vitamon experiments. Flow Recommended oral medications for diabetes for the selection of US population in the study. Head KA. The summary statistics and distributions of BMD levels were computed for all the participants. View Article Google Scholar 3.

Bone health and vitamin C -

Prrx1-Cre- expressing mice were used as controls. These observations are in line with the notion that impaired osteogenesis due to VitC deficiency is, at least in part, due to deficiency in TET enzyme activity and impaired 5hmC generation.

Thus, these results ascertain the essential role of 5hmC and VitC-dependent TET enzymes during osteogenesis and bone homeostasis. a Schematic representation of the mouse models used.

Bone tissue was collected at 11 weeks; cKO, conditional knockout. c 5hmC dot blot and relative quantification. d Principal component PC analysis and 5hmC peaks around selected bone specific genes e.

h Wordcloud representing phenotypes associated with distal intergenic loci with the strongest 5hmC loss in double knockout vs Ctrl femurs as analyzed by GREAT analysis; FDR, false discovery rate. i µCT analysis of L5 spine and relative quantification; TV total volume, BV bone volume, Tb.

trabecular number, Tb. trabecular thickness, Tb. trabecular separation j. FDR-adjusted two-tailed, unpaired t tests in g , two-sided Fishers exact test f. VitC is a unique micronutrient with multiple biochemical activities and physiological functions required for human health.

Its role as co-factor for many αKGDDs such as histone demethylases and the TET-class of cytosine hydroxylases makes VitC an epigenetic compound with broad significance in pathophysiological contexts 36 , 45 , 60 , The findings presented here reveal that bone integrity is critically dependent on the epigenetic actions of VitC that are required for osteoblastic differentiation and bone matrix mineralization.

While VitC also controls collagen matrix deposition in bone via collagen hydroxylation, this role appears mechanistically downstream from epigenetic control Supplementary Fig.

Our functional analyses on VitC-dependent epigenetic modulators during osteogenic differentiation led to several insights into physiological bone formation and osteogenic lineage differentiation. First, we found that perturbation of VitC-dependent epigenetic circuits involving histone H3 demethylation and 5hmC formation prevents adequate osteogenesis.

In human studies, lower VitC intake correlates with increased bone fracture risk, while increased VitC uptake correlates with higher BMD and reduced fractures risk 7 , 12 , Therefore, we propose that VitC is a crucial epigenetically acting agent that sustains bone homeostasis and bone health in humans.

Second, our results indicate that VitC-regulated chromatin accessibility and activation of gene expression, particularly through TET2-mediated DNA-cytosine hydroxymethylation, is a key prerequisite for osteogenic lineage commitment and progression.

VitC is continuously required throughout osteogenic differentiation, from lineage commitment of BMSCs to maturation of osteoblasts and osteocytes. Depletion of VitC in maturing osteoblasts disables further osteogenic differentiation.

These observations highlight the significance of adequate and consistent VitC intake through a balanced diet to support bone accrual and homeostasis. Interestingly, in line with the existing literature, we found that TET3 suppression enhances osteogenesis 63 , indicating that each TET enzyme may fulfill distinct biological roles 64 , 65 , It is conceivable that the specificity of TET3 during osteogenesis could differ from other TET enzymes, for example by controlling 5mC hydroxylation of non-bone-specific sites and targets genes and thus controlling different cellular functions.

Third, strikingly 5hmC marks are especially sensitive to VitC loss in bone compared to several non-osseous tissues from Gulo knockout mice and disproportionally high 5hmC levels are found in mature osteoblasts embedded within mineralized nodules in vitro. Our findings are also consistent with indirect evidence that 5hmC positively correlates with osteoblast differentiation in vitro 67 , 68 , 69 , Although neither study included bone tissue, the overall conclusion that 5hmC accumulates at tissue-specific regions near tissue-selective genes is in full agreement with our observations.

