JICDRO is a UGC approved journal (Journal no. 63927)

   Table of Contents      
Year : 2017  |  Volume : 9  |  Issue : 2  |  Page : 71-76

Magnesium and Zinc Levels in Individuals Having Generalized Chronic Periodontitis

1 Department of Periodontology, MIDSR Dental College and Hospital, Latur, Maharashtra, India
2 Department of Periodontology, Dr. Rajesh Ramdasji Kambe Dental College and Hospital, Akola, Maharashtra, India

Date of Web Publication21-Dec-2017

Correspondence Address:
Dr. Snehal Chandrashekhar Taru
Department of Periodontology, MIDSR Dental College and Hospital, Latur, Maharashtra
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jicdro.jicdro_11_17

Rights and Permissions

Background: Mineral insufficiencies may have far-reaching consequences both systemically and orally. The exact associations and roles of many of the elements are not unequivocally examined till now as far as chronic periodontitis (CP) is concerned. Aim: The present study was designed to evaluate and compare the serum levels of magnesium and zinc in CP cases as compared to healthy controls. Settings and Design: This study was conducted in the Department of Periodontology in MIDSR Dental College and Hospital, Latur. It was a cross-sectional study. Materials and Methods: This study included 60 individuals, 30 in each group, i.e. Group I –healthy controls and Group II – Generalized CP. Serum magnesium and serum zinc levels were analyzed using reagent kits. Statistical Analysis: The results obtained were analyzed by applying unpaired Student's t test. Results: Serum levels of magnesium and zinc were 1.30 + 0.78 mEq/L and 62.10 + 18.76 ug/dl, respectively, in CP cases and 1.89 + 0.48 mEq/L and 92.51 + 15.64 ug/dl, respectively, in healthy controls. Conclusion: The mean serum levels of magnesium and zinc were significantly altered in CP cases as compared to healthy controls.

Keywords: Chronic periodontitis, magnesium, zinc

How to cite this article:
Taru SC, Jawade RB, Baghele ON, Bhandari VD, Ugale GM. Magnesium and Zinc Levels in Individuals Having Generalized Chronic Periodontitis. J Int Clin Dent Res Organ 2017;9:71-6

How to cite this URL:
Taru SC, Jawade RB, Baghele ON, Bhandari VD, Ugale GM. Magnesium and Zinc Levels in Individuals Having Generalized Chronic Periodontitis. J Int Clin Dent Res Organ [serial online] 2017 [cited 2022 Dec 5];9:71-6. Available from: https://www.jicdro.org/text.asp?2017/9/2/71/221387

   Introduction Top

Periodontal disease is a microbially initiated chronic inflammatory disease, in which impaired immunoinflammatory processes are responsible for the majority of host tissue destruction and ultimately tooth loss. Periodontal disease is one of the two major dental diseases that affect human populations worldwide, the other being dental caries.

The vitality of the periodontal tissues, in both health and disease, depends strongly on an adequate source of essential nutrients being available to the host. Diet plays an important role in the maintenance of tooth structure after eruption.[1] Nutritional deficiencies are vital risk factor for periodontitis, but their direct effect on it is not well documented.[2],[3] They mainly influence the immune response in the body and subsequently the progression of periodontal disease. The integrity and maintenance of periodontium are dependent on the adequate supply of proteins, carbohydrates, fats, vitamins, and mineral salts.[4]

Certain macronutrients as well as micronutrients such as zinc (Zn), magnesium (Mg), copper (Cu), and calcium (Ca) are essential for the normal metabolism of proteins, carbohydrates, and lipids. Zinc is essential for successful growth of many internal organs, stabilizing cell membranes, and modulating membrane-bound enzymes and insulin action.[5] This micronutrient participates both in the synthesis and actions of the hormones, which are intimately linked to bone metabolism.In vitro studies have shown that Zn stimulates osteoblastic bone formation.[6] The basic mechanisms of action of these trace elements are intimately linked to the structure and action of countless enzymes involved in many different metabolic processes. Zinc and magnesium are considered to be protective with its antioxidant properties.[7] Imbalance of zinc and copper in the serum can predispose an individual to the risk of developing chronic periodontitis (CP).[8] In 2007, Orbak et al. reported, for the first time, that hyperkeratinization was more prominent in Zn-deficient rats. They also suggested that Zn deficiency is a potential risk factor for oral and periodontal diseases.[9]

