We assessed longitudinal association between calcium intake during adolescence and hypertension in adulthood. Longitudinal study data of 1611 participants from the China Health and Nutrition Survey during 1991–2011 were used. On average they were followed for 11·4 years. Dietary calcium intake during adolescence was assessed based on three 24-hour dietary recalls collected in each visit/survey between 1991 and 2009 (seven waves). The intake was recoded into quartiles. Cumulative mean±SD calcium intake was 199·9±144·8 mg/1000 kcal/day during adolescence. In total 102 participants had hypertension in adulthood (97 men and 5 women). There was a clear U-shaped association between adolescence calcium intake quartiles and adulthood hypertension: across the quartiles, hypertension prevalence was 6·7%, 4·0%, 5·2% and 9·5%, respectively. After adjustment for potential confounders including weight status and dietary pattern, odds ratios (OR, 95% CI) for hypertension were 2·32 (95% CI 1·07–5·00) for lowest quartile, 1·00 (reference), 1·34 (95% CI 0·61–2·97), and 3·10 (95% CI 1·49–6·46) across the quartiles. Lower or higher calcium intake during adolescence was associated with hypertension in adulthood independent of weight status and dietary pattern.

Pb is released from bone stores during pregnancy, which constitutes a period of increased bone resorption. A high Na intake has been found to be negatively associated with Ca and adversely associated with bone metabolism. It is possible that a high Na intake during pregnancy increases the blood Pb concentration; however, no previous study has reported on the relationship between Na intake and blood Pb concentration. We thus have investigated this relationship between Na intake and blood Pb concentrations, and examined whether this relationship differs with Ca intake in pregnant Korean women. Blood Pb concentrations were analysed in 1090 pregnant women at mid-pregnancy. Dietary intakes during mid-pregnancy were estimated by a 24 h recall method covering the use of dietary supplements. Blood Pb concentrations in whole-blood samples were analysed using graphite furnace atomic absorption spectrophotometry. Multiple regression analysis performed after adjustment for covariates revealed that maternal Na intake was positively associated with blood Pb concentration during pregnancy, but only when Ca intake was below the estimated average requirement for pregnant Korean women (P= 0·001). The findings of the present study suggest that blood Pb concentration during pregnancy could be minimised by dietary recommendations that include decreased Na and increased Ca intakes.

Adequate dietary habits are supposed to be one of the most important modifiable factors in osteoporosis prevention. However, the importance of specific nutrients is controversial. We examined relevant nutrients which are supposed to have an impact on bone parameters and compared their effect sizes with those of two known predictors of bone development: bone-related muscle mass and androgen levels. We analysed nutritional, hormonal and anthropometric data from 107 prepubertal children participating in the Dortmund Nutritional and Anthropometric Longitudinally Designed Study. Diaphyseal bone mineral content (BMC), cortical area (CA), periosteal circumference, strength strain index and muscle area of the non-dominant forearm were measured by peripheral quantitative computed tomography. Data on long-term nutrient intakes (e.g. protein, Ca and vitamin D) were derived from 3 d weighed dietary records. Twenty-four hour urinary excretion rates of androgen metabolites including the sex steroid androstenediol were measured using GC–MS. Of all considered nutrients, only protein showed a trend for an association with BMC (β = +0·11; P = 0·073) and CA (β = +0·11; P = 0·056) in stepwise linear regression models. None of the other considered dietary variables was associated with bone parameters. The size of the bone anabolic effect of protein was partly comparable with that of androstenediol. Even though boys gained more bone mass in comparison with girls, the protein effect did not differ between sexes. Bone-related muscle area and sex steroids have the strongest effects on prepubertal diaphyseal bone. However, dietary protein may have a similar bone anabolic influence compared with androstenediol. In children without explicit nutrient deficits, protein seems to be the most important dietary component for diaphyseal bone status.

Previous evidence suggests that the lactase gene C/T− 13910 polymorphism (rs4988235) is associated with avoidance of milk products and lower Ca intake. We examined whether the consumption of milk and milk products and the intakes of milk nutrients differ between the lactase genotypes from childhood to young adulthood. Subjects belong to the Cardiovascular Risk in Young Finns Study where the first cross-sectional surveys were conducted in 1980 (n 3596), with follow-up studies in 1983, 1986, 1989, 1992 and 2001 (n 2620). The same dietary questionnaire was used throughout the follow-up to collect data on habitual consumption of milk and milk products in all subjects, and daily nutrient intakes were assessed with 48 h dietary recalls in 50 % of the subjects. Subjects with the lactase non-persistence (C/C− 13910) genotype consumed less milk since childhood, but the consumption of other milk products did not differ between the genotypes. In adult females, the lactose content of milk products consumed was lower (P = 0·003), and in both sexes low-lactose and milk-free diets were more common in the C/C− 13910 genotype than in the other genotypes. Inadequate Ca intake was most common in females with the C/C− 13910 genotype as early as in childhood (15–63 %), but in males only in adulthood (24 %). In adult females, preference for low-lactose milk and milk products equalised the differences in Ca intake between the genotypes. Thus, in those with the C/C− 13910 genotype, preference for low-lactose milk and milk products may decrease the risk for inadequate Ca intake.

