What increases calcium absorption. Vitamin D’s Crucial Role in Calcium Absorption: A Comprehensive Analysis
How does Vitamin D influence calcium absorption in the intestine. What are the key mechanisms involved in this process. Which factors can affect intestinal calcium absorption. What is the significance of recent research findings on this topic.
The Fundamental Function of Vitamin D in Calcium Homeostasis
Vitamin D plays a pivotal role in maintaining calcium homeostasis within the body. Its primary function is to enhance calcium absorption from the intestine. This crucial role has been elucidated through studies on vitamin D receptor (VDR) null mice, which demonstrated that rickets and osteomalacia could be prevented, and serum calcium and parathyroid hormone (PTH) levels normalized, when these mice were fed a diet high in calcium and lactose.
When serum calcium levels decrease due to low dietary intake or increased demand (such as during growth, pregnancy, or lactation), the synthesis of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the hormonally active form of vitamin D, is upregulated. This increase leads to enhanced intestinal calcium absorption. In cases where normal serum calcium cannot be maintained through intestinal absorption alone, 1,25(OH)2D3 works in conjunction with PTH to mobilize calcium from bones and increase calcium reabsorption in the renal distal tubule.
The Mechanism of Transcellular Calcium Absorption
1,25(OH)2D3 primarily affects the process of transcellular calcium transport in the intestine. This process has traditionally been thought to involve three main steps:
- Entry of calcium via the apical calcium channel, transient receptor potential vanilloid type 6 (TRPV6)
- Translocation of calcium through the interior of the enterocyte (facilitated by the calcium-binding protein calbindin-D9k)
- Basolateral extrusion of calcium by the intestinal plasma membrane pump PMCA1b
Previous studies provided indirect evidence supporting the roles of TRPV6 and calbindin in intestinal calcium absorption. Both proteins are co-localized in the intestine and are similarly regulated, being induced at weaning (the onset of active intestinal calcium transport), under conditions of low dietary calcium, and after 1,25(OH)2D3 injection. Moreover, both TRPV6 and calbindin-D9k are induced prior to the peak of intestinal calcium absorption.
Challenging the Traditional Model: Recent Research Findings
Recent studies using knockout (KO) mice have challenged the traditional model of vitamin D-mediated transcellular calcium absorption in the intestine. These findings have sparked a reevaluation of our understanding of the process:
- Calbindin-D9k KO mice show no difference in phenotype compared to wild-type (WT) mice and maintain normal serum calcium levels.
- Active intestinal calcium transport is similarly induced in both calbindin-D9k KO mice and WT mice in response to a low calcium diet or 1,25(OH)2D3 administration.
- TRPV6 KO mice exhibit only a modest reduction in intestinal calcium absorption and maintain normal serum calcium levels when fed a regular diet.
These findings suggest that while TRPV6 and calbindin-D9k may contribute to intestinal calcium absorption, they are not essential for this process. This challenges the long-held belief in their crucial role and opens up new avenues for research into alternative mechanisms of calcium absorption.
The Role of Paracellular Calcium Absorption
In addition to transcellular calcium absorption, calcium is also absorbed through a passive paracellular pathway via tight junctions. Recent evidence suggests that 1,25(OH)2D3 can enhance paracellular calcium diffusion, adding another layer of complexity to our understanding of vitamin D-mediated calcium absorption.
How does 1,25(OH)2D3 enhance paracellular calcium absorption? It appears to regulate the expression of tight junction proteins, such as claudins, which control the permeability of the paracellular pathway. This regulation allows for increased calcium flux between cells, particularly when luminal calcium concentrations are high.
Factors Influencing Intestinal Calcium Absorption
Several factors can influence intestinal calcium absorption, adding to the complexity of this physiological process:
Estrogen
Estrogen has been shown to enhance intestinal calcium absorption, particularly during pregnancy and lactation. It acts synergistically with 1,25(OH)2D3 to upregulate calcium transport proteins and increase calcium absorption efficiency.
Prolactin
Prolactin, a hormone involved in lactation, also plays a role in calcium homeostasis. It increases intestinal calcium absorption by enhancing the responsiveness of intestinal cells to 1,25(OH)2D3 and upregulating calcium transport proteins.
Glucocorticoids
Glucocorticoids, such as cortisol, can have a negative impact on intestinal calcium absorption. Chronic exposure to high levels of glucocorticoids can lead to decreased calcium absorption, potentially contributing to osteoporosis.
Aging
Aging is associated with a decline in intestinal calcium absorption efficiency. This decrease is partly due to reduced expression of calcium transport proteins and decreased responsiveness to 1,25(OH)2D3.
The Distal Intestine: An Overlooked Player in Calcium Absorption
While the majority of calcium absorption occurs in the duodenum and proximal jejunum, recent research has highlighted the importance of the distal intestine in vitamin D-mediated calcium absorption. The distal intestine, including the ileum and colon, expresses VDR and calcium transport proteins, suggesting a role in calcium homeostasis.
What is the significance of calcium absorption in the distal intestine? It may serve as a compensatory mechanism when proximal absorption is impaired or when dietary calcium intake is low. Additionally, the longer transit time in the distal intestine may allow for more efficient absorption of calcium from food sources that release calcium slowly.
Implications for Calcium Supplementation and Vitamin D Therapy
The complex interplay between vitamin D and intestinal calcium absorption has important implications for calcium supplementation and vitamin D therapy:
- Calcium supplements may be more effectively absorbed when taken with vitamin D
- Individuals with vitamin D deficiency may require higher doses of calcium supplements to achieve optimal absorption
- Vitamin D supplementation alone may not be sufficient to improve calcium status in individuals with severe calcium deficiency
- Tailored approaches considering both vitamin D status and calcium intake may be necessary for optimal bone health
How can healthcare providers optimize calcium absorption in their patients? A comprehensive approach considering vitamin D status, dietary calcium intake, and individual factors such as age and hormone levels is essential. Regular monitoring of serum calcium, vitamin D, and PTH levels can help guide treatment decisions and ensure optimal calcium homeostasis.
Future Directions in Calcium Absorption Research
The recent challenges to the traditional model of vitamin D-mediated calcium absorption have opened up new avenues for research in this field. Some potential areas of focus for future studies include:
- Identifying alternative calcium transport proteins that may play a role in intestinal calcium absorption
- Elucidating the molecular mechanisms by which 1,25(OH)2D3 enhances paracellular calcium absorption
- Investigating the potential role of the microbiome in modulating intestinal calcium absorption
- Exploring the impact of dietary factors, such as fiber and phytates, on vitamin D-mediated calcium absorption
- Developing targeted therapies to enhance calcium absorption in individuals with impaired vitamin D metabolism or intestinal disorders
What potential breakthroughs might emerge from this research? Improved understanding of the mechanisms underlying calcium absorption could lead to the development of novel therapeutics for osteoporosis and other calcium-related disorders. Additionally, this research may inform more effective strategies for calcium supplementation and vitamin D therapy, potentially reducing the risk of calcium deficiency and related health issues in vulnerable populations.
The Interplay Between Vitamin D and Other Nutrients in Calcium Absorption
While vitamin D plays a crucial role in calcium absorption, it does not act in isolation. Several other nutrients interact with vitamin D to influence calcium homeostasis:
Vitamin K
Vitamin K is essential for the carboxylation of osteocalcin, a protein involved in bone mineralization. Research suggests that vitamin K may work synergistically with vitamin D to promote calcium absorption and utilization in bone tissue.
Magnesium
Magnesium is required for the conversion of vitamin D to its active form, 1,25(OH)2D3. Adequate magnesium intake is therefore crucial for optimal vitamin D function and, by extension, calcium absorption.
Phosphorus
Phosphorus works in concert with calcium in bone formation. However, excessive phosphorus intake can interfere with calcium absorption by forming insoluble calcium phosphate complexes in the intestine.
Zinc
Zinc is involved in the synthesis of vitamin D-dependent calcium-binding proteins. Adequate zinc status may therefore be important for optimal calcium absorption.
How does the interplay between these nutrients affect calcium absorption strategies? A balanced approach to nutrition, ensuring adequate intake of all these nutrients, may be more effective in promoting calcium absorption and bone health than focusing solely on calcium and vitamin D supplementation.
Genetic Factors Influencing Vitamin D-Mediated Calcium Absorption
Genetic variations can significantly impact an individual’s ability to absorb and utilize calcium. Several genes have been identified that influence vitamin D-mediated calcium absorption:
- VDR gene: Polymorphisms in the vitamin D receptor gene can affect the responsiveness of intestinal cells to 1,25(OH)2D3
- CYP24A1 gene: This gene encodes the enzyme responsible for the degradation of 1,25(OH)2D3. Variations in this gene can affect vitamin D metabolism and, consequently, calcium absorption
- CASR gene: The calcium-sensing receptor gene plays a role in regulating calcium homeostasis. Genetic variants can influence the body’s response to changes in serum calcium levels
- TRPV6 and TRPV5 genes: Although recent research has challenged their essential role, variations in these genes may still contribute to individual differences in calcium absorption efficiency
What are the implications of genetic variations in calcium absorption? Understanding an individual’s genetic profile may allow for personalized approaches to calcium supplementation and vitamin D therapy. In the future, genetic testing could help identify individuals at risk for calcium absorption issues and guide targeted interventions.
Clinical Applications: Optimizing Calcium Absorption in Various Health Conditions
The complex relationship between vitamin D and calcium absorption has important implications for the management of various health conditions:
Osteoporosis
In osteoporosis, enhancing calcium absorption is crucial for maintaining bone density. Combination therapy with vitamin D and calcium, along with weight-bearing exercise, forms the cornerstone of osteoporosis management.
Chronic Kidney Disease (CKD)
CKD patients often have impaired vitamin D metabolism, leading to decreased calcium absorption. Careful monitoring of vitamin D status and appropriate supplementation are essential in these patients.
Inflammatory Bowel Disease (IBD)
IBD can affect intestinal calcium absorption due to inflammation and malabsorption. Patients may require higher doses of vitamin D and calcium supplements, and alternative forms of vitamin D (such as calcitriol) may be necessary.
Bariatric Surgery
Patients who have undergone bariatric surgery often experience reduced calcium absorption due to alterations in gastrointestinal anatomy. These patients may require lifelong calcium and vitamin D supplementation, often at higher doses than the general population.
How can healthcare providers tailor calcium absorption strategies for these diverse patient populations? Individualized approaches considering the specific pathophysiology of each condition, along with regular monitoring of calcium, vitamin D, and PTH levels, are crucial for optimal management.
Emerging Technologies in Calcium Absorption Research
Advancements in research technologies are providing new insights into the mechanisms of calcium absorption and the role of vitamin D:
- Single-cell RNA sequencing: This technology allows for the detailed analysis of gene expression in individual intestinal cells, providing a more nuanced understanding of the cellular processes involved in calcium absorption
- CRISPR-Cas9 gene editing: This powerful tool enables researchers to create precise genetic modifications in animal models, allowing for more targeted studies of specific genes involved in calcium absorption
- Advanced imaging techniques: Methods such as intravital microscopy and fluorescence-based calcium imaging are providing real-time visualization of calcium transport in living tissues
- Metabolomics: This approach allows for the comprehensive analysis of metabolites involved in calcium homeostasis, potentially identifying new biomarkers of calcium absorption efficiency
How might these technologies revolutionize our understanding of calcium absorption? These advanced tools have the potential to uncover previously unknown mechanisms of calcium transport, identify new therapeutic targets, and provide a more comprehensive picture of the complex interplay between vitamin D, calcium, and other factors influencing mineral homeostasis.
As research in this field continues to evolve, our understanding of vitamin D-mediated calcium absorption will undoubtedly deepen, potentially leading to more effective strategies for maintaining optimal calcium balance and bone health across diverse populations and health conditions.
Vitamin D and Intestinal Calcium Absorption
Mol Cell Endocrinol. Author manuscript; available in PMC 2012 Dec 5.
Published in final edited form as:
PMCID: PMC3405161
NIHMSID: NIHMS306628
Department of Biochemistry and Molecular Biology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School and Graduate School of Biomedical Sciences, Newark, New Jersey 07103
To Whom Correspondence Should be Addressed: Sylvia Christakos, Ph.D., UMDNJ-New Jersey Medical School, Dept. of Biochemistry and Molecular Biology, 185 South Orange Ave., Newark, New Jersey 07103, 973 972 4033 (phone) 973 972 5594 (FAX), ude.jndmu@katsirhcSee other articles in PMC that cite the published article.
Abstract
The principal function of vitamin D in calcium homeostasis is to increase calcium absorption from the intestine. Calcium is absorbed by both an active transcellular pathway, which is energy dependent, and by a passive paracellular pathway through tight junctions. 1,25Dihydroxyvitamin D3 (1,25(OH)2D3) the hormonally active form of vitamin D, through its genomic actions, is the major stimulator of active intestinal calcium absorption which involves calcium influx, translocation of calcium through the interior of the enterocyte and basolateral extrusion of calcium by the intestinal plasma membrane pump. This article reviews recent studies that have challenged the traditional model of vitamin D mediated transcellular calcium absorption and the crucial role of specific calcium transport proteins in intestinal calcium absorption. There is also increasing evidence that 1,25(OH)2D3 can enhance paracellular calcium diffusion. The influence of estrogen, prolactin, glucocorticoids and aging on intestinal calcium absorption and the role of the distal intestine in vitamin D mediated intestinal calcium absorption are also discussed.
Introduction
Studies in vitamin D receptor (VDR) null mice have indicated that the principal function of vitamin D in mineral homeostasis is to increase calcium absorption from the intestine (Li et al., 1997, Yoshizawa et al., 1997). This conclusion was made based on the findings that rickets and osteomalacia are prevented and serum calcium and parathyroid hormone (PTH) are normalized when VDR null mice are fed a rescue diet high in calcium and lactose. In the event of decreased calcium levels in the serum due to low dietary intake or increased demand of calcium due to growth, pregnancy or lactation, the synthesis of the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is increased leading to increased intestinal calcium absorption. If normal serum calcium is unable to be maintained by intestinal absorption, then 1,25(OH)2D3 together with PTH will mobilize bone calcium and increase reabsorption of calcium from the renal distal tubule.
