Evaluation of calcium-fortified municipal water as a public health intervention to mitigate lead burdens

Lead has adverse effects on health, society, and the economy. Lead exposure results in increased blood lead levels and storage in bones. Calcium and lead are competitively absorbed and as such calcium can be used to mitigate the body lead burden. Twenty-eight quantitative research studies were reviewed that examined lead exposure (in blood, bone, or breastmilk) and calcium intake or serum calcium to evaluate the efficacy and safety of fortifying potable water supplies with calcium to mitigate lead absorption or resorption. Eighteen of the studies reported a significant inverse relationship between biomarker lead levels and calcium intake or serum calcium. The relationship was most evident with high calcium intake, suggesting a dose-dependent relationship. An intervention with calcium-fortified water could offer an accessible source of supplemental calcium to help meet the recommended dietary allowance (RDA) and mitigate lead absorption. A concentration of 60 mg-Ca/L can supply 22.0 and 16.3% of a 1,000 mg-Ca RDA for men and women, respectively, at the recommended daily water intake.

Evolution of Lactase Persistence: Turbo-Charging Adaptation in Growth Under the Selective Pressure of Maternal Mortality?

The emergence of the capacity to digest milk in some populations represents a landmark in human evolution, linking genetic change with a component of niche construction, namely dairying. Alleles promoting continued activity of the enzyme lactase through the life-course (lactase persistence) evolved in several global regions within the last 7,000 years. In some European regions, these alleles underwent rapid selection and must have profoundly affected fertility or mortality. Elsewhere, alleles spread more locally. However, the functional benefits underlying the rapid spread of lactase persistence remain unclear. Here, we set out the hypothesis that lactase persistence promoted skeletal growth, thereby offering a generic rapid solution to childbirth complications arising from exposure to ecological change, or to new environments through migration. Since reduced maternal growth and greater neonatal size both increase the risk of obstructed labour, any ecological exposure impacting these traits may increase maternal mortality risk. Over many generations, maternal skeletal dimensions could adapt to new ecological conditions through genetic change. However, this adaptive strategy would fail if ecological change was rapid, including through migration into new niches. We propose that the combination of consuming milk and lactase persistence could have reduced maternal mortality by promoting growth of the pelvis after weaning, while high calcium intake would reduce risk of pelvic deformities. Our conceptual framework provides locally relevant hypotheses to explain selection for lactase persistence in different global regions. For any given diet and individual genotype, the combination of lactase persistence and milk consumption would divert more energy to skeletal growth, either increasing pelvic dimensions or buffering them from worsening ecological conditions. The emergence of lactase persistence among dairying populations could have helped early European farmers adapt rapidly to northern latitudes, East African pastoralists adapt to sudden climate shifts to drier environments, and Near Eastern populations counteract secular declines in height associated with early agriculture. In each case, we assume that lactase persistence accelerated the timescale over which maternal skeletal dimensions could change, thus promoting both maternal and offspring survival. Where lactase persistence did not emerge, birth weight was constrained at lower levels, and this contributes to contemporary variability in diabetes risk.

Calcium Intake Is Inversely Related to the Risk of Obesity Among American Young Adults over a 30-Year Follow-Up