Increased postmenopausal bone turnover leads to bone loss and fragility fracture risk. In the absence of osteoporosis, risk preventive measures, particularly those modifying nutritional lifestyle, are appropriate. We tested the hypothesis that milk supplementation affects bone turnover related to biochemical markers in a direction that, in the long term, may be expected to reduce postmenopausal bone loss. Thirty healthy postmenopausal women aged 59·3 (sd 3·3) years were enrolled in a prospective crossover trial of 16 weeks. After a 4-week period of adaptation with diet providing 600 mg calcium plus 300 mg ingested as 250 ml semi-skimmed milk, participants were maintained during 6 weeks under the same 600 mg calcium diet and randomized to receive either 500 ml semi-skimmed milk, thus providing a total of 1200 mg calcium, or no milk supplement. In the next 6 weeks they were switched to the alternative regimen. At the end of the each period, i.e. after 4, 10 and 16 weeks, blood and urinary samples were collected. The changes in blood variables between the periods of 6 weeks without and with milk supplementation were: for parathyroid hormone, − 3·2 pg/ml (P = 0·0054); for crosslinked telopeptide of type I collagen, − 624 pg/ml (P < 0·0001); for propeptide of type I procollagen, − 5·5 ng/ml (P = 0·0092); for osteocalcin, − 2·8 ng/ml (P = 0·0014). In conclusion, a 6-week period of milk supplementation induced a decrease in several biochemical variables compatible with diminished bone turnover mediated by reduction in parathyroid hormone secretion. This nutritional approach to postmenopausal alteration in bone metabolism may be a valuable measure in the primary prevention of osteoporosis.

We aimed to describe the vitamin D status of young women living in two Chinese cities in the spring – Beijing in the north (latitude 39° north) and Hong Kong (latitude 22° north) in the south. We also examined the relationship between serum 25-hydroxyvitamin D and parathyroid hormone (PTH) concentrations to determine a threshold for serum 25-hydroxyvitamin D above which there is no further suppression of PTH. Finally, we examined whether dietary Ca intake influences this relationship. Non-pregnant women aged 18–40 years (n 441) were recruited between February and June. Fasting blood was collected and dietary intakes were assessed using 5 d food records. Mean serum 25-hydroxyvitamin D concentration was lower in Beijing than Hong Kong women (29 v. 34 nmol/l; P < 0·001). Vitamin D deficiency ( ≤  25 nmol/l) was indicated in 40 % of Beijing and 18 % of Hong Kong women, and over 90 % of women in both cities were insufficient ( ≤ 50 nmol/l). Mean Ca and vitamin D intakes were 478 mg/d and 2·0 μg/d, respectively. The relationship between 25-hydroxyvitamin D concentration and PTH was linear throughout the range with a slope of − 0·36 (different from 0; P < 0·001; R 0·26), with no apparent threshold. There was no influence of Ca intake on the relationship between 25-hydroxyvitamin D and PTH concentration. Vitamin D deficiency is common and insufficiency is very common in non-pregnant women in Hong Kong and Beijing during spring. Serum 25-hydroxyvitamin D was inversely associated with PTH with no apparent threshold. Strategies such as vitamin D fortification or supplementation may be required.

This study investigated the associations among vitamin D receptor (VDR) BsmI polymorphism, calcium intake and bone strength as indicated by the broadband ultrasound attenuation (BUA) measured by calcaneal quantitative ultrasound at the left calcaneus in community-dwelling subjects with a low calcium intake. The VDR BsmI polymorphism was analysed in 335 women older than 65 years residing in rural Asan, Korea. Calcium intake was assessed with a 2 d, 24 h recall method. The distribution of genotypes was similar to that reported in other Asian populations (92 % bb, 7 % Bb and 1 % BB). The calcaneal BUA was significantly higher (P = 0·013) in the bb genotype than in the Bb or BB genotype (Bb and BB genotypes were combined due to the small number of BB subjects) in a multiple regression model after adjusting for age, body weight, height, physical activity and nutritional factors. BUA was not significantly affected by the calcium intake regardless of the genotype, cross-sectionally. The energy-adjusted average calcium intake of this population was 439·6 mg/d (432·5 mg/d for bb and 522·3 mg/d for Bb or BB), and 96 % of the subjects had dietary intakes that were less than the recommended Dietary Reference Intake for Koreans (which for calcium is 800 mg/d for women older than 65 years). In summary, the BUA in older Korean women with a low calcium intake was significantly influenced by the VDR genotype but not by the calcium intake, cross-sectionally.

