Rickets: the Victorian disease that never quite left

Rickets carries the weight of a bygone era — think grainy photographs of bow-legged Victorian mill children. So it unsettles people to learn it still appears in twenty-first-century paediatric wards. The honest picture is more nuanced than either "eradicated" or "epidemic," and getting that picture right matters, because the disease is almost entirely preventable with food, sunlight and, where needed, a cheap supplement.

Before we look at prevention, it helps to understand what rickets is at the level of the bone itself — because the name describes a very specific mechanical failure, not simply "weak bones."

01 · DefinitionWhat rickets actually is

A child's bones grow at the epiphyseal growth plates — zones of cartilage near the ends of the long bones. Growth works like a two-stage production line: cartilage is laid down first as a soft protein scaffold called osteoid, and then calcium and phosphate crystals are deposited into that scaffold to harden it. This hardening step is called mineralisation.

Rickets is what happens when the scaffold keeps being built but cannot be mineralised. New osteoid piles up at the growth plate, never hardens, and the result is soft, pliable bone that bends under the child's own weight and the pull of their muscles. The same underlying failure in an adult — whose growth plates have long since fused — is called osteomalacia. Same defect, different stage of life, different consequences.

02 · The UK pictureRickets in modern Britain

It is tempting to frame rickets as a steady, alarming comeback. The data ask for more care. Hospital admissions for rickets in England did climb through the 2000s, reaching their highest level in five decades around 2007–2011. But primary-diagnosis admissions have since fallen by roughly 40%. The trajectory is not a runaway resurgence; it is a disease that flared and then receded, while never disappearing.

The most careful national estimate comes from a British Paediatric Surveillance Unit study, which tracked every case reported by UK consultant paediatricians over two years. It found an annual incidence of 0.48 per 100,000 children under 16, rising to 1.39 per 100,000 in the under-fives — roughly one child in every 200,000. Rare, in absolute terms. The researchers themselves described the incidence as "lower than expected."

There is a second trap worth avoiding. You may see headlines about "over 190,000 hospital admissions from vitamin deficiency." Those figures are real, but they are dominated by iron deficiency, not vitamin D — and analysts have shown that much of the apparent rise in vitamin-deficiency admissions reflects increased testing and coding rather than a genuine surge in disease. It is important, on an evidence-based site, not to borrow a frightening number that the underlying data won't support.

Deficiency is common; rickets is rare

The apparent paradox — widespread low vitamin D status alongside rare rickets — dissolves once you separate the two. The National Diet and Nutrition Survey found low vitamin D status in around 16% of adults aged 19–64 and 19% of children aged 11–18. Deficiency in the blood is genuinely common. But only a small, vulnerable subset — mostly under-fives with additional risk factors — go on to develop the bone disease itself.

Three modern factors concentrate that risk:

Geographic latitude

Northern Britain sits far enough from the equator that, for much of autumn and winter, sunlight simply isn't strong enough. The UVB wavelengths that trigger vitamin D synthesis in skin are largely absent from the UK sky between roughly October and March. Sitting by a sunny window does nothing: window glass blocks UVB.

Modern indoor lives

Screen-heavy childhoods, dense urban living and (sensible) high-factor sunscreen all reduce the skin's exposure to the little UVB that is available. The behaviours that protect against skin cancer also, unavoidably, reduce dermal synthesis.

Skin tone

Melanin is protective against UV damage, but it also absorbs the UVB needed to make vitamin D. Children with darker skin — of South Asian, Middle Eastern, African or Afro-Caribbean heritage — may need several times longer in the sun to synthesise the same amount. The surveillance data reflect this starkly: the great majority of UK rickets cases occur in Black and South Asian children.

03 · The cascadeFrom food to hormone: how vitamin D is switched on

To prevent the disease we have to follow the molecule. There are two dietary forms of vitamin D, and neither is active when you eat it.

Both forms are inert until the body performs a two-step activation, in two different organs:

Step 1 — the liver. Liver enzymes hydroxylate D2 or D3 into 25-hydroxyvitamin D — the storage-and-transport form, and the one a blood test actually measures. It circulates with a half-life of two to three weeks.

Step 2 — the kidneys. This is the tightly controlled final switch. When blood calcium falls, the parathyroid glands release parathyroid hormone, which signals the kidney to convert 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D — the active hormone that tells the gut to absorb calcium.

04 · Storage kineticsHalf-lives and the obesity paradox

Because vitamin D is lipophilic, its behaviour in the body is governed by fat. Raw, freshly made vitamin D lasts only hours to a couple of days before it is either processed by the liver or drawn into fat stores. The circulating form, 25-hydroxyvitamin D, lasts two to three weeks. But vitamin D locked deep in adipose tissue is remarkably stable, with a half-life of one to two months (up to three in deep tissues). Cut off all sun and dietary intake, and these reserves drain over roughly two to four months.

The obesity paradox

Intuition says a child with more body fat has a bigger vitamin D reserve to draw on. Biochemically, the opposite holds: higher body fat raises the risk of deficiency and rickets.

The driver is adipose sequestration. A large fat mass acts as a reservoir that vitamin D distributes into and is held within — effectively diluting it across a much bigger volume and lowering the concentration circulating in the blood, where the body actually reads and uses it. The vitamin is not gone, but it is not readily available either. The practical upshot is that children with obesity often show low blood levels of 25-hydroxyvitamin D despite adequate intake, and may need higher doses to correct it.