Interestingly, adipogenesis does not require VitC even though both osteogenic and adipogenic lineages can originate from the same BMSC culture. While this strict dependency of VitC and 5hmC towards osteogenesis requires further experimentations, this divergence might involve cell type-specific, mutually-exclusive characteristics such as differing metabolic properties or epigenetic requirements The link between 5hmC and advanced differentiation appears to be independent of cell division as osteoblasts stop proliferating at early stages of differentiation, concomitant with ECM production 71 , Supporting this observation, 5hmC induction during osteogenic differentiation appears to be largely independent of 5mC levels and activity of DNA methyltransferases DNMTs , which typically are dependent on cell divisions We also did not find evidence of further conversion of 5hmC to 5fC during osteogenic differentiation, suggesting that 5hmC accumulation rather than active DNA demethylation per se is driving bone cell maturation.

However, comprehensive detection of formylated and carboxylate cytosines 5fC and 5acC, respectively remains technologically challenging, thus precluding a more detailed characterization of these DNA modifications and their physiological roles in bone biology at present. This group includes genes that encode for osteogenic transcription factors and mediators, collagens, collagen-crosslinking enzymes, and non-collagenous extracellular matrix proteins that support mineralization.

Most of these bone genes harbor VitC-dependent 5hmC at their loci, while only a subset displays VitC-sensitive H3K27me3 or H3K9me3 demethylation. Consistent with these findings, the majority of bone genes are expressed in a VitC-dependent, 5hmC-dependent fashion, while H3K27me3 or H3K9me3 demethylation appears to play only a minor, gene-selective role in VitC-controlled gene regulation.

Both, promoter sites and distal enhancers including super-enhancers, show VitC-dependent dynamics particularly for 5hmC. To explain the primary role of 5hmC and 5hmC-generating enzymes and the more limited function of histone demethylases in orchestrating osteogenic differentiation, we propose that while 5hmC generation acts as an epigenetically active mark designated to facilitate gene expression, demethylation of H3K27me3 or H3K9me3 merely reduces or neutralizes repressive epigenetic marks; and without establishing activating signals such as H3K27ac or H3K9ac, gene expression may still be restricted.

Indeed, histone acetyltransferases which would generate such activating epigenetic marks have not been described as VitC-dependent. The latter rationalization may explain why we find 5hmC and 5hmC-generating enzymes to orchestrate a variety of physiological aspects during osteogenic differentiation, while the relevance of histone demethylases is more restricted.

In summary, our study suggests that the skeletal manifestations of scurvy and VitC deficiency represents a micronutrient-dependent epigenetic disease with secondary biochemical effects on collagen maturation. The recognition that VitC epigenetically programs the bone cell fate by both DNA hydroxymethylation and histone demethylation opens opportunities to pharmacologically facilitate bone health and prevent bone degeneration.

For example, when considering that VitC supplementation during estrogen replacement therapy in post-menopausal women further increases BMD 32 , such strategies could complement the existing standard of care that is currently applied in a broad spectrum of degenerative bone conditions that benefit from bone anabolic strategies.

Effects of Vitamin C VitC on bone were studied on homozygous B6. These mice were supplemented with Vitamin C 3. With proper VitC supplementation in the drinking water, these mice are viable, fertile and indistinguishable from their heterozygous or wild-type littermates Mice were kept on a standard mouse chow devoid of Vitamin C LabDiet, Tet1 and Tet2 expression was conditionally ablated by mating with mice expressing Cre recombinase from the Prrx1 enhancer B6.

The following primers were used for mouse genotyping. All experimental procedures involving laboratory mice were reviewed and approved by the Institutional Animal Care and Use Committee of the Mayo Clinic.

A voxel size of Using SCANCO Reconstruction software, two-dimensional data from scanned slices were used for a three-dimensional interpolation and calculation of morphometric parameters that define trabecular bone mass and micro-architecture.

A three-point bend fixture was mounted on a servohydraulic mechanical testing frame Model , MTS Systems, Eden Prairie, MN instrumented with a N capacity load cell Model , Leebow Products, Troy, MI.

Point loading was applied to the femur midshaft allowing the bones to flex about an axis aligned with the medial-lateral line. Specimens were kept moist by irrigating them with phosphate buffered saline solution.