1,25(OH)
2D3 and Transcellular Calcium Absorption
In the intestine 1,25(OH)2D3 affects the process of transcellular calcium transport which has been proposed to involve entry of calcium via the apical calcium channel, transient receptor potential vanilloid type 6 (TRPV6), translocation of calcium through the interior of the enterocyte (it has been suggested that the calcium binding protein calbindin-D9k acts to facilitate calcium diffusion through the cell) and basolateral extrusion of calcium by the intestinal plasma membrane pump PMCA1b (Wasserman 2005) (). Previous studies provided indirect evidence for a role of TRPV6 and calbindin in intestinal calcium absorption. Both are co-localized in the intestine, they are both similarly regulated [induced at weaning (the time of onset of active intestinal calcium transport), under conditions of low dietary calcium and after 1,25(OH)2D3 injection] (Song et al., 2003). TRPV6 and calbindin-D9k are both induced prior to the peak of intestinal calcium absorption (Song et al., 2003). In addition, in vitamin D receptor (VDR) KO mice, where the major defect that results in rickets is the decrease in intestinal calcium absorption, there is a 50% reduction in intestinal calbindin-D9k mRNA and a more marked decrease in TRPV6 mRNA (less than 5 – 10% of the levels in wild type (WT) mice) (Li et al., 1998, Van Cromphant et al., 2001). However, recent studies using calbindin-D9k knock out (KO) mice and TRPV6 KO mice have challenged the traditional model of vitamin D mediated transcellular calcium absorption in the intestine (Kutuzova et al., 2006, Akhter et al., 2007, Benn et al., 2008, Kutuzova et al., 2008, Bianco et al., 2008). Calbindin-D9k KO mice show no difference in phenotype compared to WT mice and they maintain normal serum calcium (Kutuzova et al., 2006, Akhter et al., 2007, Benn et al., 2008). Active intestinal calcium transport is similarly induced in both calbindin-D9k KO mice and WT mice in response to a low calcium diet or 1,25(OH)2D3, suggesting that calbindin-D9k may be compensated by another calcium binding protein (Benn et al., 2008). Calbindin may have another role in the intestine. Calbindin-D9k may be a modulator of the activity of TRPV6 and/or calbindin may act as a cytosolic buffer to prevent toxic levels of calcium from accumulating in the intestinal cell when there is an increase in apical calcium entry. TRPV6 KO mice also maintain normal serum calcium levels (Benn et al., 2008, Kutuzova et al., 2008). In response to 1,25(OH)2D3 intestinal calcium transport is similar in WT and TRPV6 KO mice (Benn et al., 2008, Kutuzova et al., 2008). However, under conditions of low dietary calcium, compared to WT mice, intestinal calcium transport is less efficient in the TRPV6 null mice (Benn et al., 2008). Also, in response to restriction of dietary calcium, although impaired bone mass accrual is comparable in WT and TRPV6 null mice, there is an increase in osteoblast activity and osteoid abundance is more pronounced in the TRPV6 null mice, suggesting a role for TRPV6 under low calcium conditions in intestinal calcium absorption to maintain proper bone mineralization (Lieben et al., 2010). When dietary supply of calcium is normal, lack of TRPV6 did not affect bone mass, remodeling parameters or growth plate morphology in young adult or aging mice. Thus, under normal calcium intake, TRPV6 is redundant for intestinal calcium transport, suggesting compensation by another channel or protein. Although the phenotype is mild, studies in the TRPV6 null mutant mice suggest that TRPV6 does contribute to the calcium absorptive process during calcium restriction. Recent studies showed that TRPV6 can interact with other proteins including calmodulin, which facilitates rapid inactivation of TRPV6, S100A10-annexin 2 protein complex which maybe involved in constitutive trafficking of TPRV6 to the plasma membrane and Rab11a which plays a role in recycling of TPRV6 to the plasma membrane (Derler et al., 2006, Van de Graaf et 2003, Van de Graaf et al, 2006). These TRPV6 associated proteins may represent novel components of the regulation by 1,25(OH)2D3 of calcium entry into the intestinal cell. Recent preliminary results show that transgenic mice overexpressing TRPV6 throughout the intestine (from duodenum to distal colon) of WT mice develop hypercalcemia, hypercalciuria and soft tissue calcification (Cui and Fleet, 2010). Although TRPV6 is not critical for 1,25(OH)2D3 mediated intestinal calcium absorption and maybe compensated by another channel yet to be identified, these studies indicate that TRPV6 does have a role in the process of intestinal calcium absorption.
Models of vitamin D mediated intestinal calcium absorption. Left panel: Transcellular intestinal calcium absorption. 1,25(OH)2D3, through its genomic actions, stimulates active intestinal calcium absorption. The traditional model of transcellular calcium transport involves calcium influx through TRPV6, intracellular calcium transfer by calbindin (CaBP) and calcium extrusion by the plasma membrane calcium ATPase (Ca pump). Recent studies using KO mice have suggested that TRPV6 and calbindin are not critical for 1,25(OH)2D3 calcium absorption and maybe compensated by another channel or protein. Right panel: Paracellular pathway. There is increasing evidence that 1,25(OH)2D3 can enhance paracellular calcium diffusion by regulating tight junction proteins. (Reproduced with permission from Wasserman RH, 2005).
Paracellular Calcium Transport
Calcium transverses the intestine by both the active transcellular pathway and the passive paracellular pathway (Hoenderop et al., 2005) (). The paracellular pathway functions throughout the entire length of the intestine and predominates in the more distal regions. This pathway is driven by the luminal electrochemical gradient and the integrity of the intercellular tight junctions (Tuskita et al., 2001). Recent evidence suggests that transjunctional transport of calcium by the paracellular pathway occurs in a regulated fashion, and may be coupled to active transcellular movement of calcium in a coordinated manner (Fujita et al., 2008). Tight junctions are specialized membrane domains located between the apical and basolateral membranes of the enterocyte, which form a barrier to the movement of ions, proteins, and other macromolecules across the intestine by maintaining a charge and size selectivity (Tuskita et al., 2001). Claudins are the major transmembrane components of tight junctions (Tuskita et al., 2001, Furuse et al., 1998) and it has been suggested that 1,25(OH)2D3 can promote paracellular calcium diffusion by increasing junction ion permeability (Fujita et al., 2008, Kutuzova and DeLuca 2004). VDR knockout mice, known to exhibit reduced intestinal calcium absorption, have decreased levels of claudin-2 and claudin-12 mRNA and protein (Fujita et al., 2008). In addition, 1,25(OH)2D3 has been shown to induce the expression of claudin-2 and claudin-12 in vitro in an intestinal epithelial cell line resulting in facilitated paracellular calcium conductance (Fujita et al., 2008). Gene array studies have shown that in addition to the known target genes, TRPV6 and calbindin-D9K, 1,25(OH)2D3 suppresses a number of intra- and intercellular matrix proteins including cadherin-17 (a cell adhesion protein) and aquaporin-8 (a tight junction channel), suggesting that vitamin D regulates intestinal calcium absorption via the paracellular pathway in addition to the transcellular pathway (Kutuzova and DeLuca 2004). It is possible that these other factors may compensate for the lack of TRPV6 in the TRPV6 KO mouse and thus may explain, in part, the mild phenotype of the TPRV6 KO mouse and the TRPV6/calbindin-D9k double KO mouse. Future studies examining different regions of the intestine and the identification of novel 1,25(OH)2D3 regulated proteins involved in transcellular and paracellular calcium absorption are needed.
Pregnancy, Lactation, Estrogen and Prolactin and Intestinal Calcium Absorption
Although 1,25(OH)2D3 is the principal hormone regulating active intestinal calcium absorption, other hormones have been shown to influence the process as well. Increased intestinal calcium transport has been observed in vitamin D deficient pregnant and lactating rats (Halloron and Deluca 1980, Boass et al., 1981, Brommage et al 1990). In addition, estradiol replacement in ovariectomized rats has been reported to result in an increase in intestinal calcium absorption without a stimulation of circulating 1,25(OH)2D3 levels (O’Loughlin and Morris, 1998). Studies by Van Cromphaut et al (Van Cromphant et al., 2003) in VDR KO mice showed that estrogen treatment after ovariectomy as well as pregnancy and lactation result in an induction of TRPV6 in the duodenum. In addition, in estrogen receptor α (ERα) KO mice, TRPV6 is reduced (Van Cromphant et al., 2003). These findings suggest that estrogens, independent of vitamin D, may be important regulators of calcium influx into the enterocyte and that these effects are mediated by ERα. In addition to estrogen, prolactin, a lacotgenic polypeptide hormone that is elevated during pregnancy and lactation, has been shown to have calcium regulatory effects. Prolactin has been reported to stimulate active intestinal calcium transport in vitamin D deficient rats (Pahuja and Deluca 1981). In addition, a direct effect of prolactin on active duodenal calcium transport was shown in studies using the Ussing chamber technique and prolactin applied to the incubation solution (Charoenphandhu et al., 2001). Studies in our laboratory indicate that prolactin can regulate TRPV6 in the duodenum independent of vitamin D, and also has cooperative effects with 1,25(OH)2D3 in regulation of both the intestinal calcium transport proteins TRPV6 and calbindin-D9K (Ajibade et al., 2010). Because both 1,25(OH)2D3 and prolactin levels are elevated during lactation (Halloron and Deluca 1980, Halloron et al. 1979, Pike et al., 1979, Meites et al 1972), prolactin may act together with 1,25(OH)2D3 to increase active intestinal calcium absorption. In addition, we found that prolactin has a direct effect on the transcription of the 1α(OH)ase gene, thus enhancing 1α(OH)ase protein expression and increasing levels of 1,25(OH)2D3 during lactation when there is an increased calcium requirement for the neonate (Ajibade et al., 2010). It has been suggested that prolactin also has an effect on the paracellular pathway of intestinal calcium absorption through upregulation of claudin-15 (Charoenphandhu et al., 2009).
Glucocortiocoids and Intestinal Calcium Absorption
Because of their potent anti-inflammatory and immunosuppressive properties, glucocorticoids are effectively used to treat inflammatory conditions such as asthma and rheumatoid arthritis. However, long term treatment with glucocorticoids reduces bone mineral density leading to osteoporosis (Reid 1997). In addition to direct effects on bone, glucocorticoids can also induce bone loss through diminished intestinal calcium absorption (Reid 1997, Huybers et al., 2007). In mice it has been reported that treatment with pharmacological doses of glucocorticoids results in decreased intestinal calcium absorption which is associated with a decrease in TRPV6 and calbindin-D9K (Huybers et al., 2007, Lee et al., 2006). Studies in cortisol treated chicks also noted an inhibition of intestinal calcium absorption which was associated with a decrease in calbindin (Feher and Wasserman, 1979). It has been suggested that the effect of glucocorticoids on calcium transport proteins can be independent of vitamin D (Huybers et al., 2007, Feher and Wasserman, 1979).
Effect of Aging
In aging, intestinal calcium absorption declines resulting in increased PTH which correlates to an age-related increase in bone turnover (Bullamore et al., 1970, Ledger et al., 1995). It has been proposed that the defect in intestinal calcium absorption is related both to low circulating levels of 1,25(OH)2D3 and to intestinal resistance to the action of 1,25(OH)2D3 (Wood et al., 1998). Either no change or a small decrease in intestinal VDR number has been reported with aging (Wood et al., 1998, Halloran and Portale, 2005). The expression of TRPV6 and calbindin-D9k declines with age and this decline is correlated to the decrease in intestinal calcium absorption and serum 1,25(OH)2D3 (Brown et al., 2005). In mice deficient in klotho (a multifunctional protein involved in phosphate and calcium homeostasis) a premature aging phenotype has been described (including short lifespan, infertility, atherosclerosis, skin atrophy and osteoporosis) (Kuro-o et al., 1997). Klotho functions as an essential cofactor for FGF23 which has been shown to regulate phosphate homeostasis and vitamin D biosynthesis (Kurosu et al). FGF23 and klotho, the FGF cofactor, suppress the expression of 1α(OH)ase and induce 24(OH)ase in kidney (Tsujikawa et al., 2003). Compared to WT mice, klotho KO mice have increased serum calcium and phosphate and decreased serum PTH (Kuro-o et al., 1997). Klotho KO mice also display increased serum levels of 1,25(OH)2D3 and increased expression of 1α(OH)ase (Tsujikawa et al., 2003, Yoshida et al., 2002). In the intestine klotho KO mice show increased expression of TRPV6 and calbindin-D9k and increased intestinal calcium absorption (Alexander et al., 2009) (in contrast to the decline observed in aging mice and rats; Brown et al., 2005). Thus the “aging” phenotype of the klotho KO mouse may reflect, at least in part, the effect of overproduction of 1,25(OH)2D3 rather than an effect on intestinal calcium absorption which contributes to bone loss in aging.
Calcium absorption, vitamin D and the distal intestine
In the calcium absorptive process the duodenum has been the major focus of research due to its highly active transport system. However, it is the distal intestine where 70- 80 % of the ingested calcium is absorbed (mostly in the ileum) (Wasserman 2005). Thus, it is important to understand the process by which the distal segment transports calcium. The vitamin D dependence of calcium absorption in the ileum and the colon has been shown (Petith et al., 1979, Lee et al., 1981, Favus et al., 1980, Favus, 1985, Vergne-Marini et al., 1976). VDR is expressed in all segments of the small and large intestine (highest levels have been reported in the cecum and colon) and in patients with extensive resection of the small intestine, calcium absorption has been reported to be significantly higher when the colon is preserved (Hirst and Feldman 1981, Stumpf et al., 1979, Xue and Fleet 2009, Hylander et al., 1990). 1,25(OH)2D3 has been shown to convert regions of net secretion of calcium in ileum and colon to net absorption (Favus 1985). The cecum has also been reported to be involved in 1,25(OH)2D3 mediated active transport (Favus and Angeid-Backman 1985). TRPV6 protein and calbindin-D9k protein are present in all segments of the mouse and rat intestine (immunocytochemical studies have indicated that the strongest expression of TRPV6 is in the cecum and colon) (Teerapornpuntakit et al., 2009, Zhang et al., 2010). Together these findings indicate that the distal segments of the intestine, in addition to the duodenum, play an important role in 1,25(OH)2D3 mediated calcium homeostasis. Our studies in the TRPV6/calbindin-D9k double KO mice indicate that we are missing important information related to the mechanisms involved in the regulation of intestinal calcium transport by 1,25(OH)2D3. Identification of multiple mechanisms by which 1,25(OH)2D3 acts to increase calcium absorption in different segments of the intestine is needed in order to identify new approaches to sustain calcium balance.