05 · Beyond vitamin DThe supporting cast: calcium, phosphate and cofactors

Rickets is so bound up with vitamin D in the public mind that a crucial fact gets lost: you can develop rickets with perfectly adequate vitamin D. The UK surveillance study was explicit that both vitamin D deficiency and dietary calcium deficiency drive the disease. Vitamin D unlocks the door to calcium absorption — but if there is little calcium in the diet to absorb, the door opens onto an empty room.

Calcium: the brick itself

Vitamin D is the foreman; calcium is the building material. A diet built on refined staples with little dairy, no fortified foods and few calcium-rich plants can produce rickets even in a sunny climate — a pattern documented in parts of the world with abundant sunshine but calcium-poor diets. For a wholefood plate, this means calcium deserves as much deliberate planning as vitamin D.

Phosphate, and the rickets diet cannot fix

Mineralised bone is calcium phosphate. Phosphate is abundant in most diets, so dietary phosphate deficiency is rare — but it matters because a family of genetic conditions causes the kidneys to waste phosphate, producing hypophosphataemic rickets. This form looks similar on an X-ray but has nothing to do with sunlight or diet, and no plate — however well built — will correct it. It is worth naming so that a child with resistant rickets is referred, not re-fed.

06 · Nutrition strategyBuilding the plate: what actually works

Dietary choices change this equation dramatically — and not always in the direction people assume.

Oily fish: the heavyweight

For those who eat it, oily fish is formidable. A 100g portion of wild salmon, mackerel or sardines can deliver 10–25 mcg of vitamin D3 — at or beyond a full day's target in a single serving. Small bone-in fish such as sardines go further still, arriving as a complete bone-building matrix: D3 alongside generous calcium and phosphorus, the exact minerals the growth plate is crying out for.

The land-meat blind spot

Here is a genuine surprise for many families: standard land meats — chicken breast, lean beef — contain almost no vitamin D, often under 0.2 mcg per serving. A child on a meat-heavy diet without fish is at essentially the same rickets risk as a child on an unplanned plant-based diet. "Eats plenty of meat" is not the reassurance it sounds like.

The wholefood vegetarian & vegan shield

Preventing rickets without meat, fish or synthetic fortification is entirely achievable — it just has to be deliberate. Three tactics do most of the work.

Eggs and dairy, working together. Two whole eggs supply roughly 3.2–3.6 mcg of vitamin D3. Paired with whole milk or cheddar — each serving bringing 240–290mg of calcium — you deliver the D3 catalyst and the calcium bricks in the same meal. It is the pairing, not either food alone, that builds bone.

Fortified foods. Plant milks, spreads and breakfast cereals typically add 1.5–2.5 mcg per serving, often using D3 sourced from lichen. Unglamorous, but a reliable everyday backstop — particularly through the northern winter.

07 · Official guidanceWhat the UK actually recommends

Food does the heavy lifting, but public-health guidance fills the winter gap. The core UK recommendations are refreshingly simple:

Everyone over the age of one should consider a daily supplement of 10 micrograms (400 IU) of vitamin D through autumn and winter, when the sun can't do the job. Groups at higher risk — people with darker skin, those who cover up or spend little time outdoors — are advised to take it year-round. Breastfed infants from birth to one year should have 8.5–10 micrograms daily, and the Healthy Start scheme provides vitamin D free to eligible families — the very support that, as the surveillance data showed, so many affected children were missing.

08 · SafetyToo much of a good thing

Because vitamin D is stored in fat, it is one of the few vitamins you can genuinely overdose on — not from sun or food, but from high-dose supplements. Excess causes hypercalcaemia, in which surplus calcium is deposited into soft tissues — the kidneys and blood vessels — risking kidney stones and, in severe cases, organ damage.

09 · ExaminationWhat a clinician looks for

When a doctor suspects rickets, they examine the places where bone is growing fastest — because those are the places the failure shows first.

Skeletal signs

As the bones stay soft, gravity and muscle pull deform them. Craniotabes is felt when a clinician presses the back of an infant's skull and finds it soft and springy, like a table-tennis ball. At the knees, weight-bearing produces genu varum (bowing) or genu valgum (knock-knees). Cartilage that expands without hardening produces a visible, knobbly broadening at the wrists and ankles.

Chest signs

The ribcage tells its own story. The rachitic rosary is a line of bead-like swellings where the ribs meet their cartilage at the costochondral junctions. Harrison's groove is a horizontal furrow drawn along the lower chest by the diaphragm tugging on ribs too soft to hold their shape. And in pectus carinatum, the pliable sternum is forced outward into a pointed "pigeon chest."

Beyond the skeleton, a clinician looks for hypotonia (a floppy, protruding "potbelly"), delayed tooth eruption with weak enamel, and motor milestone delays. Diagnosis is confirmed on wrist X-rays showing the growth plate cupping and fraying that are hallmarks of rickets, together with blood tests: a markedly raised alkaline phosphatase, high PTH, low phosphate and low 25-hydroxyvitamin D.

10 · Bottom lineKeeping rickets in the past

Rickets is one of the most preventable diseases a child can develop — which is exactly what makes each case a quiet failure of prevention rather than an act of fate. The path forward is unglamorous and reliable: sensible daylight in the months that allow it, a winter supplement for essentially everyone and year-round for those at higher risk, a plate that treats calcium as seriously as vitamin D, and particular attention to breastfed infants and children with darker skin through the northern winter.

For families choosing to exclude meat and fish, none of this is a barrier. UV-activated mushrooms, eggs and dairy or fortified alternatives, bioavailable calcium from low-oxalate greens and calcium-set tofu, and the supporting cast of magnesium and K2 together build a plate that keeps growing bones hardening on schedule. Understand the kinetics, respect the winter, and rickets stays where it belongs — in the history books.