The peak load was quantified as was the peak displacement. The stiffness was calculated from the slope of the linear region of the force displacement curve. Primers for the analyzed genes are listed in Table S1. All rt-qPCR assays were performed in triplicate and expression was evaluated using the Biorad CFX Manager 3.

For high through output next generation RNA sequencing RNA-seq RNA integrity was analyzed with a Bioanalyzer with an RNA kit Agilent Technologies. All here mentioned incubation steps were performed in the dark. Laser scanning microscopy was performed with a 40x objective on a Zeiss LSM microscope in conjunction with Zen blue edition software version 2.

Cells were then permeabilized with 0. Image acquisition and analysis was performed with a Zeiss LSM microscope or a Zeiss Axio Vert. A1 microscope in conjunction with Zen blue edition software version 2. After sonication, gDNA was concentrated using Amicon Ultra centrifugal filter units Millipore.

Inhibition of collagenous extra cellular matrix ECM deposition was achieved by treating the cells with Thereafter, cells were cultured without dexamethasone or IBMX in the media. For antioxidant experiments, mBMSCs were treated with 3 mM N-acetyl-cysteine NAC; Santa Cruz biotechnologies.

The murine osteoblast to osteocyte-like MLO-A5 cell line a generous gifted from Dr. Lynda Bonewald, Indiana University School of Medicine was maintained on collagen coated plates 0. HEK packaging cells ATCC, CRL were co-transfected with MISSION TRC2-pLKO-puroR vectors Sigma; empty vector control EVCtrl , scramble shRNA NegCtrl or shRNAs against Tet1 , anti Tet2 , anti Tet3 , Kdm4a , Kdm4b , Kdm4c , Kdm6a , Kdm6b and Jhdm1d , packaging plasmid psPAX2 Addgene plasmid and envelope plasmid pMD2.

G Addgene plasmid with Fugene transfection reagent Promega. Cells expressing puroR were selected by treatment with puromycin Santa Cruz after the third infection.

Efficiencies of shRNA knockdowns were tested beforehand by rt-qPCR and the two most efficient shRNAs were selected for experiments. Endogenous TET2, KDM4A, KDM4B, KDM4C, KDM6A, KDM6B and JHDM1D overexpression was induced using a gRNA directed, tetracycline inducible dCas9-VP64 system Addgene plasmids , in MC3T3-E1 cells.

For each gene, a screen of 5 or more promoter binding gRNAs was performed and the two gRNAs showing the highest induction activity were chosen for further experiments, as negative control the empty backbone plasmid was used Viral particles generation and cell transduction were performed as described above, gRNA sequences are listed in Table S1.

ALPL activity was determined in relation to total DNA present in samples as a surrogate for cell number. The amount of DNA was estimated using a standard curve prepared from calf thymus DNA Roche.

ALPL activity was quantified with p-nitrophenylphosphate 2. ALPL activity was expressed as arbitrary units per milligram DNA and referenced to fold change to control.

Cultured cells were dislodged from the extracellular matrix ECM using 0. The remaining ECM was thoroughly washed with PBS and ECM collagen staining was performed by Picro Sirius Red staining as shown before The pellets were transferred onto barium fluoride windows, where they were air-dried.

The collagen cross-link ratio was determined as previously described Mineralization deposits were quantified by digital image analysis using ImageJ. To remove staining excess wells were rinsed with tap water for at least 5 times. Images were digitalized and colonies were analyzed using the ImageJ software.

Total protein amounts were quantified by BCA protein assay Sigma-Aldrich and protein concentrations were equalized between the samples subsequently. Proteins were transferred to a nitrocellulose membrane and subsequently Ponceau S stain was performed to monitor equal protein loading between the samples.

Next day, membranes were washed 3 times with TBST and incubated with anti-rabbit horseradish peroxidase-conjugated secondary antibody Cell signaling, , Proteins were visualized using enhanced chemiluminescence reagents Thermo Scientific, , exposed with a ChemiDoc Touch Imaging System Biorad. Data acquisition and analysis was performed with the Biorad Image Lab software, version 5.