A high dietary P intake is suggested to have negative effects on bone through increased parathyroid hormone secretion, as high serum parathyroid hormone (S-PTH) concentration increases bone resorption. In many countries the P intake is 2- to 3-fold above dietary guidelines, whereas Ca intake is too low. This combination may not be optimal for bone health. In a previous controlled study, we found that dietary P dose-dependently increased S-PTH and bone resorption and decreased bone formation. The aim of the present study was to investigate the dose–response effects of Ca intake on Ca and bone metabolism with a dietary P intake higher than recommended. Each of the twelve healthy female subjects aged 21–40 years attended three 24-h study sessions, which were randomized with regard to a Ca dose of 0 (control day), 600 or 1200 mg, and each subject served as her own control. The meals on each study day provided 1850 mg P and 480 mg Ca. S-PTH concentration decreased (P < 0·001) and serum ionized Ca concentration increased (P < 0·001) with increasing Ca doses. The bone formation marker, serum bone-specific alkaline phosphatase, did not differ significantly (P = 0·4). By contrast, the bone resorption marker, urinary N-terminal telopeptide of collagen type I, decreased significantly with both Ca doses (P = 0·008). When P intake was above current recommendations, increased Ca intake was beneficial for bone, as indicated by decreased S-PTH concentration and bone resorption. However, not even a high Ca intake could affect bone formation when P intake was excessive.

An association between Ca intake and the risk of prostate cancer has been reported in some but not all epidemiological studies. Assuming that a pathophysiological relationship would underlie this association, a favoured hypothesis proposes that relatively high Ca consumption could promote prostate cancer by reducing the production of 1,25-dihydroxyvitamin D (1,25(OH)2D; calcitriol), the hormonal form of vitamin D. The present review analyses the plausibility of this hypothesis by considering the quantitative relationships linking Ca intake to 1,25(OH)2D production and action in healthy conditions and in prostate cancer. Changes in the plasma level of 1,25(OH)2D in response to Ca intake are of very small magnitude as compared with the variations required to influence the proliferation and differentiation of prostate cancer cells. In most studies, 1,25(OH)2D plasma level was not found to be reduced in patients with prostate cancer. The possibility that the level of 1,25(OH)2D in prostate cells is decreased with a high-Ca diet has not been documented. Furthermore, a recent randomised placebo-controlled trial did not indicate that Ca supplementation increases the relative risk of prostate cancer in men. In conclusion, the existence of a pathophysiological link between relatively high Ca intake and consequent low production and circulation level of 1,25(OH)2D that might promote the development of prostate cancer in men remains so far an hypothesis, the plausibility of which is not supported by the analysis of available clinical data.

The association of growth and anthropometric characteristics and lifestyle factors with bone mass and second metacarpal radiogrammetry parameters was evaluated in 373 healthy Chinese premenarcheal girls aged 9–11 years. Bone mineral content (BMC) and density (BMD) and bone area (BA) of distal forearm, proximal forearm and total body, bone mineral-free lean (BMFL) mass and fat mass were measured by dual-energy X-ray absorptiometry. Metacarpal bone periosteal and medullary diameters were measured. Dietary intakes were assessed by 7d food record and physical activity (PA) by questionnaire. BMFL and fat mass together explained 6·3 and 51·6% of the variation in total body BMC and BMD, respectively. BMFL mass contributed to a substantial proportion of the variation in forearm BMC and BMD and periosteal diameter (10·4–41·0%). The corresponding BA explained 14·8–80·4% of the variation in BMC. Other minor but significant predictors of total body bone mass were Ca intake, height, age and PA score (BMD only), and of forearm bone mass were PA score, bone age, height and fat mass. Nevertheless, after adjusting for bone and body size and for age or bone age, subjects with Ca intake above the median (417mg/d) had 1·8% greater total body BMC (P<0·001), and subjects with PA scores above the median had 2·4–2·5% greater distal and proximal forearm BMC (P<0·05) than those below. Vitamin D intake negatively associated with medullary diameter (partial R2 1·7%). The results indicate that premenarcheal girls should be encouraged to optimise nutrition and Ca intake and exercise regularly to achieve maximum peak bone mass.