Acknowledgments
This work was supported by National Institutes of Health Grant DK38961-22 to SC
Footnotes
Publisher’s Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
References
- Ajibade DV, Dhawan P, Fechner AJ, Meyer MB, Pike JW, Christakos S. Evidence for a role of prolactin in calcium homeostasis: regulation of intestinal transient receptor potential vanilloid type 6, intestinal calcium absorption, and the 25-hydroxyvitamin D(3) 1alpha hydroxylase gene by prolactin. Endocrinology. 2010;151:2974–2984. [PMC free article] [PubMed] [Google Scholar]
- Akhter S, Kutuzova GD, Christakos S, DeLuca HF. Calbindin D9k is not required for 1,25-dihydroxyvitamin D3-mediated Ca2+ absorption in small intestine. Arch Biochem Biophys. 2007;460:227–232. [PubMed] [Google Scholar]
- Alexander RT, Woudenberg-Vrenken TE, Buurman J, Dijkman H, van der Eerden BC, van Leeuwen JP, Bindels RJ, Hoenderop JG. Klotho prevents renal calcium loss. J Am Soc Nephrol. 2009;20:2371–2379. [PMC free article] [PubMed] [Google Scholar]
- Amling M, Priemel M, Holzmann T, Chapin K, Rueger JM, Baron R, Demay MB. Rescue of the skeletal phenotype of vitamin D receptor-ablated mice in the setting of normal mineral ion homeostasis: formal histomorphometric and biomechanical analyses. Endocrinology. 1999;140:4982–4987. [PubMed] [Google Scholar]
- Benn BS, Ajibade D, Porta A, Dhawan P, Hediger M, Peng JB, Jiang Y, Oh GT, Jeung EB, Lieben L, Bouillon R, Carmeliet G, Christakos S. Active intestinal calcium transport in the absence of transient receptor potential vanilloid type 6 and calbindin-D9k. Endocrinology. 2008;149:3196–3205. [PMC free article] [PubMed] [Google Scholar]
- Bianco SD, Peng JB, Takanaga H, Suzuki Y, Crescenzi A, Kos CH, Zhuang L, Freeman MR, Gouveia CH, Wu J, Luo H, Mauro T, Brown EM, Hediger MA. Marked disturbance of calcium homeostasis in mice with targeted disruption of the Trpv6 calcium channel gene. J Bone Miner Res. 2007;22:274–285. [PMC free article] [PubMed] [Google Scholar]
- Boass A, Toverud SU, Pike JW, Haussler MR. Calcium metabolism during lactation: enhanced intestinal calcium absorption in vitamin D-deprived, hypocalcemic rats. Endocrinology. 1981;109:900–907. [PubMed] [Google Scholar]
- Brommage R, Baxter DC, Gierke LW. Vitamin D-independent intestinal calcium and phosphorus absorption during reproduction. Am J Physiol. 1990;259:G631–638. [PubMed] [Google Scholar]
- Brown AJ, Krits I, Armbrecht HJ. Effect of age, vitamin D, and calcium on the regulation of rat intestinal epithelial calcium channels. Arch Biochem Biophys. 2005;437:51–58. [PubMed] [Google Scholar]
- Bullamore JR, Wilkinson R, Gallagher JC, Nordin BE, Marshall DH. Effect of age on calcium absorption. Lancet. 1970;2:535–537. [PubMed] [Google Scholar]
- Charoenphandhu N, Limlomwongse L, Krishnamra N. Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats. Can J Physiol Pharmacol. 2001;79:430–438. [PubMed] [Google Scholar]
- Charoenphandhu N, Nakkrasae LI, Kraidith K, Teerapornpuntakit J, Thongchote K, Thongon N, Krishnamra N. Two-step stimulation of intestinal Ca(2+) absorption during lactation by long-term prolactin exposure and suckling-induced prolactin surge. Am J Physiol Endocrinol Metab. 2009;297:E609–619. [PubMed] [Google Scholar]
- Cui M, F J. Transgenic overexpression of human TRPV6 in intestine increases calcium absorption efficiency and improves bone mass in mice. Journal of Bone and Mineral Research. 2010;25:S59. [Google Scholar]
- Derler I, Hofbauer M, Kahr H, Fritsch R, Muik M, Kepplinger K, Hack ME, Moritz S, Schindl R, Groschner K, Romanin C. Dynamic but not constitutive association of calmodulin with rat TRPV6 channels enables fine tuning of Ca2+-dependent inactivation. J Physiol. 2006;577:31–44. [PMC free article] [PubMed] [Google Scholar]
- Favus MJ. Factors that influence absorption and secretion of calcium in the small intestine and colon. Am J Physiol. 1985;248:G147–157. [PubMed] [Google Scholar]
- Favus MJ, Angeid-Backman E. Effects of 1,25(OH)2D3 and calcium channel blockers on cecal calcium transport in the rat. Am J Physiol. 1985;248:G676–681. [PubMed] [Google Scholar]
- Favus MJ, Kathpalia SC, Coe FL, Mond AE. Effects of diet calcium and 1,25-dihydroxyvitamin D3 on colon calcium active transport. Am J Physiol. 1980;238:G75–78. [PubMed] [Google Scholar]
- Feher JJ, Wasserman RH. Intestinal calcium-binding protein and calcium absorption in cortisol-treated chicks: effects of vitamin D3 and 1,25-dihydroxyvitamin D3. Endocrinology. 1979;104:547–551. [PubMed] [Google Scholar]
- Fujita H, Sugimoto K, Inatomi S, Maeda T, Osanai M, Uchiyama Y, Yamamoto Y, Wada T, Kojima T, Yokozaki H, Yamashita T, Kato S, Sawada N, Chiba H. Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. Mol Biol Cell. 2008;19:1912–1921. [PMC free article] [PubMed] [Google Scholar]
- Furuse M, Fujita K, Hiiragi T, Fujimoto K, Tsukita S. Claudin-1 and -2: novel integral membrane proteins localizing at tight junctions with no sequence similarity to occludin. J Cell Biol. 1998;141:1539–1550. [PMC free article] [PubMed] [Google Scholar]
- Halloran BP, Barthell EN, DeLuca HF. Vitamin D metabolism during pregnancy and lactation in the rat. Proc Natl Acad Sci U S A. 1979;76:5549–5553. [PMC free article] [PubMed] [Google Scholar]
- Halloran BP, DeLuca HF. Calcium transport in small intestine during pregnancy and lactation. Am J Physiol. 1980;239:E64–68. [PubMed] [Google Scholar]
- Halloran BP, P AA. Vitamin D metabolism in aging. In: P J, G F, Feldman D, editors. Vitamin D. San Diego: 2005. pp. 823–838. [Google Scholar]
- Hirst MA, Feldman D. 1,25-Dihydroxyvitamin D3 receptors in mouse colon. J Steroid Biochem. 1981;14:315–319. [PubMed] [Google Scholar]
- Hoenderop JG, Nilius B, Bindels RJ. Calcium absorption across epithelia. Physiol Rev. 2005;85:373–422. [PubMed] [Google Scholar]
- Huybers S, Naber TH, Bindels RJ, Hoenderop JG. Prednisolone-induced Ca2+ malabsorption is caused by diminished expression of the epithelial Ca2+ channel TRPV6. Am J Physiol Gastrointest Liver Physiol. 2007;292:G92–97. [PubMed] [Google Scholar]
- Hylander E, Ladefoged K, Jarnum S. Calcium absorption after intestinal resection. The importance of a preserved colon. Scand J Gastroenterol. 1990;25:705–710. [PubMed] [Google Scholar]
- Kuro-o M, Matsumura Y, Aizawa H, Kawaguchi H, Suga T, Utsugi T, Ohyama Y, Kurabayashi M, Kaname T, Kume E, Iwasaki H, Iida A, Shiraki-Iida T, Nishikawa S, Nagai R, Nabeshima YI. Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature. 1997;390:45–51. [PubMed] [Google Scholar]
- Kurosu H, Ogawa Y, Miyoshi M, Yamamoto M, Nandi A, Rosenblatt KP, Baum MG, Schiavi S, Hu MC, Moe OW, Kuro-o M. Regulation of fibroblast growth factor-23 signaling by klotho. J Biol Chem. 2006;281:6120–6123. [PMC free article] [PubMed] [Google Scholar]
- Kutuzova GD, Akhter S, Christakos S, Vanhooke J, Kimmel-Jehan C, Deluca HF. Calbindin D(9k) knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level. Proc Natl Acad Sci U S A. 2006;103:12377–12381. [PMC free article] [PubMed] [Google Scholar]
- Kutuzova GD, Deluca HF. Gene expression profiles in rat intestine identify pathways for 1,25-dihydroxyvitamin D(3) stimulated calcium absorption and clarify its immunomodulatory properties. Arch Biochem Biophys. 2004;432:152–166. [PMC free article] [PubMed] [Google Scholar]
- Kutuzova GD, Sundersingh F, Vaughan J, Tadi BP, Ansay SE, Christakos S, Deluca HF. TRPV6 is not required for 1alpha,25-dihydroxyvitamin D3-induced intestinal calcium absorption in vivo. Proc Natl Acad Sci U S A. 2008;105:19655–19659. [PMC free article] [PubMed] [Google Scholar]
- Ledger GA, Burritt MF, Kao PC, O’Fallon WM, Riggs BL, Khosla S. Role of parathyroid hormone in mediating nocturnal and age-related increases in bone resorption. J Clin Endocrinol Metab. 1995;80:3304–3310. [PubMed] [Google Scholar]
- Lee DB, Walling MM, Levine BS, Gafter U, Silis V, Hodsman A, Coburn JW. Intestinal and metabolic effect of 1,25-dihydroxyvitamin D3 in normal adult rat. Am J Physiol. 1981;240:G90–96. [PubMed] [Google Scholar]
- Lee GS, Choi KC, Jeung EB. Glucocorticoids differentially regulate expression of duodenal and renal calbindin-D9k through glucocorticoid receptor-mediated pathway in mouse model. Am J Physiol Endocrinol Metab. 2006;290:E299–307. [PubMed] [Google Scholar]
- Li YC, Pirro AE, Amling M, Delling G, Baron R, Bronson R, Demay MB. Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia. Proc Natl Acad Sci U S A. 1997;94:9831–9835. [PMC free article] [PubMed] [Google Scholar]
- Lieben L, Benn BS, Ajibade D, Stockmans I, Moermans K, Hediger MA, Peng JB, Christakos S, Bouillon R, Carmeliet G. Trpv6 mediates intestinal calcium absorption during calcium restriction and contributes to bone homeostasis. Bone. 2010;47:301–308. [PMC free article] [PubMed] [Google Scholar]
- Meites J, Lu KH, Wuttke W, Welsch CW, Nagasawa H, Quadri SK. Recent studies on functions and control of prolactin secretion in rats. Recent Prog Horm Res. 1972;28:471–526. [PubMed] [Google Scholar]
- O’Loughlin PD, Morris HA. Estrogen deficiency impairs intestinal calcium absorption in the rat. J Physiol. 1998;511:313–322. [PMC free article] [PubMed] [Google Scholar]
- Pahuja DN, DeLuca HF. Stimulation of intestinal calcium transport and bone calcium mobilization by prolactin in vitamin D-deficient rats. Science. 1981;214:1038–1039. [PubMed] [Google Scholar]
- Petith MM, Wilson HD, Schedl HP. Vitamin D dependence of in vivo calcium transport and mucosal calcium binding protein in rat large intestine. Gastroenterology. 1979;76:99–104. [PubMed] [Google Scholar]
- Pike JW, Parker JB, Haussler MR, Boass A, Toverud SV. Dynamic changes in circulating 1,25-dihydroxyvitamin D during reproduction in rats. Science. 1979;204:1427–1429. [PubMed] [Google Scholar]
- Reid IR. Glucocorticoid osteoporosis–mechanisms and management. Eur J Endocrinol. 1997;137:209–217. [PubMed] [Google Scholar]
- Song Y, Peng X, Porta A, Takanaga H, Peng JB, Hediger MA, Fleet JC, Christakos S. Calcium transporter 1 and epithelial calcium channel messenger ribonucleic acid are differentially regulated by 1,25 dihydroxyvitamin D3 in the intestine and kidney of mice. Endocrinology. 2003;144:3885–3894. [PubMed] [Google Scholar]
- Stumpf WE, Sar M, Reid FA, Tanaka Y, DeLuca HF. Target cells for 1,25-dihydroxyvitamin D3 in intestinal tract, stomach, kidney, skin, pituitary, and parathyroid. Science. 1979;206:1188–1190. [PubMed] [Google Scholar]
- Teerapornpuntakit J, Dorkkam N, Wongdee K, Krishnamra N, Charoenphandhu N. Endurance swimming stimulates transepithelial calcium transport and alters the expression of genes related to calcium absorption in the intestine of rats. Am J Physiol Endocrinol Metab. 2009;296:E775–786. [PubMed] [Google Scholar]
- Tsujikawa H, Kurotaki Y, Fujimori T, Fukuda K, Nabeshima Y. Klotho, a gene related to a syndrome resembling human premature aging, functions in a negative regulatory circuit of vitamin D endocrine system. Mol Endocrinol. 2003;17:2393–2403. [PubMed] [Google Scholar]
- Tsukita S, Furuse M, Itoh M. Multifunctional strands in tight junctions. Nat Rev Mol Cell Biol. 2001;2:285–293. [PubMed] [Google Scholar]
- Van Cromphaut SJ, Dewerchin M, Hoenderop JG, Stockmans I, Van Herck E, Kato S, Bindels RJ, Collen D, Carmeliet P, Bouillon R, Carmeliet G. Duodenal calcium absorption in vitamin D receptor-knockout mice: functional and molecular aspects. Proc Natl Acad Sci U S A. 2001;98:13324–13329. [PMC free article] [PubMed] [Google Scholar]
- Van Cromphaut SJ, Rummens K, Stockmans I, Van Herck E, Dijcks FA, Ederveen AG, Carmeliet P, Verhaeghe J, Bouillon R, Carmeliet G. Intestinal calcium transporter genes are upregulated by estrogens and the reproductive cycle through vitamin D receptor-independent mechanisms. J Bone Miner Res. 2003;18:1725–1736. [PubMed] [Google Scholar]
- van de Graaf SF, Chang Q, Mensenkamp AR, Hoenderop JG, Bindels RJ. Direct interaction with Rab11a targets the epithelial Ca2+ channels TRPV5 and TRPV6 to the plasma membrane. Mol Cell Biol. 2006;26:303–312. [PMC free article] [PubMed] [Google Scholar]
- van de Graaf SF, Hoenderop JG, Gkika D, Lamers D, Prenen J, Rescher U, Gerke V, Staub O, Nilius B, Bindels RJ. Functional expression of the epithelial Ca(2+) channels (TRPV5 and TRPV6) requires association of the S100A10-annexin 2 complex. EMBO J. 2003;22:1478–1487. [PMC free article] [PubMed] [Google Scholar]
- Vergne-Marini P, Parker TF, Pak CY, Hull AR, DeLuca HF, Fordtran JS. Jejunal and ileal absorption in patients with chronic renal disease. Effect of 1alpha-hydroxycholecalciferol. J Clin Invest. 1976;57:861–866. [PMC free article] [PubMed] [Google Scholar]
- Wasserman RH. Vitamin D and intestinal absorption of calcium: a view and overview. In: P JW, Feldman D, Glorieux F, editors. Vitamin D. Acedemin press; San Diego, CA: 2005. pp. 411–428. [Google Scholar]
- Wood RJ, Fleet JC, Cashman K, Bruns ME, Deluca HF. Intestinal calcium absorption in the aged rat: evidence of intestinal resistance to 1,25(OH)2 vitamin D. Endocrinology. 1998;139:3843–3848. [PubMed] [Google Scholar]
- Xue Y, Fleet JC. Intestinal vitamin D receptor is required for normal calcium and bone metabolism in mice. Gastroenterology. 2009;136:1317–1327. e1311–1312. [PMC free article] [PubMed] [Google Scholar]
- Yoshida T, Fujimori T, Nabeshima Y. Mediation of unusually high concentrations of 1,25-dihydroxyvitamin D in homozygous klotho mutant mice by increased expression of renal 1alpha-hydroxylase gene. Endocrinology. 2002;143:683–689. [PubMed] [Google Scholar]
- Yoshizawa T, Handa Y, Uematsu Y, Takeda S, Sekine K, Yoshihara Y, Kawakami T, Arioka K, Sato H, Uchiyama Y, Masushige S, Fukamizu A, Matsumoto T, Kato S. Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning. Nat Genet. 1997;16:391–396. [PubMed] [Google Scholar]
- Zhang W, Na T, Wu G, Jing H, Peng JB. Down-regulation of intestinal apical calcium entry channel TRPV6 by ubiquitin E3 ligase Nedd4-2. J Biol Chem. 2010;285:36586–36596. [PMC free article] [PubMed] [Google Scholar]
Calcium Supplements & Absorption | MUSC Health
Osteoporosis is a very common problem that leads to broken bones and poor posture in aging women and men.
To prevent the loss of bone mass, it is important to have sufficient calcium in the blood that is transported to the bones. Although calcium is abundant in dairy products like milk, the amount of calcium that we need increases as we age. Since many people quit eating or drinking food products with calcium, such as whole milk, due to a health-related diet, a dietary supplement with calcium is important. Older adults require approximately 1,200 milligrams of calcium per day.
The remainder of this article addresses ways to get enough calcium to keep bones strong. The healthiest sources of calcium are from foods that are rich in calcium, including most dairy products, cheeses, fortified orange juice and leafy green vegetables, which can provide at least 100 milligrams of calcium. A balanced diet provides most calcium needed by older adults. However, additional calcium must be ingested to reach a required 1,200 milligrams per day. The body can handle more than the minimum requirement of calcium. However, the body cannot manufacture calcium if too little is ingested.