Uncropped Western blot scans for the Main Figures are available as a Source Data File and uncropped Western Blot scans for the Supplementary Figures are provided at the end of the Supplementary Information file. Fluorescence signal was subtracted to media only control wells.

Data analysis was performed with the Tecan Magellan software version 7. Raw reads from RNA-seq experiments were assessed for run quality using fastqc version 0. Differential gene expression analysis was performed using featureCounts Galaxy version 1.

Fragments per kilobase of exon per million mapped fragments FPKM was performed by cufflinks v2. To further normalize for possible batch effects between the samples, RUVSeq Galaxy Version 1. Bone or fat tissue-related gene-sets as defined by DESeq2 and including already well-known bone and fat related genes, were then compared between human and mouse and only genes found in both organisms were selected for the final gene-sets.

The generated gene-sets were then used for gene-set enrichment analysis GSEA and other studies. GSEA analysis was performed with GSEA version 4.

Raw reads from 5hmC MeDIP-seq hMeDIP-seq experiments were assessed for quality using fastqc version 0. Peak size and location was visualized with IGV version 2.

MAYO by overlaying the tracks and using group auto-scale for comparable visualization of both groups. To assess significantly different peak binding between two experimental groups, peak files MACS2 from single hMeDIP-seq runs were analyzed with DiffBind Galaxy version 2.

Super-enhancer SE like analysis on 5hmC peak distribution was performed by using the package ROSE and the software NaviSE Gene-ontology analysis for gene loci near 5hmC positive cis-regulatory distal intergenic regions was performed using GREAT version 3. Raw ChIP-Seq files were assessed for read quality with fastqc version 0.

Peak calling was performed with MACS2 callpeak version 2. To assess significantly different peak binding between two experimental groups, peak files MACS2 from single ChIP-seq runs were analyzed with DiffBind Galaxy version 2. MAYO using group auto-scale for comparable visualization of all shown groups.

Gene-ontology analysis for gene loci near H3K9me3 and H3K27me3 positive cis-regulatory distal intergenic regions was performed using GREAT version 3. The most significantly FDR, DiffBind increased H3K9me3 or H3K27me3 peaks in after VitC treatment were used for the analysis.

For H3K27ac sequencing files, super enhancer analysis was performed by using the package ROSE as described above. Overlapping SE between 5hmC SE from VitC treated MC3T3-E1 cells D28 and H3K27ac SE from BMSCs were filtered with Bedtools version 2.

The vast majority of statistical data analysis and figure generation was performed with GraphPad Prism software, version 8. Statistical analysis for RNA-Seq datasets was performed by DeSeq2 Galaxy version 2.

Where representative pictures are shown, pictures showing similar results were taken from at least three independent experiments. Further information on research design is available in the Nature Research Reporting Summary linked to this article.

The raw and processed RNA-Seq, MeDIP-Seq and ChIP-Seq data-sets generated in this study have been deposited in the GEO database under accession code GSE All other data generated in this study are provided in the Supplementary Information files and the Source Data file.

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Vitamin C, through a combination of its known anti-resorptive action and the anabolic effect shown herein, may have a more profound effect on the skeleton. However, it is possible that higher doses of vitamin C will be utilized compared with those recommended by the Institute of Medicine [26] or those offered in over-the-counter supplements.

As a water-soluble vitamin, excess vitamin C is excreted in urine, and cases of vitamin C toxicity are therefore rare. The tolerable upper limit of intake of vitamin C is mg per day [26]. Beyond this level, rare side effects include mild gastrointestinal symptoms, such as abdominal cramps. However, reports for increased risk of kidney stones and of cardiovascular disease in postmenopausal women with diabetes are conflicting and inconclusive.

This begs the need for future dose-ranging and safety studies on vitamin C in humans. All animal studies were approved by the Institutional Animal Care and Use Committee at Mount Sinai School of Medicine and were performed in accordance with the guidelines of the National Institutes of Health and Mount Sinai School of Medicine.

