However, the disease occurs among older toddlers and children in these countries, which in these circumstances is attributed to low dietary calcium intakes due to a mainly cereal-based diet.Those at higher risk for developing rickets include:

Breast-fed infants whose mothers are not exposed to sunlight
Breast-fed infants who are not exposed to sunlight
Breast-fed babies who are exposed to little sunlight
Adolescents, in particular when undergoing the pubertal growth spurt
Any child whose diet does not contain enough vitamin D or calciumDiseases causing soft bones in infants, like hypophosphatasia or hypophosphatemia, can also lead to rickets.Strontium is allied with calcium uptake into bones; at excessive dietary levels strontium has a rachitogenic (rickets-producing) action. Sunlight
Sunlight, especially ultraviolet light, lets human skin cells convert vitamin D from an inactive to active state. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcaemia, leading to skeletal and dental deformities and neuromuscular symptoms, e.g. hyperexcitability. Foods that contain vitamin D include butter, eggs, fish liver oils, margarine, fortified milk and juice, portabella and shiitake mushrooms, and oily fishes such as tuna, herring, and salmon. A rare X-linked dominant form exists called vitamin D-resistant rickets or X-linked hypophosphatemia.Cases have been reported in Britain in recent years of rickets in children of many social backgrounds caused by insufficient production in the body of vitamin D because the suns ultraviolet light was not reaching the skin due to use of strong sunblock, too much "covering up" in sunlight, or not getting out into the sun.
Cases of what is believed to have been rickets have been described since the 1st century, and the condition was widespread in the Roman Empire. The disease was common into the 20th century. Early treatments included the use of cod liver oil. Signs and symptoms
Signs and symptoms of dietary deficiency rickets can include bone tenderness, and a susceptibility for bone fractures, particularly greenstick fractures. Early skeletal deformities can arise in infants such as soft, thinned skull bones – a condition known as craniotabes, which is the first sign of rickets; skull bossing may be present and a delayed closure of the fontanelles. Young children may have bowed legs and thickened ankles and wrists; older children may have knock knees. Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result as the thickening caused by nodules forming on the costochondral joints. This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest may result in the presence of Harrisons groove. Hypocalcemia, a low level of calcium in the blood can result in tetany – uncontrolled muscle spasms. Dental problems can also arise.An X-ray or radiograph of an advanced patient with rickets tends to present in a classic way: the bowed legs (outward curve of long bone of the legs) and a deformed chest.