The HbA1c test does not measure sugar alone — it measures sugar multiplied by time. The number on your lab report is the product of two ingredients: how much glucose was in your blood, and how long your red blood cells lived to record it. Almost everyone pays attention to the first ingredient. Almost nobody asks about the second. And when the time factor is disturbed — by iron deficiency, kidney disease, pregnancy, bleeding, a transfusion, or an inherited hemoglobin trait — the number moves while your blood sugar has not moved at all. This article explains when that happens, how to tell an instrument problem from a blood problem, and why that distinction changes what you should actually do. This is educational content only and is not a substitute for advice from your doctor.
What does the HbA1c test actually measure?
When glucose rises in your blood, some of it sticks to the hemoglobin inside your red blood cells. That attachment is not temporary. Cleveland Clinic puts the idea in one sentence every patient deserves to carry: "When you have glucose in your blood, it sticks to hemoglobin… it can stay there for around three months — about how long the average red blood cell lives."
Notice what that sentence says. The test's window is not three months because somebody chose that number. It is three months because that is how long a red blood cell lives. The test borrows the cell's lifespan and uses it as a logbook.
Why does this matter?
Because the logbook can close early. If a generation of red cells dies before its time, it recorded fewer days, so the number reads lower — even though your blood sugar was high the whole while. If your cells survive longer than usual, they recorded more days, so the number reads higher. In both cases your glucose did not change. What changed was the time.
So HbA1c is an excellent test — provided the second factor in the equation is normal. This article is about the situations where it is not, and how to know whether you are one of them. In substance this is the same lesson as our article on magnesium: a test can be accurate about what it measures and still be insufficient for the question you are asking it.
Two kinds of failure, not one — and the difference decides what to do
Here is the key most articles on this subject leave out. Errors in HbA1c are not one category. They are two, and they are fundamentally different.
- Analytical failure (in the instrument). Something in your blood fools the measurement method itself. The National Glycohemoglobin Standardization Program (NGSP) lists here the inherited hemoglobin traits — HbS, HbC, HbE and HbD traits — and elevated fetal hemoglobin (HbF), along with chemical modifications such as "carbamylated Hb in patients with renal failure" and "acetylated Hb in patients taking large amounts of aspirin." The crucial point: this failure depends on the instrument. That is why the program publishes a table examining each measurement method separately, and counts interference as clinically significant when it exceeds "±6% at 6 and/or 9% A1C."
- Biological failure (in the blood). Here the instrument is not fooled at all. The underlying reality has changed, because the lifespan of your cells has changed. The NGSP's sentence on this point is the single most important line in this article: "Any condition that shortens erythrocyte survival or decreases mean erythrocyte age (e.g., recovery from acute blood loss, hemolytic anemia) will falsely lower HbA1c test results regardless of the assay method used."
"Regardless of the assay method used." That clause is the dividing line between the two categories, and it is what turns a list of worries into a usable rule:
An instrument failure is fixed by changing the instrument. A blood failure cannot be fixed by any instrument — because it is not a measurement error at all. It is the right question put to the wrong tool.
Instrument failure: one sample of blood, two different numbers
In March 2026 a case was published that demonstrates the first category so plainly it needs no explanation. A 54-year-old woman with sickle cell trait (identified at age 28) and a 26-year history of type 2 diabetes presented with progressive fatigue and intermittent pain in both knees. Her blood was drawn, and her HbA1c was measured by two different methods:
- By high-performance liquid chromatography (HPLC): 10.1%
- By fluorescence immunoassay (FIA): 7.6%
One sample. One patient. One moment. And a gap of 2.5 percentage points — a difference that separates, in everyday practice, "roughly at target" from "out of control," and can separate leaving treatment alone from changing it.
The researchers explain precisely why. "Ion-exchange HPLC separates hemoglobin fractions according to their electrical charge… The presence of HbS or its glycated forms may alter hemoglobin fraction separation in ion-exchange HPLC." The other method, by contrast, relies "on the recognition of the glycated N-terminal epitope of the β-chain of HbA by specific antibodies," and the amino-acid substitution in HbS "may alter the three-dimensional structure," affecting antibody binding. In other words the two methods are measuring something physically different, and the inherited trait interferes with each of them in its own way.
Their conclusion, verbatim: "This case highlights that hemoglobin variants may cause significant analytical interference in HbA1c measurements, leading to clinically discordant results. It underscores the importance of selecting an appropriate HbA1c measurement method, as different analytical techniques may be variably affected by hemoglobin variants."
