Anaemia in older adults is a symptom, not a diagnosis

Anaemia means a reduced concentration of haemoglobin — conventionally below 130 g/L in men and 120 g/L in women. It is not a disease. It is the visible end of a process, and the useful clinical question is always which process.

Prevalence rises sharply with age: roughly 10 per cent over 65, and over 20 per cent past 85. It is associated with fatigue, reduced exercise capacity, falls, cognitive impairment, longer hospital stays, and increased mortality — associations that persist after adjustment, though causality is harder to establish.

The three broad groups

Large population studies, including analyses of the US NHANES data, divide anaemia in older adults roughly into thirds.

Nutrient deficiency — about a third. Iron predominates, with B12 and folate accounting for a smaller share.

Anaemia of chronic disease and chronic kidney disease — about a third. Inflammation raises hepcidin, which traps iron in stores and blocks absorption; the body has iron but cannot use it. Kidney disease reduces erythropoietin production.

Unexplained anaemia of ageing — about a third, where no cause is found. Some of this reflects incomplete investigation, some reflects early myelodysplasia, and some reflects the age-related decline in haematopoietic reserve.

Why the cause matters more than the number

Because iron deficiency anaemia in an older adult is, until proven otherwise, blood loss from the gastrointestinal tract.

Older adults do not commonly become iron deficient from diet alone — the requirement falls after menopause, and dietary deficiency in a person eating adequately is unusual. The iron is going somewhere. That may be an ulcer, an angiodysplasia, an NSAID-related erosion, or a colorectal cancer.

Guidelines are consistent: unexplained iron deficiency anaemia in adults over fifty warrants investigation of both the upper and lower gastrointestinal tract. Prescribing iron and rechecking in three months, without investigation, is a well-recognised route to a late cancer diagnosis.

Treating iron deficiency properly

Oral iron remains first-line, and the way it is usually prescribed is now understood to be suboptimal.

A dose of iron raises hepcidin for around 24 hours, which blocks absorption of subsequent doses. Trials have shown that alternate-day dosing of a single tablet produces greater total absorption than daily or twice-daily dosing, with substantially fewer gastrointestinal side effects. Three times a day, the traditional regimen, is close to the worst option available.

Take it with vitamin C or orange juice, which improves absorption. Avoid taking it with tea, coffee, calcium supplements or dairy, all of which impair it. Expect black stools, which is normal. Constipation is the commonest reason people stop.

Recheck at four weeks: haemoglobin should have risen by around 10 g/L. If it has not, either the diagnosis is wrong, the tablets are not being taken, or there is ongoing loss.

Intravenous iron is appropriate where oral is not tolerated, not absorbed — in coeliac disease, after gastric surgery, in inflammatory bowel disease — or where correction is needed quickly. Modern preparations are safe and often given as a single infusion.

B12 deficiency, which presents oddly

B12 deficiency in older adults is common, usually from malabsorption rather than intake, and its neurological consequences can appear before any anaemia does. Peripheral neuropathy, unsteadiness, cognitive change and mood disturbance can all occur with a normal blood count.

This matters because neurological damage from prolonged deficiency may not fully reverse. A borderline B12 level in a symptomatic person warrants further testing — methylmalonic acid is more sensitive — rather than reassurance.

Long-term metformin and proton pump inhibitor use both deplete B12 and warrant periodic checking, which is routinely forgotten.

Anaemia of chronic disease

Here the anaemia is a consequence of the underlying condition — rheumatoid arthritis, chronic infection, malignancy, heart failure, chronic kidney disease. It is typically mild to moderate, with normal or high ferritin and low transferrin saturation.

Treating it means treating the cause. Iron supplementation generally does not help and may not be absorbed, though intravenous iron has a role in some patients, particularly in heart failure where trials have shown improvement in symptoms and exercise capacity.

Erythropoiesis-stimulating agents are used in chronic kidney disease with careful targets — overcorrection increases cardiovascular events, which was a significant finding from the trials.

When to push

If you have been told you are anaemic and given iron without investigation, the reasonable questions are: what is my ferritin and transferrin saturation, has my B12 been checked, and have we established where the iron is going?

And if fatigue has been attributed to age, a full blood count is one of the cheapest tests in medicine. It will not always find something. When it does, it frequently finds something that matters.