The dose of vitamin C in our studies was fold higher than over-the-counter doses mg used as dietary supplements. However, a daily dose of mg was considered insufficient as mice synthesize the human body weight equivalent of 10, mg per day [23]. This suggests that the oral vitamin C dose was not only optimal in producing a significant change in serum vitamin C levels, but also efficacious in preventing ovariectomy-induced bone loss.

Whole body BMD minus cranium , and region-specific measurements of the spine L4—L6 , left femur, and left tibia were made. The instrument was calibrated each time before use by employing a phantom per manufacturer's recommendation.

For micro-CT estimations, the L3 vertebra was scanned non-destructively by using a Scanco μCT scanner μCT; Scanco Medical AG, Bassersdorf, Switzerland at 12 µm isotropic voxel size, with X-ray source power of 55 kV and µA, and integration time of milliseconds. The trabecular microstructure of the entire secondary spongiosa of L3 between the cranial and the caudal area was evaluated.

The reconstruction and 3D quantitative analyses were performed using software provided by Scanco. The same settings for scan and analysis were used for all samples.

Th , trabecular number Tb. N , and trabecular spacing Tb. Sp units specified in Figure 2. Parameters included mineralized surface MS , mineral apposition rate MAR , bone formation rate BFR , and TRAP surfaces Resorbed S.

Bone turnover markers, namely osteocalcin and C-telopeptide, were measured on mouse plasma using commercial kits Mouse Osteocalcin kit, Biomedical Technologies, Stoughton MA, BT and RatLaps EIA, Immunodiagnostics Systems, ACF1, respectively.

Bone marrow was isolated and stromal cell cultures performed in the absence of ascorbate for 6 or 10 days. RNA was extracted for quantitation of gene expression using established protocols [13].

Quantitative PCR was performed as described [13]. L-ascorbic acid was purchased from Sigma. The data were analyzed using Student's t-test with Bonferroni's correction.

In every case, comparisons have been made for differences between ovariectomized and sham-operated mice to examine the effect of ovariectomy. Furthermore, within the sham-operated and ovariectomized groups, comparisons were made for differences between vitamin C treated and control mice.

Conceived and designed the experiments: LP HCB MZ. Performed the experiments: LZ JC MS RZ JL YP SSM. Analyzed the data: LZ TY LG JIM JI.

Wrote the paper: ZB MZ. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Epidemiologic studies correlate low vitamin C intake with bone loss.

Introduction The diligent search for small molecules and biologics to treat osteoporosis resonates with the expanding definition of osteoporosis and the implication that many more individuals worldwide have fragile bones.

Download: PPT. Figure 1. Oral Vitamin C Prevents Ovariectomy-Induced Bone Loss in Mice. Figure 2. Oral Vitamin C Prevents Structural Deterioration in Ovariectomized Mice. Figure 3.

Oral Vitamin C Stimulates Bone Formation in Ovariectomized Mice. Table 1. Oral Vitamin C Stimulates the Expression of Osteoblast Differentiation Genes. Discussion We examined the in vivo skeletal anabolic action of vitamin C in low-turnover osteoporosis induced 8 weeks following ovariectomy in mice [14].

Materials and Methods All animal studies were approved by the Institutional Animal Care and Use Committee at Mount Sinai School of Medicine and were performed in accordance with the guidelines of the National Institutes of Health and Mount Sinai School of Medicine. Author Contributions Conceived and designed the experiments: LP HCB MZ.

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Depending on haelth and smoking Healtth, the daily-recommended intake of vitamin C can Oats and hair health greatly. For the average adult daily intake is recommended at 75mg for women and 90 mg for men. Bealth, smokers should consume at least 35 mg citamin of vitamin C per day, as healgh directly depletes the vitamin C you intake.

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Vitaimn, for the sake of this article we vifamin focus Bon its benefit for bones. While there have been many studies vitakin the effects of viyamin C on bone density, the most promising correlation has been found in postmenopausal women.