Calcium accounts for 1–2 % of adult human body weight. Over 99 % of total body Ca is found in the teeth and bones. Therefore, in addition to the obvious structural role of the skeleton, it also serves as a reservoir for Ca. Dietary Ca intake has an important impact on bone metabolism and bone health. Chronic Ca deficiency resulting from inadequate intake or poor intestinal absorption is one of several important causes of reduced bone mass and osteoporosis. It is vital, therefore, that adequate dietary Ca is consumed at all stages of life — in early life so that the genetically programmed peak bone mass can be reached and in later adulthood so that the skeletal mass can be maintained and age-related bone loss minimised. Unfortunately, there is wide variation in the estimates of daily Ca requirements made by different expert authorities. Furthermore, there is evidence that many individuals are not consuming these recommended levels. The consequence of this for bone health will be discussed in the present review. Besides the amount of Ca in the diet, the absorption of dietary Ca in foods is also a critical factor in determining the availability of Ca for bone development and maintenance. Thus, there is a need to identify food components and/or functional food ingredients that may positively influence Ca absorption in order to ensure that Ca bioavailability from foods can be optimised. This approach may be of particular value in individuals who fail to achieve the dietary recommended level of Ca.

Based on the premise that elevated blood pressure and low bone mass have both been associated with poor Ca nutriture and disturbances in Ca metabolism, a cross-sectional study was employed to determine if blood pressure and dietary Ca intake were significantly related to bone mass. Forty-seven men between 24–77 years of age with blood pressure values ranging from normal to mildly elevated comprised the study group. Blood pressure was measured with a random-zero sphygmomanometer. Bone mineral content (BMC) and density (BMD) of the hip, spine and total body were measured with dual-photon absorptiometry. Dietary intake and physical activity were also assessed. Multiple linear regression analysis was used for statistical analysis. After adjusting for known confounding variables (age, BMI, Ca intake, and others) diastolic blood pressure was negatively related to BMC (P ≤ 0·05) and BMD (P ≤ 0·01) of the total body, trochanteric region (P < 0·01) and Ward's triangle (P < 0·05), and to BMC of the femoral neck (P < 0·05) and lumbar spine, although the latter was just shy of statistical significance (P = 0·058). Systolic blood pressure was negatively related to trochanteric BMD (P = 0·04) and BMC (P = 0·06). Ca intake was positively related to total body BMD (P = 0·005), and BMC of the lumbar spine (P = 0·05). In this population of men, Ca intake was a positive predictor, and blood pressure was a negative predictor of regional measures of bone mass. These findings support the concept that independent of age, BMI and Ca intake, elevated blood pressure varies indirectly with bone mass and density, known predictors of osteoporotic fractures. Future studies are needed to determine whether elevated blood pressure is causally related to the development of low bone mass, and what role dietary Ca plays in that pathway.

Fifty-four male and forty-five female 7-week-old rats, Wistar strain, average weights 190 g and 140 g respectively, were randomized by weight into three groups of eighteen rats each (males) and three groups of fifteen rats each (females) and fed on a semi-purified diet containing (per kg) 2 (low), 5 (normal) or 20 g (high) Ca as CaCO3, for 2 weeks. Each group was then further randomized into three groups of six rats each (males) and five rats each (females) and given a meal (10 g of the same diet) containing either 2,5 or 20 g Ca as 47CaCO3. 47Ca was determined in quantitative daily collections of faeces over 7 d and fractional absorption of 47Ca estimated by extrapolating the linear portion (days 3–7) of the plot of log 47Ca retention Y. time back to the time of isotope administration. Absorption of meal Ca was higher in males than in females and was affected similarly in males and females by previous dietary Ca intake and meal Ca content. Fractional absorption of meal Ca decreased with increasing previous dietary Ca intake and with increasing meal Ca content, and the combined effect of these two variables caused fractional Ca absorption to vary from 11–89 %. Absolute absorption of meal Ca decreased with increasing previous dietary Ca intake and increased with increasing meal Ca content. The influence on Ca absorption of variations in meal Ca content (load effect) was greater than that of variations in previous dietary Ca intake (adaptive effect). These results show that previous dietary Ca intake and meal Ca content are both major determinants of Ca absorption from meals in intact rats fed in the normal way and that the rat responds to these factors in a manner similar to that reported for humans. This study provides further evidence of similarities between rats and humans in dietary Ca absorption.