G6PD deficiency (favism): the foods and drugs to avoid

In short

G6PD deficiency is a genetic condition that makes red blood cells fragile against certain foods, drugs and chemicals, which can destroy them rapidly and cause acute anaemia.
Fava beans are the most well-known food trigger, which is why the condition is popularly called favism, but fenugreek, some berries and naphthalene mothballs carry similar risk.
The most dangerous drugs include primaquine, dapsone and nitrofurantoin, and some sulphonamide antibiotics.
Most people only discover they have G6PD deficiency after their first haemolytic crisis, which makes knowing your status and memorising the avoid list more valuable than any treatment.
Males are more commonly fully affected because the gene sits on the X chromosome, but females can have the full disease too.

What this article covers

What is G6PD deficiency and why is it called favism?
How common is it in the Arab region?
Foods to avoid entirely
Drugs that trigger a haemolytic crisis
Environmental and chemical triggers
What happens during a haemolytic crisis?
Living a normal life with G6PD deficiency
G6PD deficiency in newborns and infants

What is G6PD deficiency and why is it called favism?

G6PD stands for Glucose-6-Phosphate Dehydrogenase, an enzyme that protects red blood cells from oxidative damage. When this enzyme is deficient, red blood cells become vulnerable to rapid destruction by oxidising agents. The destruction is called haemolysis and the resulting drop in haemoglobin is haemolytic anaemia.

The popular name favism comes from fava beans (Vicia faba), the food most strongly associated with triggering a crisis. Fava beans contain compounds called divicine and isouramil that generate intense oxidative stress in susceptible red blood cells, causing them to break down within hours to days of eating.

The condition is inherited in an X-linked pattern. Because males have only one X chromosome, a single defective copy produces the full disease. Females have two X chromosomes, so full disease requires two defective copies, making females more likely to be carriers with partial enzyme activity. However, some females do develop meaningful disease.

A 2021 review in Pharmacological Research documented striking regional variation in G6PD deficiency rates worldwide, with high frequencies across the Mediterranean basin, sub-Saharan Africa, the Arabian Peninsula and the Fertile Crescent. In Gaza, Palestinian researchers found G6PD deficiency to be the single most common cause of severe haemolytic anaemia in children, consistent with what is seen elsewhere in the Arab world.

How common is it in the Arab region?

G6PD deficiency is one of the most common enzyme disorders in the world, affecting an estimated 400 million people. In the Arab region it is particularly concentrated in Mediterranean populations, the Levant, the Arabian Peninsula and North Africa.

A five-year retrospective Egyptian study published in Endocrine, Metabolic and Immune Disorders Drug Targets in 2018 found that a significant proportion of acute haemolytic anaemia cases admitted to Egyptian hospitals were G6PD related, with a concentration in communities with higher rates of consanguineous marriage.

The concentration of this condition in historically malaria-endemic regions is not coincidental. Like the sickle cell trait, G6PD deficiency offers partial protection against severe falciparum malaria, giving the defective gene an evolutionary advantage that caused it to spread and persist in these populations across thousands of years. This evolutionary explanation is one of the clearest examples of population genetics in medicine, and it explains why the condition is so remarkably common in the Arab world today.

Foods to avoid entirely

Fava beans in any form are the highest-risk food. A 2019 review in Nutrition Reviews analysed the available evidence and confirmed that cooking does not reliably remove the oxidising compounds in fava beans. There is no safe quantity for someone with severe G6PD deficiency. Ful medames, fresh broad beans, split fava bean dips and beans cooked with rice or eggs are all equally risky.

Fenugreek (Helba) appears on warning lists in several clinical guidelines. In Egyptian and Levantine cooking it features in bread, stews and herbal teas. People with severe G6PD deficiency should avoid it. Black and blue currants and certain other berry varieties contain oxidising compounds that warrant caution, though the evidence is less definitive than for fava beans.

The evidence is less conclusive for other legumes such as peanuts, lentils and chickpeas. The same Nutrition Reviews analysis concluded that current data are not strong enough to prohibit these foods generally, but individual patients with severe enzyme deficiency may be advised more conservatively. The right approach is to discuss your specific diet with a doctor who knows your exact enzyme level.