One specific study focused Bons the association between vitamin C intake and the bone density in the neck. The study took techniques for blood sugar control to adjust calcium intake, physical activity, smoking, age, weight, and estrogen ehalth.

The study then measured several mg increases in vitamin C intake in participants. It was found that viramin was healgh 0. Other studies have also vitaamin credit to the Bonee correlation between vitamin Vitamih intake and bone Fleet Fuel Efficiency Management.

In fact, it has been found that decreased intake of vitamin Bone health and vitamin C is associated fitamin osteoporosis and Bodyweight tracking density loss. Boone there is some vitakin to support the claims Bone health and vitamin C vitamin C intake is directly related to bone density, many healfh and doctors still disagree on the validity of this Fleet Fuel Efficiency Management meaning more studies are required.

However, it is widely accepted that the vitamin C plays a role in collagen formation, bone matrix development, and osteoblast differentiation. Arthritis is a huge issue for many orthopedic patients and doctors. It is a disease that is difficult to combat in advanced stages, and thus much research has been done in search of ways to keep the disease at bay.

Due to studies in the early s a buzz began to spread about how a balanced intake of vitamin C can affect arthritis. A study at Duke University found that high levels of vitamin C activated a protein that causes bone spurs, which in turn actually accelerates joint damage and pain in patients with osteoarthritis.

Conversely, another study showed that people with low levels of vitamin C were 3 times more likely to develop rheumatoid arthritis than those who had normal levels of vitamin C.

Although this sounds like a mixed review, it is actually spot on with the hypothesis that a balanced intake of vitamin C keeps arthritis at bay.

The first study showed that an EXCESS of vitamin C worsens osteoarthritis while the second study showed that the proper amount of vitamin C lowers the chance of rheumatoid arthritis.

Thus, it can be deduced that if you stay within the daily recommendation of vitamin C intake you will be doing your part in keeping arthritis pains and symptoms at bay; at least from a vitamin C stand point. The goal of this article was to discuss how vitamin C intake affects the health of bones.

Although more research is needed to determine how the vitamin affects bone density, there is at least some evidence that vitamin C does increase bone strength in postmenopausal women. This is a promising sign, and a driving factor for continued research. Your bones and taste buds will thank you! Arthritis Today Staff.

Arthritis Foundation. Harvey, Edward J. University of Maryland Medical Center, Attention work-from-home and hybrid-work warriors! and the overall feeling of being trapped in your own home office can be a real downer.

Check out these simple tweaks to …. In the dynamic realm of health, young adults can also find themselves face to face with OA, which the Centers for Disease Control and Prevention identifies as the most common form ….

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thoroughly enjoy winter snow sports. request an appointment. Vitamin C: The Saving Grace for Bone Health By ProOrtho on April 19, - Posted in: News.

The entity known as vitamin C Unlike other animals, humans cannot store vitamin C, and thus we have to get it from the food we eat. Bone density While there have been many studies on the effects of vitamin C on bone density, the most promising correlation has been found in postmenopausal women.

Vitamin C and Arthritis Arthritis is a huge issue for many orthopedic patients and doctors. Vitamin C Conclusions The goal of this article was to discuss how vitamin C intake affects the health of bones. Citations: Arthritis Today Staff. ProOrtho Medical Specialties Ankle Elbow Foot Hip Knee Orthobiologics Pain Management Shoulder Spine.

