Rickets develops when a child’s bones don’t get enough calcium and phosphorus to harden properly, almost always because of insufficient vitamin D. Vitamin D is the key that unlocks your body’s ability to absorb these minerals from food. Without it, bones stay soft during the critical growth years, leading to skeletal deformities that can become permanent. While most people associate rickets with the past, the condition is actually rising in developed countries, with one nationwide study in Taiwan finding the incidence climbed by roughly 14% per year between 2008 and 2018.
Why Vitamin D Deficiency Is the Primary Cause
Vitamin D goes through two chemical conversions in your body before it becomes fully active. Once activated, it regulates how much calcium and phosphorus your intestines pull from the food you eat and push into your bloodstream. When vitamin D is too low, those minerals never make it into the blood in adequate amounts. The result is that growing bones, especially the long bones of the arms and legs, can’t mineralize correctly. They remain soft and bend under the weight of a child’s body.
Vitamin D deficiency remains the single most common cause of rickets worldwide. It happens through a few overlapping pathways: not enough sunlight, not enough vitamin D in the diet, or both at once.
Sunlight, Skin Color, and Geography
Your skin manufactures vitamin D when ultraviolet B rays hit it directly. Several factors reduce how much you can produce. Living at higher latitudes, particularly during winter months, dramatically cuts UV exposure. Dense cloud cover, high air pollution, clothing that covers most of the skin, and regular sunscreen use all limit production further.
Darker skin tones contain more melanin, which acts as a natural sunscreen. This means children with darker skin need substantially more sun exposure to produce the same amount of vitamin D as lighter-skinned children. Nearly all cases of nutritional rickets in developed countries occur in dark-skinned, breastfed infants who receive no vitamin D supplementation.
Diet and the Breastfeeding Connection
Breast milk is low in vitamin D and its related compounds, even when the mother’s own levels are adequate. This makes exclusively breastfed infants one of the highest-risk groups. The American Academy of Pediatrics recommends that all breastfed and partially breastfed infants receive 400 IU of supplemental vitamin D daily, starting in the first few days of life. Formula-fed babies need the same amount unless they’re consistently drinking at least 32 ounces of vitamin D-fortified formula per day.
In older toddlers and children, low dietary calcium can cause rickets even when vitamin D intake seems borderline acceptable. This pattern shows up most often in populations eating cereal-based diets with limited variety and little access to dairy products. In these cases, the body burns through its vitamin D stores faster trying to compensate for the missing calcium, creating a deficiency in both nutrients simultaneously. Research has shown that calcium supplements alone can heal rickets in children whose primary problem is dietary calcium rather than vitamin D.
Vitamin D deficiency and calcium deficiency represent two ends of the same spectrum. Many children with rickets fall somewhere in the middle, dealing with a combination of both.
Medical Conditions That Cause Rickets
Some children get enough vitamin D and calcium from their diet but can’t absorb or use those nutrients properly. Conditions that impair fat absorption in the intestines are a common culprit, because vitamin D is fat-soluble and rides into your body alongside dietary fat. When fat passes through unabsorbed, it binds to calcium in the gut and carries it out too, creating a double loss. Chronic liver or kidney disease can also disrupt the conversion steps that activate vitamin D, producing the same end result: bones that can’t mineralize.
Hereditary Forms of Rickets
A small percentage of rickets cases are genetic. In one hereditary form, the body can’t properly convert vitamin D into its active form. In another, the receptors that vitamin D binds to in cells don’t work correctly, so even normal levels of vitamin D have no effect. Both types lead to the same outcome: the intestines fail to absorb enough calcium and phosphorus, and bones soften.
A separate genetic category involves phosphorus rather than vitamin D. In hypophosphatemic rickets, the kidneys dump too much phosphorus into the urine instead of recycling it back into the blood. Vitamin D levels can be completely normal in these children, yet their bones still can’t mineralize because phosphorus is one of the two essential building blocks of hard bone tissue. This form is caused by overproduction of a signaling molecule that tells the kidneys to waste phosphorus. In rare cases, a tumor rather than a genetic mutation produces this same molecule, creating an acquired version of the disease.
Signs to Recognize
Rickets targets the growth plates, the soft zones at the ends of bones where new growth happens. Because these areas are actively forming, they’re the first to show problems when minerals are scarce. The classic signs include bowed legs or knock-knees, thickened wrists and ankles (from growth plates swelling outward), and a breastbone that pushes forward. Children with rickets often experience delayed growth, muscle weakness, and bone pain or tenderness. In severe cases, the softened bones fracture more easily than healthy ones.
These deformities tend to appear gradually as a child grows and begins bearing weight. Bowing of the legs, for instance, typically becomes noticeable once a toddler starts walking. If rickets is caught and treated early, many skeletal changes can reverse as the bones re-mineralize. Left untreated, some deformities become permanent.
Who Is Most at Risk
The children most likely to develop rickets share a recognizable set of risk factors:
- Exclusively breastfed infants who don’t receive vitamin D drops, particularly those with darker skin
- Children living at high latitudes or in heavily polluted cities with limited sun exposure
- Children on restricted diets that are low in dairy, fish, eggs, or fortified foods
- Children with chronic digestive conditions that reduce fat and nutrient absorption
- Children with kidney or liver disease that impairs vitamin D activation
The nutritional form of rickets is almost entirely preventable. The 400 IU daily supplement recommended for infants is inexpensive and widely available as liquid drops. For older children, vitamin D-fortified milk, fatty fish, egg yolks, and regular outdoor time in sunlight provide a reliable supply. In populations where dairy access is limited, ensuring adequate calcium through other foods or supplements addresses the other half of the equation.