G6PD Blood Test: Deficiency, Favism & Drugs to Avoid

G6PD (glucose-6-phosphate dehydrogenase) is an enzyme that protects your red blood cells from oxidative stress. When it runs short — G6PD deficiency — red cells turn fragile and can break down suddenly (hemolysis) after certain foods, infections, or medications. It is the most common enzyme deficiency in the world. This guide explains what the G6PD blood test does, how to read your normal ranges, what a deficiency means, the list of triggers to avoid, and one major trap: never test G6PD during a crisis. This marker is best understood alongside the complete blood count (CBC) and the hemolytic anemia work-up.

Key takeaways

• G6PD is an enzyme in red blood cells that defends them against oxidative stress; its deficiency is the most common inherited enzyme deficiency worldwide (~400–500 million people).¹²
• The gene sits on the X chromosome: deficiency mainly affects men and is common in people of African, Mediterranean, Middle Eastern, and Asian ancestry — regions where malaria was historically endemic.¹³
• Between crises, most people have no symptoms and live a normal life; the danger is acute hemolysis triggered by fava beans (favism), an infection, or an oxidant drug.¹⁴
• High-risk drugs include primaquine, tafenoquine, rasburicase, dapsone, methylene blue, some sulfonamides, and nitrofurantoin; also avoid naphthalene (mothballs). Your clinician sets the exact list.⁵⁶
• The test measures G6PD enzyme activity. ⚠️ The trap: don't test during a crisis — young red cells, rich in enzyme, produce a falsely normal result. Repeat the test later (2–3 months).¹⁷
• G6PD is not a cancer marker: it's a genetic and enzymatic test that mainly makes certain prescriptions safe and explains a bout of hemolysis.

What is G6PD?

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme present in every cell but vital to red blood cells. Its job is to make a protective molecule, NADPH, which lets red cells neutralize oxidative attacks (free radicals). Think of it as the red cell's antioxidant shield.¹²

The G6PD gene lies on the X chromosome. Because men have only one X, a single "deficient" copy is enough to cause the condition — so men are more often and more severely affected than women, who carry two X chromosomes and are usually carriers (sometimes partially deficient).¹⁴

More than 200 gene variants exist. Deficiency is very common in regions where malaria once thrived (sub-Saharan Africa, the Mediterranean rim, the Middle East, South and Southeast Asia): G6PD deficiency gives partial protection against malaria, which is why it spread so widely over the course of evolution.¹³

G6PD deficiency is not a constant illness. Most people with the deficiency have no day-to-day symptoms. Red cells only "break" when hit by a significant oxidative stress — it's an episodic problem, not a chronic disease in the vast majority of cases.

Why the test is done

Your clinician may order a G6PD blood test in several targeted situations:¹⁷

• to explain hemolysis (red cell destruction) after fava beans, an infection, or a medication — often once an anemia shows up with a high bilirubin and a collapsed haptoglobin;
• before prescribing a high-risk oxidant drug, especially primaquine or tafenoquine (treatment of Plasmodium vivax malaria) and rasburicase: this is a safety screen;⁸
• for neonatal jaundice (newborn jaundice) that is prolonged or severe, especially in higher-risk populations;⁹
• when there is a family history of the deficiency or unexplained hemolytic anemia.

Outside these indications, G6PD is not tested routinely. It is neither a general screening test nor a marker to monitor regularly.

Do you need to fast?

No — the G6PD test does not require fasting. It's a simple blood draw from a vein, done at any time of day. The one truly important precaution is the timing of the draw relative to a possible crisis (see below). If other tests share the same order (liver panel, glucose…), follow the overall fasting instruction you were given (see Do you need to fast before a blood test?).¹⁰

Normal ranges

The test measures G6PD enzyme activity in red blood cells, reported in units per gram of hemoglobin (U/g Hb). Values and cutoffs vary widely by lab and method — always compare against the range printed on your report. Results are often expressed as a percentage of normal activity (the median of a reference population).

Good to know: exact values depend on the lab's method. The World Health Organization classifies deficiency by residual activity, and the common variants (Mediterranean, African "A–"…) leave activity ranging from roughly 2% to 30% of normal.¹¹ To decide on antimalarial treatment, quantitative point-of-care tests use specific cutoffs — typically ≥30% activity for daily primaquine and ≥70% for single-dose tafenoquine — a decision made by your clinician.⁸¹

Understanding your results

Low G6PD (deficiency)

Low activity indicates G6PD deficiency. In practice, this means your red cells are less protected against oxidative stress and can break down suddenly (acute hemolysis) when exposed to a trigger. A typical crisis appears 1 to 3 days after the trigger: intense fatigue, pallor, dark urine (tea- or cola-colored), and sometimes jaundice. On labs it comes with an anemia, a rising bilirubin, a collapsing haptoglobin, and a jump in reticulocytes (the marrow makes fresh red cells to compensate).¹⁵

Classic triggers worth knowing and avoiding:¹⁵⁶

• fava beans (favism), raw or cooked — occasionally even through breast milk or pollen inhalation in very sensitive people;
• certain oxidant drugs: primaquine, tafenoquine, rasburicase, dapsone, methylene blue, some sulfonamides (including co-trimoxazole), and nitrofurantoin;
• naphthalene (mothballs);
• infections (a common infection alone can set off a crisis).