And here we apply the brakes immediately. This is a single case, published as a case report — not a study of a group — and it does not say that everyone with sickle cell trait will get two widely separated results. What it says is that this is possible, and that the method matters. Clinical Laboratory News fills in the rest: methods are not equal in the face of interference. Boronate affinity chromatography is "virtually free of interferences from hemoglobin variants," while immunoassays are more exposed, because "any factor that prevents glycation or any amino acid substitution in the β-chain N-terminal epitope may hinder antibody binding, leading to falsely low or undetectable HbA1c values" — particularly with fetal hemoglobin above 10%.
Blood failure: a "normal" result during an acute crisis
The second category is more dangerous, because changing laboratories will not detect it. The clearest published example appeared in January 2026. A 63-year-old woman with previously unrecognised hemoglobinopathies arrived at the emergency department with a one-week history of passing large volumes of urine, extreme thirst, and a fungal infection.
Her blood glucose on admission: 609 mg/dL. Her HbA1c at that same moment: 4.8% — a number any reader would take as entirely normal, in fact below the prediabetes threshold.
Nor was this a one-off coincidence. In previous years her fasting glucose had run between 108 and 144 mg/dL while her HbA1c stayed at 4.6–5.0%. Over two years of follow-up her fructosamine — a marker that does not depend on red cell lifespan — remained between 253 and 263 µmol/L, while her HbA1c stayed below 4.2%. The diagnosis finally came through an episode of diabetic ketoacidosis, after which she was found to have sickle cell disease (HbS 49.1%) and alpha thalassemia, with signs of long-standing undiagnosed diabetes: progressive visual changes over several months and chronic peripheral neuropathy over several years.
The authors' explanation: "In SCD, chronic hemolysis shortens RBC lifespan, reducing the time hemoglobin is available for glycation and thereby producing falsely low HbA1c values despite sustained hyperglycemia." And their conclusion, verbatim: "This case illustrates the critical limitations of HbA1c in accurately diagnosing and monitoring diabetes in niche patients with underlying hemoglobinopathies such as SCD and alpha thalassemia. In such cases, reliance on HbA1c alone can mask the presence and severity of hyperglycemia, potentially delaying diagnosis and appropriate treatment."
We report their limitations as they stated them. Laboratory evidence of hemolysis in this patient was only "minimal," and "the absence of additional hemolysis markers, such as lactate dehydrogenase, haptoglobin, and reticulocyte count, limits definitive quantification of hemolytic burden." They were equally careful about the alternative they used: "Fructosamine does not account for alterations in protein turnover or erythrocyte-independent metabolic variability." No substitute test is perfect either.
This case is exactly why the US National Institute of Diabetes and Digestive and Kidney Diseases publishes a firm rule: "Health care professionals should not use the A1C test for patients with HbSS, HbCC, or HbSC" — that is, the disease states, not merely carrier traits — and should consider "alternative forms of testing for these patients, such as glycated serum protein or glycated albumin," noting that these reflect glucose over two to three weeks rather than three months.
The common causes nobody mentions at the blood draw
If this article stopped at inherited traits it would leave a false impression. The most common reasons an HbA1c gets distorted are not genetic at all. They are ordinary things, affecting far more people, that it occurs to nobody to mention when the needle goes in.
Iron deficiency and anemia — and the direction matters
The direction is not uniform, and that is the surprise. The NGSP notes that "iron deficiency anemia… is associated with higher HbA1c and higher fructosamine," and that iron replacement therapy "lowers both HbA1c and fructosamine concentrations." So iron deficiency pushes the number up, and treating it pushes the number down — with no change in your diet and no change in your blood sugar.
A study of 7,308 adults measured what this does to diagnosis itself. The headline finding: "Approximately 65% of individuals with diabetes in our sample were concordantly classified with diabetes using both FBG and HbA1c, while 35% had a discordant diabetes classification." More importantly, the discordance did not run one way. Women with iron deficiency were less likely to be classified as having diabetes by HbA1c (relative risk ratio 0.52; 95% CI 0.29–0.95), while men with anemia were more likely to be classified as having prediabetes by HbA1c (1.81; 95% CI 1.16–2.82). The authors' conclusion, verbatim: "Estimating diabetes prevalence using HbA1c may result in under-diagnosis in women with ID and over-diagnosis in men with anemia."