Objectives It has been suggested that high calcium intake may promote weight reduction and prevent obesity, but data from longitudinal studies investigating the potential long-term associations of calcium with weight maintenance are limited and the findings are inconsistent. Therefore, we prospectively examined dietary calcium and serum calcium concentrations in relation to the incidence of obesity in a cohort of American young adults. Methods This study includes 4097 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study who were age 18–30 years at baseline in 1985–86. Participants were reexamined in 8 follow-ups over 30 years. Calcium intake from diet and supplements was estimated by the CARDIA diet history questionnaire at baseline and two re-exams (year 7 and 20). Serum calcium concentrations were measured at baseline. Incident obesity was defined as a body mass index ≥30 kg/m2. Multivariable-adjusted Cox proportional hazards regression models were used to examine the associations between calcium levels (intake and serum concentrations) and the incidence of obesity. Results During 30 years of follow-up, a total of 1675 participants became obese. Both calcium intake and serum calcium concentrations were inversely associated with obesity incidence independent of sociodemographics, major lifestyle factors, medical history, dietary quality and clinical measurements (blood pressure, lipid profiles, and fasting insulin) [hazard ratio (95% confidence interval) of quintile 5 (highest) vs. quintile 1 (lowest) calcium intake from diet and supplements: 0.76 (0.62, 0.93), P for trend = 0.02; serum calcium: 0.83 (0.71, 0.97), P for trend = 0.04]. A similar inverse association was observed between the consumption of dairy products, a major food source of calcium, and obesity incidence. Conclusions Calcium intake and serum calcium concentration are longitudinally and inversely associated with incidence of obesity among American young adults. Funding Sources The Coronary Artery Risk Development in Young Adults Study is supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham, Northwestern University, University of Minnesota, and Kaiser Foundation Research Institute. This study is also partially supported by the NIH grants.

Association between Dietary Calcium Intake and Adiposity in Male Adolescents

The aim was to investigate the possible association of dietary calcium intake with adiposity, insulin resistance, and adipocytokine values in adolescent boys. In this cross-sectional study, participants were 123 adolescent boys aged 13–15 years, who were divided into tertiles according to their dietary calcium intake. Dietary calcium intake was assessed using three 24 h dietary recalls. In addition, energy intake, body composition, physical activity (PA), and blood biochemical values were also measured. Mean body fat%, fat mass (FM), trunk FM, trunk fat%, and leptin differed between high and low tertiles of calcium intake after adjustment for age, pubertal stage, and PA. For the entire cohort, mean calcium intake was 786 ± 380 mg/day and was related to body mass index (BMI), FM, and trunk fat% but not to insulin resistance or adipocytokine values after adjusting for possible confounders. In addition, only 15.4% of the participants obtained or exceeded their mean dietary calcium intake requirements. These subjects who met their dietary calcium intake had significantly lower body fat% in comparison with subjects not meeting their dietary calcium intake. Odds ratio of being in the highest tertile of FM, trunk FM, and trunk fat% was 3.2–4.4 (95% confidence interval 1.19–12.47; p < 0.05) times higher for boys in low calcium intake tertile, compared to those boys in high calcium intake tertile. In conclusion, dietary calcium intake is inversely associated with total body and abdominal adiposity values in a specific group of healthy male adolescents with different body mass values.

Ectopic calcification and bone: a comparison of the effect of dietary carbohydrates, sugars and protein

A number of studies have shown that severe calcification of the arteries, heart and kidneys commonly coexists with<br />osteoporosis, particularly in renal disease. We have already shown that with respect to dietary fats, those that promote<br />ectopic (mainly cardiovascular) calcification are also detrimental to bone, with a similar relationship seen in fats which inhibit<br />ectopic calcification. This review of dietary carbohydrates, sugars and protein has shown a similar correspondence of effect,<br />with protein proving protective against ectopic calcification, at least in animals, and beneficial to bone. There appears to be<br />an interaction with calcium intake, with the beneficial effects of high protein being negated in a calcium deficiency, while a<br />high calcium intake enhances the dangers of a low protein intake; the cut-off for calcium intake may be around 800mg/d<br />for bone health. The results of studies on carbohydrates are unclear. Although there are no human studies on ectopic<br />calcification and intake of sugars, diabetes mellitus, insulin resistance and high blood glucose are known risk factors and are<br />also detrimental to bone. Fructose consistently promotes ectopic calcification in animals and is detrimental to bone in both<br />animals and humans, although the results for sucrose, glucose and lactose are mixed. Protein and prebiotics, both protective<br />against ectopic calcification and beneficial to bone, appear to act by increasing calcium absorption. Mechanisms of action<br />shared between inhibition of ectopic calcification and increased bone mineral density (BMD) include insulin-like growth factor<br />(IGF)-1, which can be directly induced by protein and glucose, and advanced glycation end products (AGEs), which decrease<br />expression of IGF-1 and generate reactive oxygen species, promote ectopic calcification and increased bone resorption.