Between crises, a person with the deficiency is usually symptom-free. What to avoid and how to react to a crisis is defined by your clinician, often with a card or a personalized list of drugs to avoid.

In newborns, G6PD deficiency is a common cause of neonatal jaundice that is sometimes severe — one reason to monitor bilirubin in at-risk newborns.⁹⁴

Normal or high G6PD

Normal activity is reassuring: it makes a deficiency very unlikely. A "high" value generally has no pathological meaning on its own.

⚠️ The single most important trap: a falsely normal result during a crisis. In acute hemolysis, the most deficient (oldest) red cells are destroyed first; the blood then fills with young red cells (reticulocytes) that are rich in enzyme. As a result, measured activity can look normal even though the person is genuinely deficient. The rule: don't trust a test done in the immediate aftermath of a crisis, and repeat it later — usually 2 to 3 months afterward, once the red cells have turned over.¹⁷

G6PD and cancer. G6PD is not a tumor marker, and a deficiency does not mean cancer. It's a genetic and enzymatic test that speaks to how well your red cells resist oxidative stress — nothing more.

What affects your G6PD

Several factors change the result or its interpretation: the timing of the draw relative to a crisis (the #1 factor, because of the false-negative risk), sex (female carriers can have intermediate activity that's harder to classify), a recent transfusion (normal donor blood skews the measurement — you have to wait), age (activity is slightly higher in newborns and very young children), and the lab's method. Always mention a recent transfusion or an ongoing crisis: it changes how the result is read.¹¹¹

Recent research

According to recent PubMed-indexed publications:

• Point-of-care G6PD screening before malaria treatment. To cure Plasmodium vivax malaria for good, clinicians use primaquine or tafenoquine — two drugs that cause severe hemolysis in deficient people. Quantitative rapid tests (at the bedside) now allow clinicians to measure G6PD activity before treating and tailor the drug; a study in the Brazilian Amazon confirms real-world feasibility.⁸ WHO recommends this screening before 8-aminoquinolines.¹¹ (Brito M et al., Lancet Glob Health, 2024 — DOI.)
• Treating anyway, but differently. In deficient patients, weekly low-dose primaquine regimens have been tested to cure P. vivax malaria while limiting hemolysis — showing that a deficiency doesn't close every therapeutic door, under medical supervision.¹² (Taylor WRJ et al., PLoS Negl Trop Dis, 2023 — DOI.)
• Understanding newborn jaundice. A 2022 review summarizes the pathophysiology and diagnosis of G6PD-related neonatal hyperbilirubinemia and the wide heterogeneity of gene variants.⁹
• Malaria protection confirmed. Research shows the Mediterranean variant of the deficiency reduces malaria-parasite growth, clarifying why the deficiency stayed so common in exposed populations.³

These findings concern diagnosis and research; they do not authorize self-medication and do not replace your physician's advice.

Get your G6PD interpreted by AI DiagMe

A G6PD result is never read alone: its meaning depends on context (whether a crisis is ongoing, a recent transfusion, sex), on your other markers — CBC, bilirubin, haptoglobin, reticulocytes — and on the medications you take. That cross-reading is what gives the result its real value.

👉 AI DiagMe interprets your lab results — blood, urine, or stool — in plain language, taking your whole profile into account. An informational service that does not provide a diagnosis and complements, never replaces, your physician.

Frequently asked questions

The bottom line

G6PD is your red cells' antioxidant enzyme; its deficiency — the most common in the world, and X-linked — leaves them vulnerable to acute hemolysis triggered by fava beans (favism), infections, and certain oxidant drugs (primaquine, tafenoquine, rasburicase…). The test measures enzyme activity; remember the false-negative trap during a crisis (repeat it later), that values vary by lab, and that between crises life is normal when you avoid triggers. It is not a cancer marker. No value is read alone — it's your whole set of markers and context that counts, which is what AI DiagMe provides, alongside your physician.

Sources

Official sources and peer-reviewed publications (PubMed) used for this guide: