Recent radiocarbon dating of a skeleton from Balevullin, Tiree, excavated in the early twentieth century, demonstrates that it dates to the Neolithic period, rather than the Iron Age as originally expected. Osteological examination suggests that the individual was a young adult woman, exhibiting osteological deformities consistent with vitamin D deficiency, most likely deriving from childhood rickets; an exceptionally early identification of the disease in the UK with potentially significant social implications. Isotopic analysis supports the osteological evidence for physiological stress in childhood and further suggests that the woman was most probably local to the islands. Analysis of the surviving written archive reveals that the surviving skeleton was one of several originally recovered from the site, making Balevullin an exceptionally rare example of a British Neolithic inhumation cemetery.

Introduction: Dilated cardiomyopathy is usually idiopathic and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia. Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may decline in patients with hypocalcaemia. Materials and Methods: Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology clinic. Echocardiography was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Maternal lifestyle and living conditions were investigated, and the maternal 25-OH vitamin D3 blood level was measured. Results: We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3–12 months. Laboratory results were consistent with advanced-stage rickets. Severe hypocalcaemia was detected in all patients. The maternal 25-OH vitamin D3 levels were low. Echocardiography revealed increased pre-treatment left ventricle end-systolic and end-diastolic diameters for age and reduced ejection fraction and fractional shortening. After clinical improvement, the patients were discharged. Conclusions: Severe hypocalcaemia associated with rickets must always be kept in mind among the causes of dilated cardiomyopathy and impaired cardiac function in infants. If diagnosed and treated in time, dilated cardiomyopathy and severe heart failure related to rickets respond well.

Nutritional rickets is still occasionally found in high-income countries, especially in populations at risk, and induced hypocalcaemia is a rare but possible cause of dilated cardiomyopathy. Although rare, physicians need to consider nutritional rickets in the differential diagnosis of hypocalcaemia cardiac failure, especially in high-risk populations such as immigrants. Despite being a reversible condition, the prognosis depends on the severity and time of diagnosis. We report two cases of exclusively breastfed infants with congestive cardiac failure due to hypokinetic dilated cardiomyopathy who had completely different outcomes. This report supports the need for prevention of this deficiency and underlies the role of vitamin D supplementation.

The reversibility of osteopenia secondary to isolated Ca deficiency (CaDef) is still not clear. We studied the effect of severe CaDef on Ca homeostasis and bone accrual in a ‘hypercalcaemic’ animal, the rabbit, during the post-weaning period and its reversibility on Ca supplementation. Male Belgian 5-week-old rabbit pups were fed CaDef diet (0·026% Ca) for 10 weeks. As compared with those fed with a normal chow diet (0·45% Ca), CaDef pups developed significant hypocalcaemia (P<0·05), hypocalciuria (urinary Ca 76 (sem 12) V 17 (sem 1) mg/l;P<0·005), hypophosphataemia (serum inorganic P 100 (sem 6) V. 65 (sem 4) mg/l; P<0·005), secondary hyperparathyroidism (SHPT) (serum intact parathyroid hormone human equivalent 18·2 (sem 1·4) V. 125·0 (sem 4·5) pg/ml; P<0·001) and elevated serum calcitriol levels (34·0 (sem 3·9) V. 91·0 (sem 1·0) pg/ml; v<0·005). Elevated urinary C-terminal telopeptide of class I collagen (P<0·005) and total serum alkaline phosphatase (P<0·005) suggested increased bone turnover. There was a significantly lower gain in bone mineral density (BMD) and bone mineral content (BMC) in the whole body and lumbar spine in vivo, and various sub-regions of the femur and tibia in vitro.Supplementation of adequate Ca (0·45% Ca) after 15 weeks on the normal diet resulted in rapid catch-up growth, and resolution of SHPT. Rapid gain in various BMD and BMC parameters continued at 30 weeks of age, and both were comparable with those in rabbits on a normal diet. We conclude that Ca deficiency-induced SHPT and poor bone accrual in growing rabbit pups are rapidly reversible with Ca supplementation. The present study indicates that early intervention may be a more appropriate window period for human nutritional corrective measures.

Six experiments were conducted to study the effects of exposure of young chickens to u.v. radiation. Chickens were fed a cholecalciferol (D3)-deficient diet and exposed to u.v. radiation from fluorescent lights giving total radiance (285–365nm) at 0·15m of 99·9mJ/s per m2. In Expt 1, chickens had increased body weight, bone ash and plasma Ca and decreased incidence of rickets and tibial dyschondroplasia (TD) when exposed to fluorescent light radiation 24h per d, 24h every 2d, or 24h every 3d starting with exposure on day 1 after hatching. However, when not exposed on day 1, but on days 4, 7, 10, 13 and 16, the bone ash was reduced, and the incidence of TD and rickets was increased, compared with chickens exposed on day 1 after hatching. When chickens were exposed at 1 d of age to radiation from two lamps, each of which gave a radiance (285–365nm) at 0·26m of 856mJ/s per m2, both the length of time of radiation and location of the lamps (above or below the chicken) influenced the response as measured by body weight, bone ash, plasma Ca and incidence of rickets. When chickens that received a TD-inducing diet were exposed to 30min u.v. radiation from below at 1 d of age they developed significantly less TD than did those not exposed when fed either 27·5 or 55·0μg D3/kg diet.

The first experiment was a central composite rotatable design with calculated calcium levels of 6.2, 7.0, 9.0, 11.0, and 11.8 g/kg diet and total phosphorus levels of 5.2, 6.0, 8.0, 10.0, and 10.8 g/kg diet (2.8 g phytin-P/kg by analysis). This design involved three replicates for each rotatable point and fifteen replicates of the central point. The second experiment was a 4 × 4 factorial design with calculated Ca levels of 8.0, 10.0, 12.0, and 14.0 g/kg diet and calculated total P levels of 7.0, 9.0, 11.0, and 13.0 g/kg diet (2.5 g phytin-P/kg by analysis). There were four replicates for each treatment. In both 16 d experiments maize–soya-bean diets were used and each replicate consisted of one pen containing 10-d-old broad-breasted, white tom turkeys. The Ca and total P requirements for optimum growth were estimated to be 12.5 and 10.0 g/kg diet respectively. Bone ash was adequate at these levels of Ca and total P, but maximum bone ash was not achieved until much higher levels of Ca and total P were employed. At the required levels of Ca and total P for growth the incidences of Ca- and P-deficiency rickets were very low. There were no treatment effects on feed efficiency. Increasing dietary Ca decreased the incidence of the Ca-deficiency lesion. There was a quadratic response due to dietary total P on both P-deficiency rickets and plasma dialysable P; intermediate levels of dietary P resulted in low incidence of the P-deficiency lesion and high levels of plasma dialysable P. There was a strong negative correlation between the incidence of P-deficiency rickets and plasma dialysable P. Percentage retention was very low at high levels of dietary P and low levels of Ca which corresponded with slightly higher P-deficiency rickets and low plasma dialysable P. No such obvious relationships existed between Ca retention, incidence of Ca-deficiency rickets, and plasma Ca. The incidence of tibial dyschondroplasia was very low in the present study. There were pronounced dietary treatment effects on phytin-P retention; at 14 d percentage phytin-P retention treatment means ranged from 18 to 46 in Expt 1 and from 0 to 40 in Expt 2 with the highest retention of phytin-P at low levels at both Ca and total P.

Calcium: Phosphorus: Phytin-phosphorus retention: Rickets: Tibial dyschondroplasia: Turkey