Their own limitations: no oral glucose tolerance test (the gold standard) was used; fasting glucose and HbA1c were each measured only once per participant; no data on inherited hemoglobin variants were available; and pregnant women were excluded. So this is a strong signal about the size of the problem, not a verdict on any individual patient.
Kidneys, pregnancy, transfusion and bleeding
The NGSP on kidneys is direct: "HbA1c underestimates glycemic control in diabetic patients on dialysis," with glycated albumin described as "a more robust indicator" in that setting. Pregnancy alters red cell turnover and blood volume, which is one reason HbA1c alone is not relied on to assess diabetes in pregnancy — a subject we covered separately in our article on gestational diabetes. A transfusion introduces cells of a different age into the logbook, and bleeding or recovery from it shortens mean cell age — all of these belong to the second category, the one no change of instrument will fix.
Cleveland Clinic publishes a practical list worth reading before any test. Among the causes of a falsely low result: blood transfusion, chronic kidney failure, erythropoietin-stimulating agents, hemorrhage, iron supplementation, liver cirrhosis, pregnancy, sickle cell anemia, and hemolytic anemia. Among the causes of a falsely high result: iron-deficiency anemia, thalassemia, vitamin B12 deficiency, high triglycerides, and certain medications.
The Saudi picture: two facts in one file that never met
Here the question becomes distinctly Saudi, and in a way we have not encountered in any topic we have written about before. The national premarital screening program, in an analysis published in the Journal of Epidemiology and Global Health in 2024, examined data from 1,871,184 individuals between 2011 and 2018 (mean age 30.2 years). The result: HbS was present in 4.7% of those screened — roughly one person in every twenty-one — accounting for 78.5% of all abnormal findings; beta thalassemia was present in 1.2%. The geographical spread is dramatic: sickle cell trait peaks in Jazan (135.7 per 1,000) and the Eastern Region (114.4 per 1,000), and falls to just 2.0 per 1,000 in Hail. This is consistent with an earlier analysis of the same program covering 1,572,140 people from 2004 to 2009: 45.1 per 1,000 nationally, peaking in the Eastern Region.
Now set that beside another fact: diabetes is very common in Saudi Arabia, and HbA1c is the most widely used tool for diagnosing and monitoring it. The consequence is that hundreds of thousands of Saudis already know they carry a hemoglobin trait — because a national program told them so, by name, before they married. The information is not missing and does not require a new test. It is in the person's own hands, written on a sheet of paper they either kept or forgot.
But it was created inside a system that talks about marriage and childbearing, and it is needed now inside a system that talks about diabetes — and the two systems have never spoken to each other. The patient is not asked to mention it at the blood draw, nobody enquires, and it does not travel automatically onto the test request. In every previous topic, the Saudi gap has been an appointment that was never made, or care that arrived too late, or a box on an order form that nobody ticked. Here the gap is a new kind: the information exists, is accurate, and is owned by the person it describes — but it is filed in the wrong drawer. Moving it requires no budget, no equipment and no policy. It requires one sentence, said by the patient.
Before you distrust your test: what the evidence says about its reliability
If this article ended at the previous paragraph it would be worse than not written. The real risk of a piece like this is not that someone neglects their test, but that they lose confidence in a good tool and stop using it. So we put the brakes before the advice, not after it.
- HbA1c remains the cornerstone. According to a professional report on the American Diabetes Association's 2026 Standards of Care (published March 2026), the standards "reaffirm it as a cornerstone of diabetes screening and monitoring, with continued emphasis on National Glycohemoglobin Standardization Program-certified methods" — while at the same time stressing "the importance of recognizing when results may be unreliable."
- Standardization is not a formality. "About 99% of U.S. clinical laboratories use methods certified by the National Glycohemoglobin Standardization Program."
- And the most important brake: modern instruments have largely solved the common-trait problem. The same report quotes an expert at an instrument manufacturer — and we flag it as a manufacturer's testimony rather than independent evidence — saying that modern assays "can now report accurate HbA1c results in the presence of common hemoglobin variants like hemoglobin S, hemoglobin C, or hemoglobin D." That is borne out by the NGSP's own table: most methods in use today show no clinically significant interference from HbS or HbC trait.
The honest reading, then, is not "don't trust your test." It is: for most people on most modern instruments, HbA1c is accurate and sufficient. What this article is about is a set of identifiable groups — and the common biological situations (iron deficiency, kidney disease, pregnancy, bleeding, transfusion) that better instruments do not address at all.