Calcium Supplementation
All calcium ingested is not absorbed into the body. The small intestine, which is the part of the digestive system just beyond the stomach, is where calcium is taken by the blood and transported to bone and other tissues. The amount of calcium absorbed is dependent on several key factors:
- Amount of calcium already in the blood
- Form of calcium (diet or formulation)
- Small intestine conditions
Calcium typically comes as a liquid or tablet carbonate or citric acid preparation. The carbonate requires acid in the intestine that generally is generated with food in the stomach. Therefore, carbonate pills should be taken with meals by people taking calcium to increase calcium absorption. Calcium citrate is soluble and does not require meals for absorption. Most commonly used calcium supplements come as a carbonate form and should be taken during or immediately after meals. Check the label of your calcium supplement to determine which form you have and when to take it.
Approximately 500 milligrams of calcium can be taken at one time. Therefore, do not take all supplements at the same time. If you and your doctor have agreed you need supplementation, be sure to take it three times a day or approximately one-third at a time. To avoid taking too much, do not take more than 2,500 milligrams per day.
Vitamin D also is required for calcium absorption. The best source of vitamin D is sunshine for approximately 20 minutes per day, which is not a problem for most people who live in the South. Vitamin D also is found in many other sources and generally is not responsible for poor calcium absorption. On the other hand, estrogen facilitates calcium absorption. After menopause, some women lose their ability to easily take up calcium. For this reason, calcium generally is given at menopause as a vitamin supplement.
The Bottom Line
As we age, we need calcium to prevent weak bones and fractures. Both women and men should take an additional 1,000 to 1,500 milligrams a day after first consulting a physician. Three doses of 500 milligrams of calcium should be taken each day, preferably with a meal, for healthier bones and other tissues.
Did you know that certain foods block calcium absorption?
Self Care, Diet and Nutrition
You try to eat a healthy, calcium-rich diet. You watch your weight. You exercise. You do everything in your power to maintain strong bones because you want to be active well into your 70s and 80s.
You even make sure you have a nutritious breakfast of natural whole wheat squares topped cold, vitamin-D-fortified milk.
It sounds like a nutritious way to your day. But eating whole-wheat cereal and milk together may not be the best menu choice if you are trying to increase your bone mass. There are certain foods, like wheat, that block calcium absorption.
Phytates bind calcium.
High-fiber foods contain phytates, which prevent the body from absorbing calcium in other foods. Eating a high-fiber, whole-wheat cereal with milk, macaroni and cheese, or drinking a tall, cold glass of milk with Boston baked beans and hot dogs may be great-tasting combinations, but they do not boost bone-building nutrition.
Phytates found in whole-grains, legumes (dried beans), nuts and soy products bind the calcium of other foods eaten when they are eaten at the same time. When calcium is bound, the body cannot use it.
Oxalic acid hinders calcium absorption.
Foods high in oxalic acid also impede the absorption of calcium by binding the mineral.
Spinach is naturally high in calcium, but it is also high in oxalic acid. The body is unable to process the calcium it provides. Other foods that contain oxalic acid include beet greens, rhubarb and sweet potatoes.
Though these foods should not be considered for their calcium value, they do provide other nutrients and minerals that help the body stay healthy.
Does protein interfere with calcium absorption?
Historically, nutritionists have warned that eating large amounts of protein causes the kidneys to flush calcium out of the body. But recent studies show protein also may increase intestinal calcium absorption.
More study is needed to determine protein’s effect on the body’s ability to process calcium. To make the most of your calcium intake, don’t drink milk with your beef stew, chili or steak dinner. Eat your meal and then drink your milk later.
Beer, cheese and snacks are a trifecta for calcium loss.
Alcohol and salty foods are catalysts for calcium flushing. As calcium levels in the blood decrease, the body extracts (resorbing) calcium from the bones to obtain the calcium it needs to function properly. Calcium flushing can make the bones porous, which can lead to the development of osteoporosis.
To minimize calcium flushing:
- Avoid eating foods that have a sodium content higher than 20 percent of the daily recommended value.
- Don’t drink more than two or three alcoholic drinks a day.
You can eat your spinach and build your calcium, too.
Wheat and other “bad-to-the-bone” foods provide many other vitamins and minerals vital to your health. You should still eat these types of foods, just not at the same time that you drink milk or eat calcium-rich foods.
The best way to maximize the nutrition from foods that bind or flush calcium and continue to boost your calcium levels is just a matter of scheduling. Eat calcium-binding foods at least two hours before or after you eat calcium-rich foods. This timing allows your body to maximize the vitamins and minerals of all food types. By making this timely adjustment to your meals, you gain all the nutritional benefits without interfering with your body’s ability to absorb the calcium it needs every day.
Source:
The National Institutes of Health Office of Dietary Supplements
Other e-Motion articles added in October 2017:
What are the benefits of anterior hip replacement?
Hand, back and burn injuries. Who knew Thanksgiving could be so dangerous?
Hoop it up!
Meet C. Kevin Martin, PA-C
Calcium Absorption – an overview
Intestinal Calcium Absorption
Calcium absorption is moderately efficient in humans, with 35% of dietary intake typically absorbed. The transfer of calcium across the intestinal barrier occurs through both saturable (presumably transcellular) and nonsaturable (presumably paracellular diffusion) pathways. Calcium absorption is saturable in the duodenum (proximal segment of small intestine) and to a lesser extent in the jejunum (midportion of the small intestine). Animal studies suggest that saturable calcium transport may also occur in the large intestine. The saturable pathway is energy dependent. Calcium moves from the mucosal to serosal side of the intestine, even against a concentration gradient. This pathway is under nutritional and physiologic regulation. For the standard recommended calcium intake (i.e., 400–500 mg per meal), the saturable transport accounts for more than 60% of total calcium absorption in the small intestine, thus demonstrating the importance of the saturable calcium absorption pathway under normal dietary loads.
In contrast, passive transport, involving claudins-2, -12, and -15, occurs throughout the entire intestine. Passive transport is a nonsaturable, linear function, dependent on the calcium concentration found in a given segment of the intestinal lumen.
When calcium intake is adequate to high, the proportion of calcium transported in any given intestinal segment is determined by the following: (1) the presence of saturable and nonsaturable pathways, (2) the transit time through the intestinal tract, and (3) the solubility of calcium within the intestinal segment. As a result, even though calcium solubility is low and the saturable pathway is absent or downregulated in the ileum (the final segment of the small intestine), the total amount of calcium absorbed is actually greatest in the ileum because transit time through this segment is 10 or more times longer than through the more proximal intestinal segments.
Habitual consumption of a low-calcium diet stimulates processes to increase small intestine calcium absorption efficiency. This effect is mediated in part through changes in the plasma concentrations of the most active vitamin D metabolite, 1,25(OH)2D. There are four different models for regulated calcium transport (Fig. 13.3).
Figure 13.3. Intestinal calcium absorption. Passive paracellular transport following the concentration gradient involves claudin-2, claudin-12, and claudin-15. Although passive, this process can be regulated by 1,25(OH)2D and prolactin through changes in gene transcription. Active transport may occur through multiple mechanisms: facilitated diffusion, vesicular transport, and transcaltachia. Facilitated diffusion (middle right, middle left) uses the transient receptor potential cation channel subfamily V member 6 (TRPV6), calbindin-D9K, basolateral transport via plasma membrane Ca2+ ATPase 1 (PMCA1), and the sodium-calcium exchanger 1 (NCX1). Gene transcription for expression of these proteins is upregulated by 1,25(OH)2D. Transcaltachia (lower left) refers to the rapid action of 1,25(OH)2D on either a membrane form of the vitamin D3 receptor (VDR) or membrane-associated, rapid-response steroid-binding protein (MARRS), triggering a rapid increase in transport through TRPV6 or through lysosomal cycling, independent of gene transcription. Vesicular transport (lower right, lower left) occurs through endocytosis or entry of cytoplasmic calcium into vesicles for transport and basolateral exocytosis.
In the facilitated diffusion model, calcium enters epithelial cells through the apical membrane calcium channel TRPV6. TRPV6 delivers calcium to calbindin-D9K, a low molecular weight, cytosolic, calcium-binding protein proposed to facilitate transcellular calcium movement. Calcium is then actively extruded across the basolateral membrane. This is primarily mediated by PMCA1b moving calcium against a concentration gradient, though the NCX1 sodium-calcium exchanger also contributes. Each of these proteins are transcriptionally regulated by 1,25(OH)2D.
The validity of the facilitated diffusion model has been challenged. Animals lacking TRPV6 or calbindin-D9K still increase the efficiency of intestinal calcium absorption in response to dietary calcium restriction, and 1,25(OH)2D still increases calcium absorption in TRPV6 knockout mice. Furthermore, mice without calbindin-D9K have normal calcium absorption, both at baseline and in response to 1,25(OH)2D. However, mice with the combined knockouts of TRPV6 and calbindin-D9K have a limited response to 1,25(OH)2D. These studies suggest that other mechanisms in addition to facilitated diffusion contribute to the process of active calcium transport across enterocytes.
The vesicular transport model predicts that calcium absorption required cycling of calcium-containing lysosomes in enterocytes (as in Fig. 13.3). In enterocytes, 1,25(OH)2D increases both lysosomal number and calcium content. Lysosomal calcium uptake models occurring after TRPV6 transport and endocytosis into cells have been proposed. Transient receptor potential cation channel subfamily V member 5 (TRPV5) and TRPV6 may be present in some vesicular structures and facilitate calcium transport. Enterocyte vesicle calbindin-D28K is also reported in chicks. However, it is not clear whether calcium accumulation in vesicles is specific to mammalian transcellular calcium transport regulation.
Transcaltachia refers to a rapid, 1,25(OH)2D-stimulated increase in calcium transport (Fig. 13.3). In contrast to the facilitated diffusion model, transcaltachia does not require gene transcription, although, like in the vesicular transport model, transportation across the cell may still involve vesicles. In ex vivo perfused chick intestine, exposure to 1,25(OH)2D for 14 min dramatically increases calcium transport across enterocytes.
Transcaltachia appears to be mediated by a basolateral membrane receptor: either by a unique role for the vitamin D3 receptor (VDR) at the basolateral surface, by a novel membrane vitamin D receptor called the membrane-associated, rapid response steroid-binding protein (MARRS), or by the PTH-PTHrP receptor. However, MARRS knockout mice do not have disrupted transcellular calcium absorption or whole body calcium metabolism.
Regulated paracellular transport also contributes to calcium absorption. 1,25(OH)2D increases production of the tight junction proteins claudin-2 and claudin-12 in the jejunum and ileum facilitating passive transport. However, vitamin D regulates active calcium absorption in the proximal duodenum and jejunum, as opposed to the ileum, where claudin-2 and claudin-12 expression is highest. Prolactin upregulates claudin-15 during pregnancy and lactation, contributing to paracellular calcium absorption, as well as TRPV5, TRPV6, and calbindin-D9K also upregulating transcellular calcium transport. In addition, the voltage-dependent L-type calcium channel subunit alpha-1D (also known as voltage-gated calcium channel subunit alpha Cav1.3) may also contribute to intestinal calcium absorption. However, this protein’s gene is not vitamin D regulated and Cav1.3 knockout mice do not have strong disruptions in either calcium or bone metabolism.
In sum, no single model is able to explain fully intestinal calcium transport mechanisms and the timing of responses to 1,25(OH)2D. Data support both transcriptional and more rapid responses of calcium transport to 1,25(OH)2D; more rapid increases in calcium transport suggest that mechanisms such as vesicular transport may be important. Redundancy in this system likely enables greater control and efficiency of calcium absorption, given that relative dietary deficiency is common and excess calcium consumption can also occur. Further studies are necessary to delineate the relative contributions of these various models and their mechanisms.
Vitamin D, calcium homeostasis and aging
Peacock M . Calcium metabolism in health and disease. Clin J Am Soc Nephrol 2010; 5 (Suppl 1): S23–S30.
CAS
Article
Google Scholar
Morris HA, Need AG, Horowitz M et al. Calcium absorption in normal and osteoporotic postmenopausal women. Calcif Tissue Int 1991; 49: 240–243.
CAS
Article
Google Scholar
Ensrud KE, Duong T, Cauley JA et al. Low fractional calcium absorption increases the risk for hip fracture in women with low calcium intake. Study of Osteoporotic Fractures Research Group. Ann Intern Med 2000; 132: 345–353.
CAS
Article
Google Scholar
Christakos S . Recent advances in our understanding of 1,25-dihydroxyvitamin D(3) regulation of intestinal calcium absorption. Arch Biochem Biophys 2012; 523: 73–76.
CAS
Article
Google Scholar
Brown EM . The calcium-sensing receptor: physiology, pathophysiology and CaR-based therapeutics. Subcell Biochem 2007; 45: 139–167.
CAS
Article
Google Scholar
Plum LA, DeLuca HF . Vitamin D, disease and therapeutic opportunities. Nat Rev Drug Discov 2010; 9: 941–955.
CAS
Article
Google Scholar
Bikle DD, Adams J, Christakos S . Vitamin D: production, metabolism and clinical requirements//Rosen C. Primer on Metabolic Bone Diseases. Hoboken: John Wiley and Sons, 2013: 235–245.
Zhu J, DeLuca HF . Vitamin D 25-hydroxylase – four decades of searching, are we there yet? Arch Biochem Biophys 2012; 523: 30–36.
CAS
Article
Google Scholar
Cheng JB, Motola DL, Mangelsdorf DJ et al. De-orphanization of cytochrome P450 2R1: a microsomal vitamin D 25-hydroxylase. J Biol Chem 2003; 278: 38084–38093.
CAS
Article
Google Scholar
Zhu JG, Ochalek JT, Kaufmann M et al. CYP2R1 is a major, but not exclusive, contributor to 25-hydroxyvitamin D production in vivo . Proc Natl Acad Sci USA 2013; 110: 15650–15655.
CAS
Article
Google Scholar
Chun RF, Peercy BE, Orwoll ES et al. Vitamin D and DBP: the free hormone hypothesis revisited. J Steroid Biochem Mol Biol 2014; 144: 132–137.
CAS
Article
Google Scholar
Nykjaer A, Dragun D, Walther D et al. An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. Cell 1999; 96: 507–515.
CAS
Article
Google Scholar
Kitanaka S, Takeyama K, Murayama A et al. Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. N Engl J Med 1998; 338: 653–661.
CAS
Article
Google Scholar
Jones G, Prosser DE, Kaufmann M . 25-Hydroxyvitamin D-24-hydroxylase (CYP24A1): its important role in the degradation of vitamin D. Arch Biochem Biophys 2012; 523: 9–18.
CAS
Article
Google Scholar
Veldurthy V, Wei R, Campbell M et al. 25-Hydroxyvitamin D(3) 24-hydroxylase: a key regulator of 1,25(OH)(2)D(3) catabolism and calcium homeostasis. Vitam Horm 2016; 100: 137–150.
CAS
Article
Google Scholar
St-Arnaud R, Arabian A, Travers R et al. Deficient mineralization of intramembranous bone in vitamin D-24-hydroxylase-ablated mice is due to elevated 1,25-dihydroxyvitamin D and not to the absence of 24,25-dihydroxyvitamin D. Endocrinology 2000; 141: 2658–2666.
CAS
Article
Google Scholar
Schlingmann KP, Kaufmann M, Weber S et al. Mutations in CYP24A1 and idiopathic infantile hypercalcemia. N Engl J Med 2011; 365: 410–421.
CAS
Article
Google Scholar
Henry HL . Regulation of vitamin D metabolism. Best Pract Res Clin Endocrinol Metab 2011; 25: 531–541.
CAS
Article
Google Scholar
Brenza HL, DeLuca HF . Regulation of 25-hydroxyvitamin D3 1alpha-hydroxylase gene expression by parathyroid hormone and 1,25-dihydroxyvitamin D3. Arch Biochem Biophys 2000; 381: 143–152.
