategy to Prevent Kernicterus? Curr Pediatr Rev. 2017;13(3):210-219. Abstract Full text (in our servers)
  2. Bichali S, Brault D, Masserot C, Boscher C, Couec ML, Deslandes G, Pissard S, Leverger G, Vauzelle C, Elefant E, Rozé JC, Cortey A, Chenouard A. Maternal consumption of quinine-containing sodas may induce G6PD crises in breastfed children. Eur J Pediatr. 2017 Oct;176(10):1415-1418. Abstract
  3. AEHH: Asociación Española de Hematología y Hemoterapia. EL DEFICIT DE GLUCOSA-6-FOSFATO DESHIDROGENASA (G6PD). EL FAVISMO AEHH 2012 Full text (link to original source) Full text (in our servers)
  4. Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis. 2009 May-Jun;42(3):267-78. Abstract
  5. Kaplan M, Vreman HJ, Hammerman C, Schimmel MS, Abrahamov A, Stevenson DK. Favism by proxy in nursing glucose-6-phosphate dehydrogenase-deficient neonates. J Perinatol. 1998 Nov-Dec;18(6 Pt 1):477-9. Abstract
  6. Schiliro G, Russo A, Curreri R, Marino S, Sciotto A, Russo G. Glucose-6-phosphate dehydrogenase deficiency in Sicily. Incidence, biochemical characteristics and clinical implications. Clin Genet. 1979 Feb;15(2):183-8. Abstract
  7. Belsey MA. The epidemiology of favism. Bull World Health Organ. 1973;48(1):1-13. Abstract Full text (link to original source) Full text (in our servers)
  8. Taj-Eldin S. Favism in breast-fed infants. Arch Dis Child. 1971 Feb;46(245):121-3. No abstract available. Abstract Full text (link to original source) Full text (in our servers)
  9. Kattamis C. Favism in breast-fed infants. Arch Dis Child. 1971 Oct;46(249):741. No abstract available. Abstract Full text (link to original source) Full text (in our servers)
  10. HARLEY JD, ROBIN H. "Late" neonatal jaundice in infants with glucose-6-phosphate dehydrogenase-deficient erythrocytes. Australas Ann Med. 1962 Aug;11:148-55. No abstract available. Abstract
  11. EMANUEL B, SCHOENFELD A. Favism in a nursing infant. J Pediatr. 1961 Feb;58:263-6. No abstract available. Abstract
  12. CASPER J, SHULMAN J. Bilateral cortical necrosis of the kidneys in an infant with favism. Am J Clin Pathol. 1956 Jan;26(1):42-7. No abstract available. Abstract

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