Avoid list for G6PD deficiency

Substance	Risk level	Notes
Fava beans (broad beans)	High risk: avoid completely	Cooking does not remove the danger
Fenugreek (Helba)	High risk in severe deficiency	Common in Arab breads and herbal teas
Naphthalene mothballs	High risk: avoid any exposure	Fumes absorbed through skin and breathing
Black currants and blueberries	Caution: moderation or avoidance	Depends on severity of deficiency
Black henna products	Caution: chemical additives	Pure henna is less concerning; check labels

Drugs that trigger a haemolytic crisis

Primaquine and tafenoquine, used to treat and prevent relapsing malaria caused by Plasmodium vivax, are among the most dangerous drugs for people with G6PD deficiency. Exposure can cause life-threatening haemolysis. G6PD testing before prescribing these drugs is mandatory in international treatment guidelines.

Dapsone, used in leprosy treatment, some skin conditions and as prophylaxis against Pneumocystis pneumonia, and nitrofurantoin, sometimes prescribed for urinary tract infections, carry high risk. Some sulphonamide antibiotics and aspirin at high doses also belong on the list. Before any new prescription, tell your doctor and pharmacist that you have G6PD deficiency.

A landmark 2014 review in the British Journal of Haematology by Luzzatto and Seneca described G6PD deficiency as the classic example of pharmacogenetics, where drug safety depends entirely on the patient's genetic makeup. The practical implication is that every prescriber who treats you needs to know about this condition.

High-risk drugs in G6PD deficiency

Drug	Common use	Risk level
Primaquine	Malaria treatment (vivax)	Very high: G6PD test required first
Tafenoquine	Malaria treatment and prevention	Very high
Dapsone	Leprosy, skin conditions	High
Nitrofurantoin	Urinary tract infection	High: safer alternatives exist
Rasburicase	Tumour lysis syndrome	Very high
Sulphonamides	Various infections	High in severe deficiency

Environmental and chemical triggers

Naphthalene mothballs are one of the most dangerous environmental triggers. The chemical releases vapours that are absorbed through breathing and even through the skin. In households where mothballs are placed in wardrobes year-round, a person with G6PD deficiency may be exposed to a continuous low-level oxidative stress without realising it.

Henna is a topic of some debate. Pure natural henna is generally considered relatively safe, but many products sold as henna contain Para-phenylenediamine or other chemical additives that are strongly oxidising. Black henna in particular carries a clear warning. If you use henna, choose products that guarantee purity and check with your doctor.

Bacterial and viral infections themselves can trigger a haemolytic crisis in someone with G6PD deficiency, independent of any food or drug. Inflammation increases oxidative stress throughout the body, destabilising red blood cells that are already fragile. Any febrile illness in a person with known G6PD deficiency therefore warrants close monitoring of symptoms.

What happens during a haemolytic crisis?

A crisis typically begins within 24 to 72 hours of exposure to the trigger. The G6PD-deficient red cells, lacking their protective enzyme, are oxidised and destroyed in a process called haemolysis. Their internal haemoglobin is released into the bloodstream and the kidneys attempt to clear it, turning the urine dark brown or cola-coloured. This dark urine is the most distinctive warning sign and the one that should prompt immediate action.

At the same time, the haemoglobin level in the blood drops rapidly, producing symptoms of acute anaemia: pallor, dizziness, shortness of breath and a racing heart. In severe cases acute kidney injury can develop if the haemoglobin load overwhelms the kidneys. Hospital treatment including intravenous fluids and sometimes blood transfusion is required in serious crises. Prevention by avoiding triggers is always preferable to treating a crisis that has already started.

The good news is that most G6PD crises are self-limiting. Once the trigger is removed, the bone marrow produces new, healthy red cells and blood values recover in two to four weeks in most cases. Crises in newborns and infants are more dangerous because blood volume is smaller and deterioration is faster.

The severity of crises also varies with the degree of enzyme deficiency. People with mild deficiency may tolerate small quantities of a trigger without a noticeable crisis, while those with severe deficiency can develop significant haemolysis from a much smaller exposure. Knowing your specific enzyme level helps calibrate how strictly you need to apply the avoid list.

Living a normal life with G6PD deficiency

The great majority of people with G6PD deficiency live entirely normal lives once they know their triggers. Routine blood tests are not necessary unless there is a reason for concern. The key is awareness: knowing your status and telling every prescriber and pharmacist before any new medication is issued. This single step prevents most crises.

Practical habits that help include keeping a brief note on your phone or a card in your wallet stating that you have G6PD deficiency and listing the main drugs to avoid. This makes a real difference in emergency situations where speed matters and medical staff may not know your history. Replacing naphthalene mothballs with cedar blocks, lavender sachets or other chemical-free options is a simple household change worth making immediately.