CAS
Article
Google Scholar
Hu MC, Shiizaki K, Kuro-o M et al. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol 2013; 75: 503–533.
CAS
Article
Google Scholar
Pike JW, Meyer MB . Fundamentals of vitamin D hormone-regulated gene expression. J Steroid Biochem Mol Biol 2014; 144: 5–11.
CAS
Article
Google Scholar
Christakos S, Dhawan P, Verstuyf A et al. Vitamin D: metabolism, molecular mechanism of action, and pleiotropic effects. Physiol Rev 2016; 96: 365–408.
CAS
Article
Google Scholar
Amling M, Priemel M, Holzmann T et al. Rescue of the skeletal phenotype of vitamin D receptor-ablated mice in the setting of normal mineral ion homeostasis: formal histomorphometric and biomechanical analyses. Endocrinology 1999; 140: 4982–4987.
CAS
Article
Google Scholar
Li YC, Amling M, Pirro AE et al. Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. Endocrinology 1998; 139: 4391–4396.
CAS
Article
Google Scholar
Benn BS, Ajibade D, Porta A et al. Active intestinal calcium transport in the absence of transient receptor potential vanilloid type 6 and calbindin-D9k. Endocrinology 2008; 149: 3196–3205.
CAS
Article
Google Scholar
Lieben L, Benn BS, Ajibade D et al. Trpv6 mediates intestinal calcium absorption during calcium restriction and contributes to bone homeostasis. Bone 2010; 47: 301–308.
CAS
Article
Google Scholar
Cui M, Li Q, Johnson R et al. Villin promoter-mediated transgenic expression of transient receptor potential cation channel, subfamily V, member 6 (TRPV6) increases intestinal calcium absorption in wild-type and vitamin D receptor knockout mice. J Bone Miner Res 2012; 27: 2097–2107.
CAS
Article
Google Scholar
de Groot T, Bindels RJ, Hoenderop JG . TRPV5: an ingeniously controlled calcium channel. Kidney Int 2008; 74: 1241–1246.
CAS
Article
Google Scholar
Ajibade D, Benn BS, Christakos S. Mechanism of action of 1.25 dihydroxyvitamin D3 in intestinal calcium absorption and renal calcium transport//Holick MF. Vitamin D: Physiology, Molecular, Biological and Clinical Applications. Totowa: Humana Press, 2010: 175–187.
Hoenderop JG, Dardenne O, Van Abel M et al. Modulation of renal Ca2+ transport protein genes by dietary Ca2+ and 1,25-dihydroxyvitamin D3 in 25-hydroxyvitamin D3-1alpha-hydroxylase knockout mice. FASEB J 2002; 16: 1398–1406.
CAS
Article
Google Scholar
Hoenderop JG, van Leeuwen JP, van der Eerden BC et al. Renal Ca2+ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5. J Clin Invest 2003; 112: 1906–1914.
CAS
Article
Google Scholar
Armbrecht HJ, Zenser TV, Bruns ME et al. Effect of age on intestinal calcium absorption and adaptation to dietary calcium. Am J Physiol 1979; 236: E769–E774.
CAS
PubMed
Google Scholar
van Abel M, Huybers S, Hoenderop JG et al. Age-dependent alterations in Ca2+ homeostasis: role of TRPV5 and TRPV6. Am J Physiol Renal Physiol 2006; 291: F1177–F1183.
CAS
Article
Google Scholar
Brown AJ, Krits I, Armbrecht HJ . Effect of age, vitamin D, and calcium on the regulation of rat intestinal epithelial calcium channels. Arch Biochem Biophys 2005; 437: 51–58.
CAS
Article
Google Scholar
Matkovits T, Christakos S . Variable in vivo regulation of rat vitamin D-dependent genes (osteopontin, Ca,Mg-adenosine triphosphatase, and 25-hydroxyvitamin D3 24-hydroxylase): implications for differing mechanisms of regulation and involvement of multiple factors. Endocrinology 1995; 136: 3971–3982.
CAS
Article
Google Scholar
Johnson JA, Beckman MJ, Pansini-Porta A et al. Age and gender effects on 1,25-dihydroxyvitamin D3-regulated gene expression. Exp Gerontol 1995; 30: 631–643.
CAS
Article
Google Scholar
Armbrecht HJ, Zenser TV, Davis BB . Effect of age on the conversion of 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 by kidney of rat. J Clin Invest 1980; 66: 1118–1123.
CAS
Article
Google Scholar
Pattanaungkul S, Riggs BL, Yergey AL et al. Relationship of intestinal calcium absorption to 1,25-dihydroxyvitamin D [1,25(OH)2D] levels in young versus elderly women: evidence for age-related intestinal resistance to 1,25(OH)2D action. J Clin Endocrinol Metab 2000; 85: 4023–4027.
CAS
PubMed
Google Scholar
Ebeling PR, Sandgren ME, DiMagno EP et al. Evidence of an age-related decrease in intestinal responsiveness to vitamin D: relationship between serum 1,25-dihydroxyvitamin D3 and intestinal vitamin D receptor concentrations in normal women. J Clin Endocrinol Metab 1992; 75: 176–182.
CAS
PubMed
Google Scholar
Horst RL, Goff JP, Reinhardt TA . Advancing age results in reduction of intestinal and bone 1,25-dihydroxyvitamin D receptor. Endocrinology 1990; 126: 1053–1057.
CAS
Article
Google Scholar
Kinyamu HK, Gallagher JC, Prahl JM et al. Association between intestinal vitamin D receptor, calcium absorption, and serum 1,25 dihydroxyvitamin D in normal young and elderly women. J Bone Miner Res 1997; 12: 922–928.
CAS
Article
Google Scholar
Wood RJ, Fleet JC, Cashman K et al. Intestinal calcium absorption in the aged rat: evidence of intestinal resistance to 1,25(OH)2 vitamin D. Endocrinology 1998; 139: 3843–3848.
CAS
Article
Google Scholar
Weinstein JR, Anderson S . The aging kidney: physiological changes. Adv Chronic Kidney Dis 2010; 17: 302–307.
Article
Google Scholar
Reichel H, Deibert B, Schmidt-Gayk H et al. Calcium metabolism in early chronic renal failure: implications for the pathogenesis of hyperparathyroidism. Nephrol Dial Transplant 1991; 6: 162–169.
CAS
Article
Google Scholar
Quarles LD . Role of FGF23 in vitamin D and phosphate metabolism: implications in chronic kidney disease. Exp Cell Res 2012; 318: 1040–1048.
CAS
Article
Google Scholar
Armbrecht HJ, Wongsurawat N, Zenser TV et al. Differential effects of parathyroid hormone on the renal 1,25-dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 production of young and adult rats. Endocrinology 1982; 111: 1339–1344.
CAS
Article
Google Scholar
Mulroney SE, Woda C, Haramati A . Changes in renal phosphate reabsorption in the aged rat. Proc Soc Exp Biol Med 1998; 218: 62–67.
CAS
Article
Google Scholar
Raisz LG . Pathogenesis of osteoporosis: concepts, conflicts, and prospects. J Clin Invest 2005; 115: 3318–3325.
CAS
Article
Google Scholar
Cosman F, de Beur SJ, LeBoff MS et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int 2014; 25: 2359–2381.
CAS
Article
Google Scholar
Riggs BL, Khosla S, Melton LJ 3rd . Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev 2002; 23: 279–302.
CAS
Article
Google Scholar
Cauley JA . Estrogen and bone health in men and women. Steroids 2015; 99: 11–15.
CAS
Article
Google Scholar
Cauley JA, LaCroix AZ, Wu L et al. Serum 25 hydroxyvitamin D concentrations and the risk of hip fractures: the women’s health initiative. Ann Intern Med 2008; 149: 242–250.
Article
Google Scholar
Ross AC, Manson JE, Abrams SA et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011; 96: 53–58.
CAS
Article
Google Scholar
Holick MF, Binkley NC, Bischoff-Ferrari HA et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011; 96: 1911–1930.
CAS
Article
Google Scholar
Gallagher JC, Sai A, Templin T 2nd et al. Dose response to vitamin D supplementation in postmenopausal women: a randomized trial. Ann Intern Med 2012; 156: 425–437.
Article
Google Scholar
Priemel M, von Domarus C, Klatte TO et al. Bone mineralization defects and vitamin D deficiency: histomorphometric analysis of iliac crest bone biopsies and circulating 25-hydroxyvitamin D in 675 patients. J Bone Miner Res 2010; 25: 305–312.
CAS
Article
Google Scholar
Zhou Y, Zhao LJ, Xu X et al. DNA methylation levels of CYP2R1 and CYP24A1 predict vitamin D response variation. J Steroid Biochem Mol Biol 2014; 144: 207–214.
CAS
Article
Google Scholar
Gallagher JC . Vitamin D and aging. Endocrinol Metab Clin North Am 2013; 42: 319–332.
Article
Google Scholar
Tella SH, Gallagher JC . Prevention and treatment of postmenopausal osteoporosis. J Steroid Biochem Mol Biol 2014; 142: 155–170.
CAS
Article
Google Scholar
Ralston SH, Binkley N, Boonen S et al. Randomized trial of alendronate plus vitamin D3 versus standard care in osteoporotic postmenopausal women with vitamin D insufficiency. Calcif Tissue Int 2011; 88: 485–494.
CAS
Article
Google Scholar
Weber K, Kaschig C, Erben RG . 1 Alpha-hydroxyvitamin D2 and 1 alpha-hydroxyvitamin D3 have anabolic effects on cortical bone, but induce intracortical remodeling at toxic doses in ovariectomized rats. Bone 2004; 35: 704–710.
CAS
Article
Google Scholar
Li M, Healy DR, Simmons HA et al. Alfacalcidol restores cancellous bone in ovariectomized rats. J Musculoskelet Neuronal Interact 2003; 3: 39–46.
CAS
PubMed
Google Scholar
Orimo H, Shiraki M, Hayashi Y et al. Effects of 1 alpha-hydroxyvitamin D3 on lumbar bone mineral density and vertebral fractures in patients with postmenopausal osteoporosis. Calcif Tissue Int 1994; 54: 370–376.
CAS
Article
Google Scholar
Shikari Kushida M, Yamazaki K, Nagai K et al. H. Effects of 2 years’ treatment of osteoporosis with 1 alpha-hydroxy vitamin D3 on bone mineral density and incidence of fracture: a placebo-controlled, double-blind prospective study. Endocr J 1996; 43: 211–220.
Article
Google Scholar
Hayashi Y, Fujita T, Inoue T . Decrease of vertebral fracture in osteoporotics by administration of 1α-hydroxy-vitamin D3. J Bone Miner Metab 1992; 10: 50–54.
Article
Google Scholar
Nuti R, Bianchi G, Brandi ML et al. Superiority of alfacalcidol compared to vitamin D plus calcium in lumbar bone mineral density in postmenopausal osteoporosis. Rheumatol Int 2006; 26: 445–453.
CAS
Article
Google Scholar
Kubodera N, Tsuji N, Uchiyama Y et al. A new active vitamin D analog, ED-71, causes increase in bone mass with preferential effects on bone in osteoporotic patients. J Cell Biochem 2003; 88: 286–289.
CAS
Article
Google Scholar
Abe M, Tsuji N, Takahashi F et al. Overview of the clinical pharmacokinetics of eldecalcitol, a new active vitamin D3 derivative. Jpn Pharmacol Ther 2011; 39: 261–274.
CAS
Google Scholar
Ritter CS, Brown AJ . Suppression of PTH by the vitamin D analog eldecalcitol is modulated by its high affinity for the serum vitamin D-binding protein and resistance to metabolism. J Cell Biochem 2011; 112: 1348–1352.
CAS
Article
Google Scholar
Kondo S, Takano T, Ono Y et al. Eldecalcitol reduces osteoporotic fractures by unique mechanisms. J Steroid Biochem Mol Biol 2015; 148: 232–238.
CAS
Article
Google Scholar
Harada S, Mizoguchi T, Kobayashi Y et al. Daily administration of eldecalcitol (ED-71), an active vitamin D analog, increases bone mineral density by suppressing RANKL expression in mouse trabecular bone. J Bone Miner Res 2012; 27: 461–473.
CAS
Article
Google Scholar
Saito M, Grynpas MD, Burr DB et al. Treatment with eldecalcitol positively affects mineralization, microdamage, and collagen crosslinks in primate bone. Bone 2015; 73: 8–15.
CAS
Article
Google Scholar
Matsumoto T, Ito M, Hayashi Y et al. A new active vitamin D3 analog, eldecalcitol, prevents the risk of osteoporotic fractures–a randomized, active comparator, double-blind study. Bone 2011; 49: 605–612.
CAS
Article
Google Scholar
Matsumoto T, Takano T, Saito H et al. Vitamin D analogs and bone: preclinical and clinical studies with eldecalcitol. Bonekey Rep 2014; 3: 513.
Article
Google Scholar
Sakai A, Ito M, Tomomitsu T et al. Efficacy of combined treatment with alendronate (ALN) and eldecalcitol, a new active vitamin D analog, compared to that of concomitant ALN, vitamin D plus calcium treatment in Japanese patients with primary osteoporosis. Osteoporos Int 2015; 26: 1193–1202.
CAS
Article
Google Scholar
Plum LA, Fitzpatrick LA, Ma X et al. 2MD, a new anabolic agent for osteoporosis treatment. Osteoporos Int 2006; 17: 704–715.
CAS
Article
Google Scholar
Ke HZ, Qi H, Crawford DT et al. A new vitamin D analog, 2MD, restores trabecular and cortical bone mass and strength in ovariectomized rats with established osteopenia. J Bone Miner Res 2005; 20: 1742–1755.
CAS
Article
Google Scholar
DeLuca HF, Bedale W, Binkley N et al. The vitamin D analogue 2MD increases bone turnover but not BMD in postmenopausal women with osteopenia: results of a 1-year phase 2 double-blind, placebo-controlled, randomized clinical trial. J Bone Miner Res 2011; 26: 538–545.
CAS
Article
Google Scholar
Zella JB, Plum LA, Plowchalk DR et al. Novel, selective vitamin D analog suppresses parathyroid hormone in uremic animals and postmenopausal women. Am J Nephrol 2014; 39: 476–483.
CAS
Article
Google Scholar
Calcium Information | Mount Sinai
Aloia JF, Dhaliwal R, Shieh A, Mikhail M, Islam S, Yeh JK. Calcium and vitamin d supplementation in postmenopausal women. J Clin Endocrinol Metab. 2013;98(11):E1702-E1709.
Avgerinos DV, Leitman IM, Martinez RE, Liao EP. Evaluation of markers for calcium homeostasis in a population of obese adults undergoing gastric bypass operations. J Am Coll Surg. 2007;205(2):294-297.
Barrett-Connor E, Wade SW, Downss RW, et al. Self-reported calcium use in a cohort of postmenopausal women receiving osteoporosis therapy: results from POSSIBLE US. Osteoporosis Int. 2015;26(8):2175-2184.
Bauman WA, Shaw S, Jayatilleke E, Spungen AM, Herbert V. Increased intake of calcium reverses vitamin B12 malabsorption induced by metformin. Diabetes Care. 2000;23(9):1227-1231.
Bendich A. The potential for dietary supplements to reduce premenstrual syndrome (PMS) symptoms [review]. J Am Coll Nutr. 2000;19(1):3-12.
Bonithon-Kopp C, Kronborg O, Giacosa A, Rath U, Faivre J. Calcium and fibre supplementation in prevention of colorectal adenoma recurrence: a randomised intervention trial. European Cancer Prevention Organisation Study Group. Lancet. 2000;356(9238):1300-1306.