So what should you do?
In September 2026 a review in Frontiers in Endocrinology proposed a clinical-laboratory framework for exactly this situation. Two of its sentences matter most. The first extinguishes any hope of a magic replacement: "The framework does not replace hemoglobin A1c with a single alternative marker" — there is no one test that takes its place, only options (continuous glucose monitoring, structured self-monitoring, laboratory plasma glucose, glycated albumin, fructosamine) chosen according to the decision at hand. The second is the best advice in this entire subject: "discordance is a reason to slow interpretation before making any changes to treatment."
We record the review's limitation as its authors stated it, verbatim: "This is a narrative review with a proposed interpretive framework, not a systematic review, meta-analysis, guideline, or prospectively validated algorithm," and its present role is "to support clinician-laboratory communication and to define testable research questions." It is a way of thinking, not a prescription.
The practical steps are few:
- Say the sentence at the blood draw. If you know you have a hemoglobin trait (from premarital screening or any previous test), or anemia, or iron deficiency, or kidney disease, or a recent transfusion, or you are pregnant — mention it. One sentence can change how the whole number is interpreted.
- Keep your premarital screening result, and if you cannot find it, ask for it. It is permanent medical information about you, not a one-time document.
- If your HbA1c contradicts your day-to-day readings, the contradiction is information, not noise. Your home meter or continuous monitor says something about your glucose now; HbA1c says something about three months. A large disagreement between them is the beginning of a question, not the end of an answer.
- Ask your doctor one specific question: "Is there anything in my case that makes HbA1c unreliable for me, and if so what is the right alternative?" And follow up at the same laboratory, since a change of method alone can move the number. This is a question for your doctor, not a decision for you to make.
Who should pay closer attention, and when is it an emergency?
This article is educational and does not replace advice from your doctor. No test reading and no medication decision should be based on an article.
Signs that call for urgent medical care right away — and these are precisely how the patient in the case above arrived at the emergency department: heavy urination and severe thirst that will not settle, rapid unintended weight loss, nausea, vomiting and abdominal pain, fast deep breathing or an unusual smell on the breath, confusion or extreme drowsiness. Do not wait for an HbA1c to tell you something. Seek care.
Those with the strongest reason to raise the reliability question with their doctor:
- Anyone who knows they have a hemoglobin trait or disorder — especially HbSS, HbSC or HbCC, where the published rule is not to use the test at all.
- Anyone with anemia of any kind, or iron deficiency, or who has recently started iron supplements or treatment for anemia.
- People with chronic kidney disease, particularly those on dialysis or receiving erythropoiesis-stimulating agents.
- Anyone recently transfused, bleeding, or recovering from blood loss.
- Pregnant women and those planning pregnancy, and anyone with a family history of hemoglobin disorders.
- Anyone who finds a persistent contradiction between their HbA1c and their daily readings.
And any decision about medication — starting, stopping or changing a dose — belongs to your doctor, not to something you read.
Where does Bakery 8 stand in this, and what we will not say about ourselves
Here we have to say something that does not serve our interests, and we say it because it is true.
The entire healthy-baking category — ourselves included — ultimately sells itself through a number. The most persuasive testimonial in our marketing is the customer who says: "My HbA1c was this, and after I switched my bread it became that." That testimonial works. We know it works.
But this article has just spent thousands of words explaining that this number can fall for reasons that have nothing to do with food: a transfusion, kidney disease, bleeding, or — as the NGSP itself states — simply starting treatment for iron deficiency, which "lowers both HbA1c and fructosamine concentrations." A customer who began iron tablets in the same month they began our bread may see a drop we deserve no credit for whatsoever.
So: we cannot know which explanation is the true one in any individual customer's case — and neither can the customer. The only honest conclusion is that a fall in a customer's test result is not evidence about a product, and we will not use it as evidence. Our customers' lab numbers are not marketing material, and they will not become it.
What we do claim is far narrower: our products are low in carbohydrate, free of added sugar and gluten-free, which means they reduce one carbohydrate load in one meal. They do nothing for the lifespan of your red blood cells, nothing for your inherited trait, nothing for your kidney function and nothing for your iron stores — the very factors this article says may be the reason for your number. No bread — not ours, not anyone's — repairs an unreliable test.
So if lowering carbohydrate is part of a plan you agreed with your doctor, we have low-carb bread and keto granola. Healthy and delicious — a description of what is in the loaf, not a test result on your behalf. That is all we claim.