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: Bone health and vitamin C

Publication types	EMBO Rep. Primers for the analyzed genes are listed in Table S1. Head KA. Snoddy AME, Buckley HR, Elliott GE, Standen VG, Arriaza BT, Halcrow SE. Acerola cherry. A study from the United States of America indicated that vitamins B12 and B9 were beneficial for osteoporosis prevention in the elderly women [ 10 ]. Most notably, vitamin C is known to function as a co-factor for lysine and proline hydroxylation during type 1 collagen synthesis [22].
Vitamin C (Ascorbic acid)	Consult your Minster chiropractor to determine the appropriate daily dosage of Vitamin C for you to protect your bones and enhance your bone mineral density throughout your life. Vitamin C is Good for Your Bones, Too! This celebrated, familiar vitamin is proclaimed for its antioxidant function and part in the support of a healthy immune system 1. But did you know that nutrition research into Vitamin C has revealed its task in forming bone and protecting it? Minster Chiropractic Center desires to relay to you the nutritional gains, and how Minster chiropractic patients can take advantage of this to augment their care for spinal pain management. References Bsoul SA et al: Vitamin C in health and disease. J Contemp Dent Pract. Sahni S et al: High vitamin C intake is associated with lower 4-year bone loss in elderly men. J Nutr Oct; 10 Ruiz-Ramos M et al: Supplementation of ascorbic acid and alpha-tocopherol is useful to preventing bone loss linked to oxidative stress in elderly. J Nutr Health Aging. Morton DJ et al: Vitamin C supplement use and bone mineral density in postmenopausal women. J Bone Miner Res. Depending on age and smoking habits, the daily-recommended intake of vitamin C can vary greatly. For the average adult daily intake is recommended at 75mg for women and 90 mg for men. However, smokers should consume at least 35 mg more of vitamin C per day, as smoking directly depletes the vitamin C you intake. So what exactly does vitamin C do for our bodies? Well, it repairs tissues and builds collagen, which is important for making new skin cells, cartilage, tendons, ligaments, and blood vessels. So, for the sake of this article we will focus on its benefit for bones. While there have been many studies on the effects of vitamin C on bone density, the most promising correlation has been found in postmenopausal women. One specific study focused on the association between vitamin C intake and the bone density in the neck. The study took care to adjust calcium intake, physical activity, smoking, age, weight, and estrogen use. The study then measured several mg increases in vitamin C intake in participants. It was found that there was a 0. Other studies have also attributed credit to the positive correlation between vitamin C intake and bone density. In fact, it has been found that decreased intake of vitamin C is associated with osteoporosis and bone density loss. Although there is some evidence to support the claims that vitamin C intake is directly related to bone density, many scientists and doctors still disagree on the validity of this statement; meaning more studies are required. However, it is widely accepted that the vitamin C plays a role in collagen formation, bone matrix development, and osteoblast differentiation. Arthritis is a huge issue for many orthopedic patients and doctors. It is a disease that is difficult to combat in advanced stages, and thus much research has been done in search of ways to keep the disease at bay. Due to studies in the early s a buzz began to spread about how a balanced intake of vitamin C can affect arthritis. A study at Duke University found that high levels of vitamin C activated a protein that causes bone spurs, which in turn actually accelerates joint damage and pain in patients with osteoarthritis. Conversely, another study showed that people with low levels of vitamin C were 3 times more likely to develop rheumatoid arthritis than those who had normal levels of vitamin C. Although this sounds like a mixed review, it is actually spot on with the hypothesis that a balanced intake of vitamin C keeps arthritis at bay. The first study showed that an EXCESS of vitamin C worsens osteoarthritis while the second study showed that the proper amount of vitamin C lowers the chance of rheumatoid arthritis. Thus, it can be deduced that if you stay within the daily recommendation of vitamin C intake you will be doing your part in keeping arthritis pains and symptoms at bay; at least from a vitamin C stand point. The goal of this article was to discuss how vitamin C intake affects the health of bones. Although more research is needed to determine how the vitamin affects bone density, there is at least some evidence that vitamin C does increase bone strength in postmenopausal women. This is a promising sign, and a driving factor for continued research. Your bones and taste buds will thank you! Arthritis Today Staff. Arthritis Foundation. Harvey, Edward J.