Boonen S, Lips P, Bouillon R, Bischoff-Ferrari HA, Vanderschueren D, Haentjens P. Need for additional calcium to reduce the risk of hip fracture with vitamin d supplementation: evidence from a comparative metaanalysis of randomized controlled trials. J Clin Endocrinol Metab. 2007;92(4):1415-1423.
Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002;346(2):77-84.
Bostick RM, Fosdick L, Grandits GA, Grambsch P, Gross M, Louis TA. Effect of calcium supplementation on serum cholesterol and blood pressure. Arch Fam Med. 2000;9(1):31-38.
Caan B, Neuhouser M, Aragaki A, Lewis CB, Jackson R, LeBoff MS, et al. Calcium plus vitamin D supplementation and the risk of postmenopausal weight gain. Arch Intern Med. 2007;167(9):893-902.
Chan JM, Stampfer MJ, Ma J, Gann PH, Gaziano JM, Giovannucci EL. Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study. Am J Clin Nutr. 2001;74(4):549-554.
Chen Y, Strasser S, Cao Y, Wang KS, Zheng S. Calcium intake and hypertension among obese adults in United States: associations and implications explored. J Hum Hypertens. 2015;29(9):541-547.
Consensus Opinion. The role of calcium in peri- and postmenopausal women: consensus opinion of the North American Menopause Society. Menopause. 2001;8(2):84-95.
Dagnelie PC, Schuurman AG, Goldbohm RA, Van den Brandt PA. Diet, anthropometric measures and prostate cancer risk: a review of prospective cohort and intervention studies. BJU Int. 2004;93(8):1139-1150.
Davies KM, Heaney RP, Recker RR, et al. Calcium intake and body weight. J Clin Endocrinol Metab. 2000;85(12):4635-4638.
Emkey R, Emkey G. Calcium metabolism and correcting calcium deficiencies. Endocrinology and Metabolism Clinics. 2012;41(3):527-556.
Giovannucci E, Liu Y, Stampfer MJ, Willett WC. A prospective study of calcium intake and incident and fatal prostate cancer. Cancer Epidemiol Biomarkers Prev. 2006;15(2):203-210.
Gonnelli S, Campagna MS, Montagnani A, et al. Calcium bioavailability from a new calcium-fortified orange beverage, compared with milk in healthy volunteers. Int J Vitam Nutr Res. 2007;77(4):249-254.
Grau MV, Baron JA, Sandler RS, et al. Prolonged effect of calcium supplementation on risk of colorectal adenomas in a randomized trial. J Natl Cancer Inst. 2007;99(2):129-136.
Gulson BL, Mizon KJ, Palmer Jm, Korsch MJ, Taylor AJ. Contribution of lead from calcium supplements to blood lead. Environ Health Perspect. 2001;109(3):283-288.
Heaney RP, Dowell SD, Bierman J, Hale CA, Bendich A. Absorbability and cost effectiveness in calcium supplementation. J Am Coll Nutr. 2001;20(3):239-246.
Hermensen K. Diet, blood pressure and hypertension. Br J Nutr. 2000;83(Suppl 1):S113-S119.
Hiller JE, Crowther CA, Moore VA, Willson K, Robinson JS. Calcium supplementation in pregnancy and its impact on blood pressure in children and women: follow up of a randomised controlled trial. Aust N Z J Obstet Gynaecol. 2007;47(2):115-121.
Hofmeyr G, Duley L, Atallah A. Dietary calcium supplementation for prevention of pre-eclampsia and related problems: a systematic review and commentary. BJOG. 2007;114(8):933-943.
Jänne PA, Mayer RJ. Chemoprevention of colorectal cancer. N Engl J Med. 2000;342(26):1960-1968.
Kampman E, Slattery ML, Caan B, Potter JD. Calcium, vitamin D, sunshine exposure, dairy products and colon cancer risk (United States). Cancer Causes Control. 2000:11(5):459-466.
Krall EA, Wehler C, Garcia RI, et al. Calcium and vitamin D supplements reduce tooth loss in the elderly. Am J Med. 2001;111(6):452-456.
Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines. Revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation. 2000;102(18):2284-2299.
Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007;85(6):1586-1591.
Larsson SC, Orsini N, Wolk A. Dietary calcium intake and risk of stroke: a dose-response meta-analysis. Am J Clin Nutr. 2013;97(5):951-957.
Lin Y-C, Lyle RM, McCabe LD, et al. Dairy calcium is related to changes in body composition during a two-year exercise intervention in young women. J Am Coll Nutr. 2000;19(6):754-760.
Martin BR, Davis S, Campbell WW, Weaver CM. Exercise and calcium supplementation: effects on calcium homeostasis in sportswomen. Med Sci Sports Exerc. 2007;39(9):1481-1486.
Myers VH, Champagne CM. Nutritional effects on blood pressure. Curr Opin Lipidol. 2007;18(1):20-24.
Nakamura K, Saito T, Kobayashi R, et al. Effect of low-dose calcium supplements on bone loss in perimenopausal and postmenopausal Asian women: a reandomized controlled trial. J Bone Miner Res. 2012;27(11):2264-2270.
NAMS Consensus. Consensus Opinion: the role of calcium in peri-and postmenopausal women: consensus opinion of The North American Menopause Society. Menopause. 2001;8(20):84-95.
Napoli N, Thompson J, Civitelli R, Armamento-Villareal RC. Effects of dietary calcium compared with calcium supplements on estrogen metabolism and bone mineral density. Am J Clin Nutr. 2007;85(5):1428-1433.
NIH Consensus Development Panel. Osteoporosis prevention, diagnosis, and therapy. JAMA. 2001;285(6):785-795.
Ochner CN, Lowe MR. Self-reported changes in dietary calcium and energy intake predict weight regain following a weight loss diet in obese women. J Nutr. 2007;137(10):2324-2328.
Palacios C, Benedetti P, Fonseca S. Impact of calcium intake on body mass index in Venezuelan adolescents. P R Health Sci J. 2007;26(3):199-204.
Park SY, Murphy SP, Wilkens LR, Stram DO, Henderson BE, Kolonel LN. Calcium,vitamin D, and dairy product intake and prostate cancer risk: the Multiethnic Cohort Study. Am J Epidemiol. 2007;166(11):1259-1269.
Park Y, Leitzmann MF, Subar AF, Hollenbeck A, Schatzkin A. Dairy food, calcium, and risk of cancer in the NIH-AARP Diet and Health Study. Arch Intern Med. 2009;169(4):391-401.
Park Y, Mitrou PN, Kipnis V, Hollenbeck A, Schatzkin A, Leitzmann MF. Calcium, dairy foods, and risk of incident and fatal prostate cancer: the NIH-AARP Diet and Health Study. Am J Epidemiol. 2007;166(11):1270-1279.
Peacock M, Liu G, Carey M, et al. Effect of calcium or 25OH vitamin D3 supplementation on bone loss at the hip in men and women over the age of 60. J Clin Endocrinol Metabol. 2000;85(9):3011-3019.
Petti S, Cairella G, Tarsitani G. Nutritional variables related to gingival health in adolescent girls. Community Dent Oral Epidemiol. 2000;28(6):407-413.
Ross EA, Szabo NJ, Tebbett IR. Lead content of calcium supplements. JAMA. 2000;284(11):1425-1429.
Sacks FM, Svetkey LP, Volmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet. N Engl J Med. 2001;344(1):3-10.
Shahar DR, Schwarzfuchs D, Fraser D, et al. Dairy calcium intake, serum vitamin D, and successful weight loss. Am J Clin Nutr. 2010;92(5):1017-1022.
Shin CS, Kim KM. Calcium, Is It Better to Have Less? J Cell Biochem. 2015;116(8):1513-1521.
Straub DA. Calcium supplementation in clinical practice: a review of forms, doses, and indications. Nutr Clin Pract. 2007;22(3):286-296.
Tang BM, Eslick GD, Nowson C, Smith C, Bensoussan A. Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet. 2007;370(9588):657-666.
Tavani A, Bertuccio P, Bosetti C, et al. Dietary intake of calcium, vitamin D, phosphorus and the risk of prostate cancer. Eur Urol. 2005;48(1):27-33.
Thys-Jacobs S. Micronutrients and the premenstrual syndrome: the case for calcium. J Am Coll Nutr. 2000;19(2):220-227.
Torkos S. Drug-nutrient interactions: a focus on cholesterol-lowering agents. Int J Integrative Med. 2000;2(3):9-13.
Varenna M, Binelli L, Casari S, Zucchi F, Sinigaglia L. Effects of dietary calcium intake on body weight and prevalence of osteoporosis in early postmenopausal women. Am J Clin Nutr. 2007;86(3):639-644.
Wagner G, Kindrick S, Hertzler S, DiSilvestro RA. Effects of various forms of calcium on body weight and bone turnover markers in women participating in a weight loss program. J Am Coll Nutr. 2007;26(5):456-461.
Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC. Regulation of adiposity by dietary calcium. FASEB. 2000;14(9):1132-1138.
%PDF-1.4
%
840 0 obj
>
endobj
xref
840 82
0000000016 00000 n
0000002638 00000 n
0000002785 00000 n
0000003417 00000 n
0000003563 00000 n
0000003709 00000 n
0000003738 00000 n
0000004044 00000 n
0000004356 00000 n
0000004901 00000 n
0000005177 00000 n
0000005668 00000 n
0000005948 00000 n
0000006547 00000 n
0000006574 00000 n
0000006686 00000 n
0000006833 00000 n
0000007137 00000 n
0000007424 00000 n
0000008007 00000 n
0000008525 00000 n
0000008639 00000 n
0000011802 00000 n
0000011948 00000 n
0000012334 00000 n
0000015597 00000 n
0000018656 00000 n
0000021801 00000 n
0000024966 00000 n
0000028065 00000 n
0000028448 00000 n
0000028889 00000 n
0000029150 00000 n
0000029263 00000 n
0000029660 00000 n
0000029933 00000 n
0000030515 00000 n
0000030782 00000 n
0000031143 00000 n
0000031546 00000 n
0000032033 00000 n
0000032427 00000 n
0000035043 00000 n
0000036546 00000 n
0000079497 00000 n
0000079787 00000 n
0000080034 00000 n
0000080440 00000 n
0000080683 00000 n
0000081179 00000 n
0000102974 00000 n
0000113481 00000 n
0000115019 00000 n
0000115089 00000 n
0000116737 00000 n
0000127704 00000 n
0000167269 00000 n
0000167372 00000 n
0000186552 00000 n
0000186622 00000 n
0000186713 00000 n
0000200317 00000 n
0000200607 00000 n
0000200881 00000 n
0000200908 00000 n
0000201283 00000 n
0000208681 00000 n
0000208953 00000 n
0000209316 00000 n
0000228132 00000 n
0000228411 00000 n
0000228806 00000 n
0000249703 00000 n
0000249952 00000 n
0000250320 00000 n
0000255519 00000 n
0000271956 00000 n
0000272408 00000 n
0000272655 00000 n
0000272801 00000 n
0000002439 00000 n
0000001936 00000 n
trailer
]/Prev 479596/XRefStm 2439>>
startxref
0
%%EOF
921 0 obj
>stream
hb“d`x Ā
90,000 How do you get your calcium intake and help your body absorb it properly?
Calcium is found in many foods. But simply eating them to provide calcium is not enough. This macronutrient is pretty moody. It is difficult to digest, requiring special conditions for this. If we do them, we will get strong bones and healthy teeth and beautiful hair.
Calcium is not at all alone. In order for it to be assimilated in the body, it needs companions.Magnesium and phosphorus are best suited. If these substances are enough (which by the way is rare), then calcium will be assimilated. But if magnesium, for example, is in short supply, then calcium, on the contrary, will be intensively excreted from the body. In order to prevent such a development of the plot, it is worth eating cottage cheese more often. It contains all the participants in this game: calcium, phosphorus, and magnesium. Alternatively, eggs, fresh herbs, and certain types of fish are good options.
Legumes are also a good option for getting your calcium requirement.Soups made from peas or chickpeas, beans and tofu contain calcium, magnesium and phosphorus in the required proportions. You can also get additional magnesium from whole grain bread or cocoa.
Product selection
Milk and dairy products contain calcium in the form of lactate. It is easy to digest and almost completely fulfills its purpose. Slightly worse, by 80 percent, citrate and similar calcium compounds from broccoli, collard greens (except spinach), almonds, turnips and fish are absorbed.But sesame is full of easily digestible calcium. Having eaten 100 g, you can supply your body with a daily norm.
But this does not mean that from now on sesame must be eaten with spoons. You can add it to leafy greens and broccoli salads with cottage cheese, or drink a tablespoon of sesame oil in the morning on an empty stomach. And as a dessert, eat figs and almonds.
Chia seeds are also rich in calcium. 100 grams contains about 600 mg of an important macronutrient. Chia seeds can be conveniently added to smoothies, desserts, or yogurt.
By the way, calcium is also found in large quantities in plant milk, especially oat milk. There is 120 mg of calcium per 100 ml. It can be added to hot and cold drinks, used as a smoothie base, or cooked into porridge.
Avoid Waste
Choosing the right calcium-rich foods is only half the battle. At the same time, it is better to exclude foods that contribute to its loss from the diet. The macronutrient is washed out under the influence of caffeine, salt and hydrogenated fats.In this regard, it is better to avoid eating margarine, creamy spreads and canned sauces. As for coffee, you can, of course, drink it, but no more than 3 cups a day. If you can’t meet this amount, then at least compensate for the losses with additional milk.
Beets, spinach, sorrel and rhubarb, or rather the acids they contain, will interfere with the absorption of calcium. They should be consumed in moderation. But dried apricots, on the contrary, should be added to the diet.It contains potassium, which will prevent the loss of an important macronutrient.
Conductors for calcium
It is possible to increase the absorption of calcium. For example, if you use it together with vitamin D. It not only increases the absorption of the microelement by 30-40%, but also normalizes its balance with phosphorus. In addition, vitamin D is actively involved in calcium metabolism.
Highest vitamin D content in liver, eggs and seafood. Such as shrimp, lobster, crabs, herring, salmon, sardines and mackerel.But we get all such main amount thanks to ultraviolet rays. Therefore, on a sunny day, be sure to walk in the fresh air for at least a quarter of an hour.
Physical activity
Calcium will be absorbed much better if we have enough physical activity in our lives. If you run or walk, do exercises with a barbell or dumbbells, then the bone tissue will grow.
And you shouldn’t even sweat to a sweat. Because with sweat, the loss of calcium only increases.It is enough to lose 400-450 kcal during the lesson. Typically, a standard power set and thirty minutes of cardio will suffice for this. The sauna should not be overused. And if you still sweat, then make up for the loss with a glass of kefir or oat milk with the addition of chia seeds.
Supplements for sports and beyond
Even if you do not exercise professionally, pay attention to whey protein isolate. It contains not only essential amino acids, but also bioavailable calcium.
It is believed that after 25 years, 800 mg of calcium should be consumed per day. And after 50 and even more – 1200-1500 mg, as well as for pregnant and lactating women. In addition, American scientists also advise adding 100 mg of vitamin B6 and 400 mg of magnesium oxide to your daily diet. It improves mood and helps to flush excess water from the body.
Minimum stress
When we are nervous, our body produces the stress hormone cortisol. It negatively affects the absorption of calcium in the intestine and promotes its excretion in the urine.Therefore, the more stress we experience, the more calcium we lose.
Remember this and try to avoid unnecessary worries. Allow yourself to rest and eat well. And do not deprive yourself of the joys in the form of a piece of dark chocolate. It contains antioxidants, vitamins A, C, E, as well as selenium, magnesium, iron, potassium and calcium, of course.