Frequently asked questions
Does sickle cell trait mean my HbA1c is wrong?
Not necessarily. Most methods in use today show no clinically significant interference from HbS trait. But methods are not equal, and a case has been published in which one sample of blood gave 10.1% by one method and 7.6% by another. Mention your trait, and ask your doctor whether your laboratory's method is appropriate for it.
What is the difference between an instrument error and a blood error?
An analytical error means something in your blood fooled the measurement method; it depends on the instrument and can be resolved by changing the method. A biological error means the lifespan of your red cells genuinely changed, so the underlying reality changed — and that kind, in the NGSP's words, happens "regardless of the assay method used," so no instrument fixes it.
Does iron deficiency raise or lower the result?
Iron deficiency is associated with a higher HbA1c, and treating the deficiency brings the number down. So someone can appear to have prediabetes when they do not. Conversely, a study of 7,308 adults found the direction differed by group: under-diagnosis in women with iron deficiency, over-diagnosis in men with anemia.
What is the alternative if my test is unreliable?
There is no single alternative. The options include glycated albumin and fructosamine (which reflect two to three weeks rather than three months), continuous glucose monitoring, and laboratory plasma glucose. Choosing between them depends on the clinical decision being made, and is determined by your doctor together with the laboratory — not by an article.
References
- National Glycohemoglobin Standardization Program (NGSP). Factors that Interfere with HbA1c Test Results. Page updated 23 June 2026.
- National Glycohemoglobin Standardization Program (NGSP). HbA1c Assay Interferences (method-by-method interference table; clinical-significance criterion >±6% at 6 and/or 9% A1C).
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Sickle Cell Trait and Other Hemoglobinopathies and Diabetes: Important Information for Providers.
- Cleveland Clinic. A1C Test (diagnostics page).
- Rakotonjafiniarivo FH, Fenomanana J, Rakotomalala SM, Rakoto Alson AO, Ranaivosoa MK. Major Discordance in Hemoglobin A1c Measurement in Sickle Cell Trait: Effect of Analytical Methods. Cureus. 2026;18(3):e105572. doi:10.7759/cureus.105572
- Toperzer K, Moon A. Diagnostic Limitations of Hemoglobin A1c in the Setting of Compound Hemoglobinopathy: A Case Report of Sickle Cell Disease, Alpha Thalassemia, and Occult Diabetes. Cureus. 2026;18(1):e101623. doi:10.7759/cureus.101623
- Wu T, Guan Z, Cai W. Glycemic assessment when hemoglobin A1c is unreliable: a clinical-laboratory framework for kidney disease, anemia, and hemoglobinopathies. Frontiers in Endocrinology. 2026;17:1898713. doi:10.3389/fendo.2026.1898713 (published 1 September 2026)
- Attard SM, Herring AH, Wang H, Howard A-G, Thompson AL, Adair LS, Mayer-Davis EJ, Gordon-Larsen P. Implications of iron deficiency/anemia on the classification of diabetes using HbA1c. Nutrition & Diabetes. 2015;5(6):e166. doi:10.1038/nutd.2015.16
- Aljabry M, Sulimani S, Alotaibi G, Aljabri H, Alomary S, Aljabri O, Sallam M, Alsultan A. Prevalence and Regional Distribution of Beta-Hemoglobin Variants in Saudi Arabia: Insights from the National Premarital Screening Program. Journal of Epidemiology and Global Health. 2024;14(3):1242–1248. doi:10.1007/s44197-024-00281-x
- Memish ZA, Owaidah TM, Saeedi MY. Marked regional variations in the prevalence of sickle cell disease and β-thalassemia in Saudi Arabia: Findings from the premarital screening and genetic counseling program. Journal of Epidemiology and Global Health. 2011;1(1):61–68. doi:10.1016/j.jegh.2011.06.002
- Sofronescu AG. Navigating Hemoglobin A1C Measurements for Diabetes Care. Clinical Laboratory News (ADLM), 9 September 2025.
- Arnett A. Diabetes Testing Moves Earlier — and Gets More Complex (report on the ADA 2026 Standards of Care and their laboratory impact). Clinical Lab Products, 17 March 2026.
Related keywords: HbA1c test accuracy, when HbA1c is unreliable, glycated hemoglobin, sickle cell trait and A1C, iron deficiency and HbA1c, hemoglobin variants A1C interference, glycated albumin, fructosamine, premarital screening Saudi Arabia, diabetes diagnosis.