Latest ProOrtho News	Due to its presence in many normal foods it is pretty easy to get your daily-recommended intake of vitamin C. Depending on age and smoking habits, the daily-recommended intake of vitamin C can vary greatly. For the average adult daily intake is recommended at 75mg for women and 90 mg for men. However, smokers should consume at least 35 mg more of vitamin C per day, as smoking directly depletes the vitamin C you intake. So what exactly does vitamin C do for our bodies? Well, it repairs tissues and builds collagen, which is important for making new skin cells, cartilage, tendons, ligaments, and blood vessels. So, for the sake of this article we will focus on its benefit for bones. While there have been many studies on the effects of vitamin C on bone density, the most promising correlation has been found in postmenopausal women. One specific study focused on the association between vitamin C intake and the bone density in the neck. The study took care to adjust calcium intake, physical activity, smoking, age, weight, and estrogen use. The study then measured several mg increases in vitamin C intake in participants. It was found that there was a 0. Other studies have also attributed credit to the positive correlation between vitamin C intake and bone density. In fact, it has been found that decreased intake of vitamin C is associated with osteoporosis and bone density loss. Although there is some evidence to support the claims that vitamin C intake is directly related to bone density, many scientists and doctors still disagree on the validity of this statement; meaning more studies are required. However, it is widely accepted that the vitamin C plays a role in collagen formation, bone matrix development, and osteoblast differentiation. Arthritis is a huge issue for many orthopedic patients and doctors. It is a disease that is difficult to combat in advanced stages, and thus much research has been done in search of ways to keep the disease at bay. Due to studies in the early s a buzz began to spread about how a balanced intake of vitamin C can affect arthritis. A study at Duke University found that high levels of vitamin C activated a protein that causes bone spurs, which in turn actually accelerates joint damage and pain in patients with osteoarthritis. Conversely, another study showed that people with low levels of vitamin C were 3 times more likely to develop rheumatoid arthritis than those who had normal levels of vitamin C. Although this sounds like a mixed review, it is actually spot on with the hypothesis that a balanced intake of vitamin C keeps arthritis at bay. The first study showed that an EXCESS of vitamin C worsens osteoarthritis while the second study showed that the proper amount of vitamin C lowers the chance of rheumatoid arthritis. Thus, it can be deduced that if you stay within the daily recommendation of vitamin C intake you will be doing your part in keeping arthritis pains and symptoms at bay; at least from a vitamin C stand point. The goal of this article was to discuss how vitamin C intake affects the health of bones. Although more research is needed to determine how the vitamin affects bone density, there is at least some evidence that vitamin C does increase bone strength in postmenopausal women. This is a promising sign, and a driving factor for continued research. Your bones and taste buds will thank you! Arthritis Today Staff. Arthritis Foundation. Take some supplements. Add some lemon juice to your water. Whatever it takes…because while many scientists and doctors still disagree on the validity of vitamin C intake improving bone density, several studies show vitamin C plays a role in collogen formation, bone matrix development, and osteoblast differentiation. The most promising correlation between vitamin C and bone density was discovered in postmenopausal women. One specific study focused on the association between vitamin C intake and bone density in the neck. The study considered several variables, then measured mg increases in vitamin C intake in participants, finding there was a 0. Other studies also lend credence to the positive correlation between vitamin C intake and bone density. According to Cambridge University Press, greater dietary vitamin C intake is associated with higher bone mineral density at the femoral neck and lumbar spine. Furthermore, reduced risk of hip fracture and osteoporosis is associated with greater dietary vitamin C intakes. A study at Duke University found that an excess of vitamin C worsens osteoarthritis, while another study showed that normal recommended levels of vitamin C lowers the chance of rheumatoid arthritis. Yet another indication that life is all about balance : staying within the daily recommended intake of vitamin C keeps arthritis pain at bay. And what is that recommended intake you may ask? The adult daily recommended intake is 75 mg 1. Easy enough. So what have you got to lose? A supplement here, and orange there, or maybe even some shudder red cabbage with dinner is all it takes to keep your bones in tip top shape. Stay healthy and bone-strong as we enter our rather-dark-and-cold-but-joyous winter season. If you have any questions about osteoporosis, arthritis, our orthopedic services, or anything else, reach out today. Arthritis Today Staff. Arthritis Foundation. Harvey, Edward J. University of Maryland Medical Center, Harvinder S. Attention work-from-home and hybrid-work warriors! and the overall feeling of being trapped in your own home office can be a real downer. Check out these simple tweaks to ….

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Use THIS FORM of Vitamin C!