Useful calcium
We tend to think about a lack of calcium when external reasons for concern appear: dental problems, hair loss, peeling and brittle nails.But do we know everything about him?
Calcium is necessary not only for the tissues of teeth and bones, it also affects many metabolic processes in the body. Therefore, signs of calcium deficiency are not only brittle nails, problems with tooth enamel, hair, but also tingling in the fingers, numbness of the limbs and cramps.
The problem with calcium is that it is difficult to assimilate. Even with the use of milk, fish and vegetables, only 25-30% will be assimilated. It is extremely difficult to replenish the daily supply of calcium through food alone.Biologically active additives are an additional source of calcium.
1
The highest concentration of the basic substance is found in supplements containing calcium carbonate. It is also necessary to look for it in the composition of the drug.
2
The best “allies” of calcium are vitamin D3 (cholecalciferol) and vitamin C. The first will help calcium to be absorbed in the body, the second for additional strengthening of the walls of blood vessels.
3
In order for calcium to have a beneficial effect on the body, vitamin K is added to the vitamin complexes.It helps direct calcium to its destination, namely bones, hair, nails and tooth enamel. And vitamin B6 reduces the excretion of calcium from the body.
There are innumerable amounts of vitamin complexes with calcium on the market today. You can choose for every taste: for children and for pregnant women, for the elderly and for general use, foreign and Russian. How to choose a really good product in such a variety? You need to pay attention to the composition. It is important that for better absorption of the vitamin complex with calcium there are all the trace elements mentioned above, namely vitamins C, B6, D and K.
These parameters correspond to the Multivita Calcium plus complex in the form of effervescent tablets. A significant advantage of this product is the absence of sugar in the composition, therefore, it is included by the Russian Diabetes Association in an expanded assortment list of goods for a healthy lifestyle and for the nutrition of consumers with diabetes mellitus. And due to the release form, it is convenient for taking, especially by elderly people: 1 tablet must be dissolved in a glass of water at room temperature.
Dietary supplement Vitamir Calcium D3 chewing with orange flavor 100 tablets
In the dietary supplement “VITAMIR D3 Calcium with orange / lemon / mint flavor” calcium is present in the form of carbonate, it contains 40% elemental calcium.In addition, the dietary supplement contains vitamin D3 (cholecalciferol), which significantly increases the absorption of calcium, normalizes the formation of the bone skeleton and teeth in children, and helps to preserve the structure of bones.
Ingredients: active ingredients: calcium carbonate – 1250 mg (equivalent to elemental calcium – 500 mg), vitamin D3 (cholecalciferol equivalent to -2.5 μg (100 IU)), auxiliary components: sucrose, talc (anti-caking agent), calcium stearate (anti-caking agent), potato starch, natural orange / lemon / mint flavor.
Information on biologically active substances and their properties:
- Calcium (Ca) is a common macronutrient in the human body, which is the main building material of bones (99% of calcium is contained in bones), teeth, an important component of hair and nails. Also, calcium ensures the normal functioning of the body as a whole.
- Calcium requirements may vary at different times in life. For example, in adolescence, the consumption of a sufficient amount of this element is very important due to the intensive growth of the skeleton, for example, with a lack of calcium, children begin to lag behind in growth.
- During menopause and postmenopause, calcium helps prevent fractures, this is especially important for those who are not receiving hormone replacement therapy.
- Reduced bone density can result in joint pain, and in older people, increased bone fragility increases the risk of fractures. With an increase in calcium deficiency, the mineralization of bone mass decreases, which can lead to a pathological decrease in bone density, its rarefaction with a loss of natural strength.
- In the human body, calcium deficiency can manifest itself in the form of deterioration of the condition of teeth, hair and nails, as well as increased fatigue, general weakness and a decrease in the usual ability to work. At the same time, muscle spasms, nervousness, irritability can be observed.
- The key role of vitamin D3 , included in “ VITAMIR calcium D3″ is to maintain calcium-phosphorus balance in the blood. Vitamin D3 is important for the normal absorption of calcium in the intestines, as well as for maintaining the strength of teeth and bones.
Scope: as a biologically active food supplement – an additional source of calcium, vitamin D3.
BAA, is not a drug.
Contraindications: individual intolerance to the components.
Before use, it is recommended to consult a doctor, before using dietary supplements for children, it is recommended to consult a pediatrician.
With caution: persons with dental inserts in the oral cavity (braces, dentures) – due to their possible damage.
Method of administration and dosage: children 3 – 7 years old, 1 tablet a day with meals; children over 7 years old – 1 tablet 2 times a day with meals; adults 1-2 tablets 2 times a day with meals. Duration of admission is 1-2 months. If necessary, the reception can be repeated.
Storage conditions: in a dry, dark place, out of reach of children, at a temperature not exceeding 25 ° C.
Expiration date: 3 years.
CALCIUM D3 VITAMIR N30 JEW TAB WITH ORANGE TASTE
Calcium – Impact of Protein Intake and Vegan Research
I am posting the penultimate part of the article about vitamin D and calcium.This section discusses how protein intake affects calcium absorption and how much protein is involved in leaching calcium out of bones. Also discussed is a study conducted by the University of Oxford, which showed that the incidence of bone fractures in vegans was 30% higher than in groups of people who eat other types of food. To find out why they had more fractures, see cat.
This google dox document can be found here. Tomorrow, I will be exhibiting the last part of this article, which will show a chart of plant foods for the richest in calcium and give tips on how to meet your calcium needs in a vegan diet.So don’t miss the next and final episode! 🙂
Proteins
As mentioned above, there is a theory according to which proteins, especially sulfur-containing amino acids, increase the acid load in the body, thereby provoking the excretion of calcium in the urine. Sulfur-containing amino acids predominate in animal products, although they are also found in high amounts in many cereals. Another theory, in contrast, claims that proteins increase the absorption of calcium in the intestinal system, which in turn neutralizes the loss of calcium in the urine (29).
In the 2004 summer issue of Soy Connection magazine, an article was published on this topic, titled “Are Protein and Calcium Friends or Foes?” It concluded:
Recent evidence suggests that high protein intake does not necessarily have a negative effect on bone health. Protein source composition and other dietary factors determine acid load. It appears that healthy people who eat high-protein foods in the context of a typical diet do not reach the point where calcium homeostasis (balance) is disturbed.
In December 2009, a meta-analysis of studies examining bone health and protein intake was published in the American Journal of Clinical Nutrition (33). It included seven cohort studies analyzing protein intake and fracture risk. The meta-analysis concluded:
The bulk of the evidence suggests that protein intake has little or no positive effect on the skeleton.However, the long-term clinical effect is not yet fully clear. There was also no reduction in fracture risk. More research is needed to resolve the controversy over the effects of protein intake on bone health. In the meantime, when planning a healthy diet, you can rely on the quantitative recommendations for protein intake and balancing different protein sources provided in the government’s healthy eating guidelines.
It is possible that a protein intake of two to three times the daily intake may increase the risk of osteoporosis.However, research shows that for ovo-lactic vegetarians and non-vegetarians, animal protein does not pose a significant threat to bone health.
Vegan Studies
Very little data exists to date on the health of vegans. Several small cross-sectional studies have shown that vegans have the same or slightly lower bone density than non-vegans (9-12, 13, 30). These studies were conducted with vegans who may not have been getting enough vitamin D or trying to meet the recommended calcium intake.
In 2009, researchers from Vietnam and Australia conducted a meta-analysis of studies examining bone density among vegetarians (23). They concluded: “Vegetarian and especially vegan diets have little effect on bone density. In addition, it is unlikely that this impact will lead to clinically important changes in the risk of bone fractures. ”
In 2007, published the first study discussing fracture risk among vegans (14).For EPIC-Oxford, the study recruited 57,000 participants, of whom over 1,000 were vegans and nearly 10,000 ovo-lactic vegetarians. The study was conducted from 1993 to 2000. At the beginning, participants were asked to fill out questionnaires to find out what they eat. Five years after the start of the study, participants were sent out new questionnaires asking about any fractures that have occurred in the past five years (to be paraphrased).
After scientists adjusted the study for age, the incidence of fractures in vegans was 37% higher than in non-vegetarians.After adjusting for age, smoking, alcohol consumption, body weight, physical activity, marital status, number of births, and hormone replacement therapy, vegan fracture rates were still 30% higher than meat eaters. The incidence of fractures in non-vegetarians, sand vegetarians, and ovo-lacto vegetarians did not differ in all analyzes.
However, there was some good news in this study. After adjusting the study results for calcium intake, vegans lost the lead in fracture rates (paraphrase?).Among participants who consumed at least 525 mg of calcium per day (only 55% of vegans and 95% of those on other diets), the incidence of fractures in vegans was the same as in non-vegans.
Does this mean that insufficient calcium intake is the cause of fractures? It is possible that participants who consumed more calcium also consumed more or less vitamin D or protein. However, the authors noted that the incidence of fractures was not associated with protein or vitamin D intake.A separate analysis of the EPIC-Oxford (20) study found that calcium intake was associated with an increased risk of fractures for women but not for men. The relative risk averaged 1.75 (1.33-2.29) for women who consumed less than 525 mg per day compared to women who consumed more than 1200 mg per day.
Today, we have to assume that vegans with a lot of fractures were lacking calcium.
Tags: veganhealth
90,000 TOP-11 calcium preparations – rating of good products 2021
Calcium is one of the electrolytes in the body.It is a mineral that carries an electrical charge when dissolved in blood. The role of calcium in the body can hardly be overestimated, since it is a building material for bone structures, maintains the health of cell membranes and takes part in the transmission of nerve impulses. Also, calcium has a detoxifying, anti-inflammatory and anti-allergenic effect.
About 99% of the calcium in the body is stored in the bones. However, cells (especially muscle cells) and blood also contain calcium.Calcium is needed for:
- the formation of bones and teeth;
- muscle contractions;
- blood clotting;
- maintaining the functions of enzymes and hormones;
- ensuring a normal heart rate.
The body precisely controls the amount of calcium in cells and blood. As needed, the mineral is transferred from the bones to the blood to maintain a constant balance.When people don’t get enough calcium, calcium is taken from the bones, which weakens them. Osteoporosis can be the result. To maintain normal blood calcium levels without weakening bones, you need to consume at least 1000-1500 mg of calcium per day. This requires a balanced diet or medication.
The best calcium supplements are presented in the ranking below. The TOP is compiled depending on the effectiveness and safety of medicines, as well as on the basis of reviews.An equally important criterion is the price-quality ratio. Finding a medicine on your own is not easy. To begin with, you should consult a doctor and, if necessary, undergo an examination to clarify the diagnosis.
Classification of calcium preparations
Calcium deficiency often creeps up and then goes unnoticed for a long time. This condition can have a negative impact on bone health. Thus, the risk of developing osteoporosis and bone fractures increases.
In the presence of a significant deficiency, the following symptoms are possible:
- tingling in the limbs;
- muscle twitching;
- cramps and numbness;
- excessive anxiety;
- deterioration of the condition of the skin and hair;
- excessive brittleness of the nails;
- periodontal disease and caries;
- increased heart rate;
- disorders of digestive functions.
Experts recommend that calcium supplements only be taken if there is a proven deficiency of this mineral and vitamin D, or if there is existing osteoporosis. The main thing is to choose the right drug and dosage.
Calcium preparations are classified as follows:
- Lactate. Absorbed by the body at any pH value. Can be taken regardless of food intake. This pharmacological group successfully neutralizes the insufficient effect of estrogen-containing drugs.As monotherapy, it does not allow to replenish the calcium requirement.
- Gluconate. It is used as a topical agent or as a solution for injection. The drugs included in this group physiologically stimulate the release of the active form of the calcitonin molecule. It has a positive effect on kidney function, providing a natriuretic and vasodilating effect. Calcium gluconate is a safe and effective form of calcium that can be used to increase bone density in premature babies.
- Citrate. An exceptional form of calcium that is the most effective and safest. The advantage is complete dissolution in water and assimilation, regardless of the acidity of the gastric juice and food intake. Calcium citrate is the drug of choice for people with low gastric acidity and elderly patients who are taking proton pump inhibitors and antacids. Also, this group of calcium preparations helps dissolve kidney stones.
Less safe are inorganic calcium salts: phosphate and carbonate.Calcium carbonate antacid may not be completely absorbed by the body, which depends on the acidity of the gastric juice and the general condition of the gastrointestinal tract. Phosphates are also practices that completely neutralize acid, therefore, they have a number of contraindications for use.
Causes of calcium deficiency in the body
To properly perform its various tasks, calcium must be present in the body in sufficient quantities. But what is enough? Daily requirements vary according to age group.Unlike many other nutrients, your need for calcium is not sex-specific. Men and women need the mineral equally.
Table – Daily calcium requirement depending on age
Age group | Calcium amount, mg / day |
1 to 4 years old | 600 |
4-7 years old | 750 |
7 to 10 years old | 900 |
10 to 15 years old | 1100 |
15 to 19 years old | 1200 |
19 years and older | 1000 |
Pregnant and lactating women | +100 |
It is not only amazing that men and women need the same amount of calcium.In addition, the fact that the need of pregnant and lactating women is practically not increased, distinguishes calcium from other nutrients. However, women should individually coordinate their nutritional needs with an obstetrician to rule out deficiencies.
Given the basic functions that calcium takes on in the body, it is clear that a deficiency in minerals can seriously affect health.
Among the main causes of deficiency states are:
- Monotonous food.Calcium is present in sufficient quantities, primarily in dairy products of animal origin. Mineral deficiency is diagnosed primarily in vegans and people with lactose intolerance.
- Disorders of the gastrointestinal tract. For digestive disorders associated with problems such as vomiting, nausea, bloating, and diarrhea, absorption of nutrients may be difficult or prevented.
- Kidney disease (kidney failure).Reduces the excretion of the mineral phosphate. Although phosphate is not actually harmful to the body, an increased concentration can alter calcium levels in the body. As a result, a deficiency state develops.
- Thyroid dysfunction (hypothyroidism). The thyroid gland produces a hormone that regulates calcium balance. With inflammation of the pancreas, the function of assimilating nutrients from food is disrupted. Therefore, as a consequence of this disease, the absorption of calcium is also impaired.
Diuretics can cause calcium deficiency. Medicines of this group are used for renal failure, as well as for liver diseases, edema, hypertension and heart failure.
With age, the performance of our digestive system decreases. As a result, it becomes more difficult for the body to release and absorb nutrients from food. However, older adults are at a particularly high risk of developing calcium deficiency. Bone substance also weakens with age.
Vitamin D deficiency is one of the most common causes of calcium deficiency. As we already know, it is absorbed mainly in the intestines. Vitamin D (cholecalciferol) promotes absorption from the small intestine and the incorporation of calcium into bones. Thus, vitamin D plays a crucial role in calcium absorption.
Vitamin D is, in fact, not a vitamin at all, but a precursor to a hormone that the body can produce itself. The main requirement for this is sunlight, because exposure to ultraviolet rays on the skin leads to the formation of vitamin D, and then further processes in the kidneys and liver to produce an effective substance called calcitriol.
It is already reliably known that 91% of women and 82% of men are insufficiently provided with vitamin D. Therefore, regular consumption of foods rich in vitamin D is strongly recommended. But, as practice shows, in most cases this is not enough to fill deficiency states. In this case, good calcium tablets are needed.
Rating of calcium preparations
First, it is recommended to normalize the power supply. The most famous calcium-rich foods are milk and dairy products.Already 200 ml of cow’s milk provides about 240 mg of calcium and thus covers almost of the daily calcium requirement. By the way, the fat content of milk does not matter, it does not affect the mineral content.
Cheeses, especially hard varieties such as Parmesan or Tilsit, are especially rich in calcium. For example, 30 g of Tilsit provides about 250 mg of calcium.