In fava bean season, particularly in Egypt, Syria and the Levant, children with G6PD deficiency may face social pressure to eat what everyone else is eating. It helps if teachers, carers and family members understand why the child avoids fava beans, so the child is not pressured and those preparing food take appropriate care.

Always check the ingredients list of any herbal remedy, food supplement or over-the-counter product before using it. Some essential oils and herbal extracts contain oxidising compounds. Asking a pharmacist to check unfamiliar products against the G6PD drug list is a simple precaution that takes seconds and can prevent a crisis.

Practical steps after a G6PD diagnosis

1Learn the food avoid list and tell everyone who cooks for you
2Tell every doctor and pharmacist about G6PD deficiency before any new prescription
3Remove naphthalene mothballs from your home and replace with safe alternatives
4Check henna product labels before use and avoid black henna
5If urine turns dark or you develop sudden pallor, go to the emergency department immediately
6Tell close family members because G6PD deficiency is inherited and others may be affected

G6PD deficiency in newborns and infants

Newborns with G6PD deficiency are at particular risk of severe neonatal jaundice in the first days of life. Their fragile red cells break down at a higher rate than normal, raising bilirubin to levels that can cause permanent brain damage if not treated promptly with phototherapy. This is why prompt recognition of significant neonatal jaundice in any baby requires checking whether G6PD deficiency is present.

Newborn screening programmes in several Arab countries now include G6PD testing alongside the routine heel prick test performed on the second or third day of life. Research in Gaza published in Clinical Genetics in 2016 recommended establishing a national newborn G6PD screening programme given the high local prevalence, and similar recommendations have been made in Egypt and parts of the Gulf.

Breastfeeding mothers of infants with G6PD deficiency need to be aware that oxidising compounds from foods they eat can pass into breast milk and trigger a crisis in the baby. Avoiding fava beans and other high-risk foods during breastfeeding is therefore important when the infant has confirmed G6PD deficiency. The midwife or paediatrician can advise on specific dietary modifications needed during the breastfeeding period.

If you or one of your children has been diagnosed with G6PD deficiency, Sihtak lets you record medications, foods eaten before any crisis episode and the symptoms that followed, building a clear picture that helps your doctor manage your care more precisely.

Frequently asked questions

Can G6PD deficiency be cured?

No, G6PD deficiency is a lifelong condition. There is currently no treatment that corrects the underlying gene defect. However, the absence of a cure does not mean a difficult life. The vast majority of people with G6PD deficiency live entirely normally once they know and avoid their triggers.

Are females protected from G6PD deficiency?

Not entirely. Females are less commonly fully affected because they carry two X chromosomes, so a defective copy on one is partially compensated by the normal copy on the other. However, females with two defective copies develop full disease, and some with one defective copy can have partial deficiency with real clinical symptoms.

Is paracetamol safe in G6PD deficiency?

Yes, paracetamol at standard doses is considered safe for people with G6PD deficiency and is generally preferred over aspirin, which can be risky at higher doses. Always inform your doctor of your G6PD status before any new medication regardless.

Can someone with G6PD deficiency eat lentils, chickpeas and peas?

These legumes are generally not on the strict prohibited list the way fava beans are, and the scientific evidence for avoiding them is much weaker. Whether they cause problems depends partly on the severity of the individual's enzyme deficiency. Discuss your specific diet with a doctor who knows your enzyme level.

Does G6PD deficiency affect pregnancy?

A pregnant woman with G6PD deficiency should avoid the usual trigger foods and drugs. If the fetus inherits G6PD deficiency, the baby may develop neonatal jaundice requiring phototherapy. Newborn screening identifies this quickly and treatment is straightforward when given promptly.

Do I need G6PD testing before travelling to malaria areas?

Yes, this is important because some malaria prevention drugs, particularly primaquine and tafenoquine, are very dangerous in G6PD deficiency. A travel medicine doctor needs to know your status to choose a safe antimalarial drug for prophylaxis or treatment.

When is the right time to test for G6PD?

The best time to test is at least two to four weeks after any haemolytic crisis has resolved. During or immediately after a crisis, the most fragile cells have already been destroyed, leaving behind only the newer, less deficient cells, which can give a falsely normal enzyme reading and miss the diagnosis.

Sources

This content is for health education only and is not a substitute for medical advice. If you have symptoms that worry you, see your doctor.