Calcium Intake and Metabolic Bone Disease after Eight Years of Roux-en-Y Gastric
Bypass
Duran deCampos C, et al.
Obes Surg, 2008; 18(4):386-90.
Roux-en-Y gastric bypass (RYGBP) has been found to be the most efficient way to lose weight and maintain the
weight loss in morbid obesity. However, with the formation of a new stomach and the modification of intestinal
anatomy, there are significant changes on physiological properties of these organs that lead to nutrient deficiency,
including calcium. The objectives of this study were to evaluate calcium intake, bone metabolism, and prevalence
of metabolic bone disease in women subjected to RYGBP after 8 years. Food frequency questionnaire and 3-day
dietary recall, laboratory tests of bone metabolism and bone mineral density were accessed. Calcium intake was
below the recommendation in all women. Serum PTH and alkaline phosphatase were elevated, whereas vitamin D
and urinary calcium were significantly lower. Also, a higher prevalence of metabolic bone disease than the one
expected for the normal population at the same age was noted. These data suggest that metabolic bone disease
could be a complication of this type of surgery.
Reproductive and Neurobehavioral Outcome of Drinking Purified Water Under
Magnesium Deficiency in the Rat’s Diet
Zeng H, et al.
Food Chem Toxicol; May 2008; 46(5):1495-502.
Taking magnesium deficient diet and drinking soft water (including purified water, essentially mineral free) are
commonly consumed in the world. The present study was conducted to assess the potential combined influence of
maternal drinking purified water and taking magnesium deficient diet on postnatal development and behavior in the
offspring of exposed rats. Sprague-Dawley (SO) rat were assigned to four groups: group 1 fed with control diet
(Mg(2+) 0.4 g/kg) and control water (Mg(2+) 12.7 mg/L), group 2 fed with control diet and purified water
(Mg(2+) 0.015 mg/L), group 3 fed with magnesium deficient diet (Mg(2+) 0.2 g/kg) and control water, group 4
fed with magnesium deficient diet and purified water from 5 weeks of age of the FO generation to 3 weeks of the
F1 generation, respectively. Reproductive and neurobehavioral parameters were measured. Maternal body weights
significantly decreased during treatment (before mating) and lactation periods in the group fed with magnesium
deficient diet and purified water. There were no significant differences of the reproductive outcome in the groups.
Offspring's body weight, development of reflexes significantly reduced in the group 4. Although there were no
significant differences in the four groups, the data showed a trend toward a decreased risk for offspring body
weight, neurobehavioral development as follows: group 1 >group 2>group 3>group 4. Therefore, purified water
cannot obviously affect the reproductive outcome when magnesium is sufficient or half of the estimated average
requirement (EAR) in the diet. However, drinking purified water can decrease maternal magnesium level slightly,
induce offspring's development retardation, especially with the magnesium deficiency in the diet. Furthermore,
magnesium deficiency in the diet (half of the EAR) can produce growth delay and reflex development retardation in
F1-offspring. Therefore, drinking purified water should be carefully considered, especially for susceptible
population.
Possible Roles of Zinc Nutriture in the Fetal Origins of Disease
Maret W, et al.
Exp Gerontol; May 2008; 43(5):378-81.
Risk of diseases of metabolism such as atherosclerosis and adult onset diabetes mellitus is increased by fetal
malnutrition. Deficiencies of micronutrients essential for methylation are believed to contribute to the phenomenon in
part through epigenetic abnormalities. Zinc is one of the nutrients essential for the epigenome. Because the worldwide
prevalence of zinc deficiency is at least 20%, fetal zinc deficiency is common. We suggest fetal zinc deficiency
contributes to the pathogenesis of metabolic diseases in adults. In support of our thesis, research in experimental
models and humans established the essentiality of zinc at all stages of intrauterine and infant life. Experiments in
rodents and/or non-human primates found that fetal and/or suckling zinc deficiency impairs neuropsychological
functions of progeny and that the effects persist in spite of nutritional rehabilitation. In addition, maternal zinc
deficiency in mice is reported to impair immunity of progeny; effects persist in spite of nutritional rehabilitation into
the next generation. We suspect that zinc deficiency is a far greater human health problem than is generally
recognized.
Prenatal Zinc Deficiency: Influence on Heart Morphology and Distribution of Key Heart
Proteins in a Rat Model
Lopez V.
Biol Trace Elem Res; June 2008: 122(3):238-55.
The etiology of congenital heart disease is multifactorial, with genetics and nutritional deficiencies recognized as
causative agents. Maternal zinc (Zn) deficiency is associated with an increased risk for fetal heart malformations;
however, the contributing mechanisms have yet to be identified. In this study, we fed pregnant rats a Zn-adequate diet
(ZnA), a Zn-deficient (ZnD), or a restricted amount of Zn adequate diet (RF) beginning on gestation day (GD) 4.5, to
examine whether increased cell death and changes in cardiac neural crest cells (NCC) play a role in Zn deficiencyinduced
heart defects. Fetuses were collected on GD 13.5, 15.5, and 18.5 and processed for GATA-4, FOG-2,
connexin43 (Cx43), HNK-1, smooth muscle alpha-actin (SMA) and cleaved caspase-3 protein expression. Fetuses
from ZnA-fed dams showed normal heart development, whereas fetuses from dams fed with the ZnD diet exhibited a
variety of heart anomalies, particularly in the region of the outflow tract. HNK-1 expression was lower than normal in
the hearts of GD13.5 and 15.5 ZnD fetuses, particularly in the right atrium and in the distal tip of the interventricular
septum. Conversely, Cx43 immunoreactivity was increased throughout the heart in fetuses from ZnD dams compared
to fetuses from control dams. The distribution and intensity of expression of SMA, GATA-4, FOG-2, and markers of
apoptosis were similar among the three groups. We propose that Zn deficiency induced alterations in the distribution
of Cx43 and HNK-1 in fetal hearts contribute to the occurrence of the developmental heart anomalies.
Iron and Zinc Deficiencies in China: What is a Feasible and Cost-Effective Strategy?
Ma G, et al.
Public Health Nutr; June 2008; 11(6):632-8.
In order to prioritize interventions for micronutrient deficiencies in China, the populations affected by iron and zinc
deficiencies were assessed based on data from the 2002 China National Nutrition and Health Survey. The costs and
cost-effectiveness of supplementation, food diversification and food fortification were estimated using the standard
World Health Organization ingredients approach. Results indicated that 30% of children (60 years), pregnant and
lactating women, and 20% of women of reproductive age were anaemic, some 245 million people. Approximately
100 million people were affected by zinc deficiency (zinc intake inadequacy and stunting), the majority living in rural
areas. Among interventions on iron and zinc deficiency, biofortification showed the lowest costs per capita, I$0.01 (international dollars), while dietary diversification through health education represented the highest costs at I$1148.
The cost-effectiveness of supplementation, food fortification and dietary diversification for iron deficiency alone was
I$179, I$66 and I$103 per disability-adjusted life-year (DALY), respectively. Data for biofortification were not
available. For zinc deficiency, the corresponding figures were I$399, I$153 and I$103 per DALY, respectively. In
conclusion, iron and zinc deficiencies are of great public health concern in China. Of the two long-term intervention
strategies, i.e. dietary diversification and biofortification with improved varieties, the latter is especially feasible and
cost-effective for rural populations. Supplementation and fortification can be used as short-term strategies for specific
groups.
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