But even through herbal products, we can meet our calcium needs. Recommended especially:
- green leafy vegetables such as cabbage, arugula or fennel;
- herbs such as parsley or dill;
- nuts and seeds also contribute to the targeted supply of calcium.
Many people are unaware that mineral water can also be a good source of calcium. Mineral waters can contain more than 500 mg / l of this mineral. From 150 mg calcium / liter, mineral water can be said to be rich in calcium.
Medicines and dietary supplements are rich sources of calcium. To achieve the result declared by the manufacturer, you must strictly follow the instructions for use.
TOP-11 calcium preparations
From this list you can choose the most suitable one:
No. 1 – “Calcium-D3 Nycomed” (Takeda, Russia)
Combined preparation based on calcium carbonate.The clinical and pharmacological group is aimed at regulating the exchange of phosphorus and calcium in the body. Chewable tablets improve the condition of nails, hair, teeth and muscle structures. Available with lemon, orange, mint and strawberry-watermelon flavors 60 and 120 pcs.
“Calcium-D3 Nycomed” is included in the list of the best calcium preparations, since it increases bone density and replenishes the lack of vitamin D3 in the body. As a result, nerve conduction improves, muscle contractions are normalized and blood clotting indicators are normalized.The drug is widely used during growth, pregnancy and lactation, excluding deficiency conditions.
No. 2 – “Calcium Magnesium plus zinc” (Solgar, USA)
Biologically active food supplement, which is an additional source of minerals:
- calcium – maintains the strength of bone structures;
- magnesium – ensures an even distribution of calcium throughout the body and promotes its absorption;
- zinc – takes part in the production of its own collagen in bone structures.
The tablets are in second place in the ranking of calcium preparations due to the fact that the combination of minerals is presented in a special chelated form. The active substances are absorbed by the body as much as possible.
No. 3 – Calcemin Advance (Bayer, USA)
The drug belongs to such a pharmacotherapeutic group as a calcium-phosphorus metabolism regulator. The composition includes micro and macro elements, as well as vitamins. The action of the tablets is due to the properties of the active ingredients:
- forms bone tissue, increasing its density and reducing resorption;
- prevents the development of diseases of the musculoskeletal system;
- strengthens the skeletal system and articular structures.
Calcium citrate is absorbed regardless of the secretory functions of the gastrointestinal tract. Thanks to vitamin D3, mineral metabolism in the body is regulated.
It is prescribed for the prevention and complex treatment of osteoporosis in women in menopause, with the use of immunosuppressants and glucocorticosteroids, as well as in the treatment of various diseases of the musculoskeletal system. Also, the drug “Calcemin Advance” is indicated for adolescents to replenish the deficiency of trace elements in the body.
No. 4 – Calcemin (Bayer, USA)
The regulator of calcium-phosphorus metabolism. The drug “Kalcemin” is developed on the basis of calcium, vitamin D3 and osteotropic minerals that regulate metabolic processes.
The action of film-coated tablets is due to the active ingredients:
- calcium – forms bone tissue, increasing and preventing disorders of the musculoskeletal system;
- colecalciferol – preserves the structure of bones, improves the absorption of minerals in the intestinal area;
- zinc – synthesizes sex hormones, preventing the destruction of bone structures;
- copper – synthesizes elastin and collagen, normalizing the formation of bone mass;
- manganese – forms proteoglycans that form a protein matrix.
Not recommended for hypercalcinuria and hypercalcemia, in case of vitamin D3 hypervitaminosis, nephrolithiasis, severe renal failure. Among the absolute contraindications, one should highlight the active form of tuberculosis, children under 5 years of age and decalcifying neoplasms.
If you do not know which calcium tablets to choose for pregnant women, then “Calcemin” is the most suitable option. A preliminary consultation with an obstetrician-gynecologist leading a pregnancy is mandatory.
No. 5 – “Calcium Citrate + Vitamin D / Calcium Citrate + D” (Alpha Vitamins Laboratories, USA)
The drug is developed on the basis of minerals and is intended for the prevention and complex treatment of idiopathic, steroid or postmenopausal osteoporosis. It is used for complications such as bone fractures, and is also prescribed for the elimination of deficiency conditions.
Recommended to be taken when the body’s need for vitamin D3 and calcium is increased, for example during pregnancy and lactation, as well as in childhood and adolescence during periods of intensive development.
No. 6 – Complivit Calcium D3 (Pharmstandard-Leksredstva, Russia)
Orange flavored chewable tablets regulate the mineral and vitamin balance, improving the condition of muscle and bone structures. The drug effectively copes with osteomalacia associated with impaired mineral metabolism in people aged 45 and older.
Recommended to be taken from the age of 12, swallowed or chewed whole. Adverse reactions include hypercalciuria and hypercalcemia, diarrhea, pain in the abdomen or stomach, and allergic reactions.
No. 7 – “Calcium gluconate” (Renewal, Russia)
The tablets are designed to replenish the mineral deficiency in the body. Formulated on the basis of calcium gluconate monohydrate. The active substance is involved in the formation of bone tissue and in the process of blood coagulation. It is used to support cardiac activity and improve the transmission of nerve impulses.
The drug “Calcium gluconate” improves the contractile activity of muscle structures, helping to cope with myasthenia gravis, muscular dystrophy and increased vascular permeability.The effect is achieved by stimulating the sympathetic nervous system and enhancing adrenaline secretion by the adrenal glands. The tablets have a moderate diuretic effect.
No. 8 – “Vitamins” Calcium + Vitamin D “(PharmaMed, USA)
Chewable lozenges contain natural vegetable and fruit extracts. Designed to enrich the child’s body with minerals and vitamins. The action is aimed at:
- reducing the risk of caries development;
- strengthening teeth and bones.
It is prescribed for children aged 3 years and older, 1 lozenge 2 times a day. Children from 7 years of age and older – 2 lozenges 2 times a day. Recommended to be taken with meals.
No. 9 – “Calcium 600 from oyster shells with D3” (Solgar, USA)
It helps prevent calcium deficiency in children and adults, eliminating the development of rickets, osteolysis (destruction of bone structures), seizures and muscle spasms. It also eliminates the likelihood of diseases such as bowel cancer and high blood pressure, which are associated with a lack of calcium in the body.
The course of treatment contributes to an increase in bone density and growth, the development and normal functioning of muscle structures. Calcium carbonate, obtained from oyster shells, protects bones and teeth from lead, a harmful metal that accumulates in the body during deficiency conditions.
No. 10 – “Calcium D3” (Renewal, Russia)
Chewable tablets are a biologically active food supplement, providing an additional source of minerals and vitamins.It is not recommended to take in the presence of individual intolerance, with renal failure and with an increased concentration of calcium and vitamin D in the blood or urine.
No. 11 – “Doppelherz Active Magnesium + Calcium” (Queisser Pharma, Germany)
Tablets are prescribed for increased physical and mental stress, as well as to reduce the risk of developing atherosclerosis and diseases of the cardiovascular system. Doctors recommend taking an additional source of minerals if you have an unbalanced diet and an unhealthy lifestyle.Among the absolute indications, one should highlight living in regions with a deteriorated environmental situation and frequent stressful situations.
The effectiveness of the drug is due to its composition:
- magnesium – improves the function of the heart muscle, restoring contractility;
- calcium – normalizes blood clotting processes, takes part in the contraction of smooth and skeletal muscles, and also removes salts of radionuclides and heavy metals.
The drug is intended for adults.It is recommended to take 1 tablet a day, unless otherwise prescribed by your doctor.
Which drugs are absorbed better
Calcium preparations are better absorbed if they are formulated on the basis of citrate. This compound is biologically very valuable and is a tool for delivering building material to bone structures. Calcium citrate is beneficial because it alkalizes urine, preventing the development of kidney stones and urinary tract infections.It also regulates energy metabolism and slows down the synthesis of parathyroid hormone, preventing the leaching of minerals from the body.
But about 85% of the drugs on the pharmaceutical market are based on carbonate, which is less effective. But carbonic acid has its advantage, which lies in the high content of elemental calcium – more than 50%. But the carbonate, unfortunately, is absorbed only by 15-20%. And such drugs cause disorders of the gastrointestinal tract, which should be considered before use.This is due to the fact that when carbonic acid breaks down, carbon dioxide is formed, which is the cause of bloating.
Due to the fact that the formation of bone structures obeys general biological laws, calcium is not the only necessary mineral for the processes to proceed continuously and in a reasonable ratio. It is important to restore the mechanisms of calcium metabolism before oversaturation of the body with calcium. To improve the processes of assimilation of minerals and their fixation in skeletal tissues, not only vitamin D3 is needed, but also B6 (thiamine).The complex effect allows you to achieve a more pronounced and lasting result.
Conclusions
The market for calcium-containing products is vast, but not many of the pharmaceutical diversity really deserve attention. This is due to the fact that not all pills are equally effective and safe.
The rating of calcium supplements will help determine which of the presented funds is better. But it should be understood that a preliminary consultation with a specialist is the key to effective treatment and the exclusion of the likelihood of developing adverse reactions.It is possible to choose the best calcium in tablets only on the basis of the results of the diagnostic tests carried out. The doctor, when prescribing a particular drug, repels from the root cause of deficiency conditions, prescribing concomitant therapy to eliminate it.
Prevention of hypocalcemia includes not only taking pills, but also a balanced diet, taking vitamin D3 and daily walks in the fresh air. Maintaining physical activity and practicing feasible sports are also important.
Literature:
https://www.vidal.ru/drugs/atc/a12ax
https://www.lvrach.ru/2014/11/15436097
https://cyberleninka.ru/article/n/sravnitelnyy -analiz-soderzhaniya-kaltsiya-v-kaltsiysoderzhaschih-f …
https://www.vidal.ru/drugs/molecule-in/154
Calcium and boron deficiency in plants. Consequences and methods of struggle
For a plant to develop normally, it must receive all the necessary micro and macro elements. In nature, the balance of the required substances is not always achieved.But under artificial conditions, this is easy to achieve. The main thing is to responsibly treat the growing process and apply fertilizers in a timely manner. Which? We’ll cover in this article. But first, let’s decide what role calcium and boron play in plant life.
The role of calcium in plant life
Calcium is an essential element for proper growth and development. Mostly leaves. With its help, the exchange of proteins and carbohydrates occurs. It is part of the cell membrane and holds them together.
Plants need calcium for the entire growing season. But the main requirement is its presence at the beginning of growth. This contributes to the correct construction and further development.
The effectiveness of using this element depends on the type of soil, its acidity, the type of plants and weather conditions. Different species need this element in different ways.
The effect of calcium on plants is manifested in the following:
- It has a positive effect on the development of the root system, regulates the water balance.
- Reduces soil acidity.
- Increases endurance and immunity to harmful organisms.
- Reduces the intake of radioactive elements, eliminates the negative effects of ammonia.
- Normalizes the acid-base balance in plant cells.
- Increases immunity to fungal infections.
- The liming of soils with a lack of calcium significantly improves its health. This increases air aeration and soil permeability.
- With its help, plants absorb the necessary nutrients better.
Lack of calcium in plants
The plant reacts very painfully to a deficiency of this element. Since calcium tends to accumulate in old parts and leaves, young leaves and shoots are most affected:
- Plant cells are deformed. The stems become weak and hollow. They can crack easily.
- Top leaves wither first.Their growth slows down, spots appear and they die off.
- New leaves take on an ugly shape. They curl down, turn yellow, then fall off.
- Roots gradually rot and die off. They become susceptible to root diseases.
- A weak, drooping peduncle develops.
Feeding plants with calcium will help to completely avoid such negative consequences. Next, we will consider with what fertilizers you can do this.
How to make up for the lack of calcium in plants
After the plant dies off, this element again enters the soil. Therefore, other plants get it as a result of the natural cycle. But if the soil for some reason is depleted in calcium, it is fertilized or lime.
Enough calcium enters the soil with manure. Also, plants are sprayed with a solution of calcium nitrate or potassium chloride. But unknowingly, you can worsen the condition of the plants.Therefore, it is better to use high-quality, proven fertilizers. It is safer and easier to buy calcium for plants than to prepare it yourself.
Let’s take a closer look at the best calcium fertilizers:
Plagron Calcium Kick additive 5 kg. An excellent tool that improves the quality of the soil. With its help, the optimal pH level is established (5.5-6.5). It also improves the structure of the soil, accelerates the absorption of microelements. As a result, the plant develops faster.The soil in which Calcium Kick was applied can be reused. Only used in soil-based substrates.
Set of mineral fertilizers Flora Series 3×60 ml. Fertilizers that will significantly increase yields. Using this kit, your plants will receive the care they need to thrive. Suitable for hydroponic and soil cultivation.
Fertilizer set Plagron Top Grow Box Bio. A universal set for a beginner. It allows you to get beautiful, strong plants and an excellent harvest as quickly as possible.It includes all the supplements you need for successful cultivation. Can be used in any type of substrate, soil and hydroponics.
Powder Feeding Calcium 1kg. This powder additive is used to enrich water with calcium. It strengthens your plant and protects it from pests. Suitable for use in soil and hydroponics.
Mineral fertilizer FloraDuo Grow HW 500 ml. Fertilizer used in hard water.It develops and strengthens the root system well. Increases the absorption of essential elements. It is used in hydroponics and soil.
Mineral fertilizer FloraMicro HW 1 l. Contains all the necessary micro and macro elements. It is applied using hard water. Stabilizes pH. Can be used for hydroponic and soil cultivation.
The role of boron in plant life
It is from this microelement that the quantity and quality of the crop most depends.Boron for plants is necessary for the entire growing season. The most in need of it is dicotyledonous plants, which absorb 10 times more boron than monocotyledons.
Together with calcium, boron participates in the formation of cell walls. Therefore, it is necessary for the normal development of young parts. Lack of it at any stage of growth inevitably leads to disease.
The effect of boron on plants is that:
- It accelerates the formation, movement and exchange of carbohydrates from leaves to roots.
- Improves photosynthesis, increases chlorophyll content.
- Positively influences the absorption of calcium.
- Promotes an increase in the number of flowers, fruits, pollen does not germinate without it.
- Increases resistance to bacterial and fungal diseases.
- Improves the growth of leaves, roots, buds. Increases the absorption of nutrients.
Boron deficiency in plants
Boron deficiency symptoms are similar to those of calcium.With a slight lack of it, plants can look healthy. But they will not bear fruit and bloom.
At first, the problem manifests itself on young shoots and leaves. Wherein:
- the upper part of the shoot is affected and dies off, the so-called. growth point;
- small leaves grow, curl and fall off early;
- the development of the upper kidneys stops, they gradually die off;
- the stem is bent;
- due to the growth of lateral shoots, the plant becomes like a bush;
- flowers fall or there are no inflorescences at all;
- the fruit does not set or has an ugly shape.
How to Replenish Boron Shortage
Boron is contained in the soil in the form of boric acid salts. When liming or washing out by precipitation, its content is significantly reduced. Therefore, fertilization of plants with boron is an important stage in their development.
Do you want to significantly improve the quality of your crop? Use proven boron fertilizers:
Fertilizer set Bio Sevia Bloom + Bio Sevia Grow 2×1 l.It is the first certified organic fertilizer for hydroponics. It is quickly absorbed by the plant, promotes increased absorption of nutrients. This unique product gives excellent results in soil and hydroponic cultivation.
Mineral fertilizer 1 Component Soil Bloom B.A.C. 1 l. Fertilizer necessary during flowering. The solution prepared from it increases the immunity of the plant, strengthens the roots, accelerates the ripening of fruits. Suitable for use in soil.
Powder Feeding Long Flowering 0.