Magnesium is a macronutrient which acts as a critical cofactor involved in the carbohydrate, lipid, and protein metabolism. In all, magnesium activates over 300 cellular enzymes and helps in electron transport chain in cell cycle.[5] Magnesium is involved in a number of processes, including hormone receptor binding and gating of calcium channels, transmembrane ion flux, regulation of adenylate cyclase, muscle contraction and neuronal activity, control of vascular tone, cardiac excitability, and neurotransmitter release. Magnesium increases the body's ability to utilize calcium, phosphorus, sodium, potassium, Vitamins C, E, and B complex.[10] Magnesium is also a fundamental element of the structure of cellular and subcellular membranes with the major function of offering membrane stability.[11],[12]

Magnesium is necessary for a wide range of cellular functions. Low magnesium intake has been linked to periodontitis.[13] Meisel et al. have observed lower levels of magnesium in the blood of individuals with periodontal disease.[14]

Periodontitis, inspite of its localized nature, may lead to various responses beyond the confines of the periodontium, through passage of bacteria and their products into the bloodstream and adjacent tissues, through uptake of various molecules such as enzymes, prostaglandins, cytokines, immunobiological mediators, lipid, and protein molecules. Literature reveals that trace mineral insufficiency has far-reaching consequences both systemically and orally.[15] The exact associations and roles of these trace elements are not unequivocally examined till now as far as pathogenesis of CP is concerned. The relationship between serum zinc and serum magnesium levels with CP is hazy.

Thus, hereby, we hypothesize that the serum levels of magnesium and zinc are significantly altered in otherwise healthy but with CP individuals as compared to individuals who are systemically and periodontally healthy.

The present study aimed to evaluate and compare the serum zinc and magnesium levels and investigate their association in CP versus healthy controls.

   Materials and Methods Top

Source of data

The present study was carried out on 60 individuals in the age group of 30–50 years who visited the Outpatient Department of Periodontology, MIDSR Dental College and Hospital, Latur, inclusive of both gender and were divided into 2 groups of 30 individuals each. It was a cross-sectional study. The study was approved from the Institutional Ethical Boards.

Methods of collection of data

All potential participants were selected and explained the need and objectives of the study. Verbal and written informed consent was obtained from those who agreed to participate voluntarily in this study.

Blood serum samples were collected and were categorized into two groups based on their clinical findings as follows:

  1. Group I: 30 individuals as healthy controls
  2. Group II: 30 individuals with generalized CP.

Inclusion criteria:

  1. Age group 30–50 years
  2. Parameters for categorization of periodontitis patients

    1. Mean probing depth of more than or equal to 5 mm and clinical attachment loss more than or equal to 3 mm measured with the William's periodontal probe in at least 40% teeth.[5]

  3. The controls with relatively healthy gingival and periodontal status with no clinical attachment loss and probing depth of ≤3 mm. Individuals with gingival index score of maximum up to 0.6 were included which were considered to be relatively healthy [16]
  4. Patients who had not undergone any kind of periodontal therapy for at least 6 months before sampling
  5. Presence of more than or equal to 20 permanent teeth.

Exclusion criteria:

  1. Patients consuming tobacco in any form
  2. Drug abusers
  3. History of any antibiotic therapy within 6 months before study
  4. History of any systemic diseases having direct influence on macro- and micronutrients such as thyroid dysfunction, hyperparathyroidism, Addison's disease, tetany, multiple sclerosis, neuromuscular discrepancy, hypertension, and type 2 diabetes mellitus
  5. History of any systemic disease for the control group
  6. Individuals who were pregnant
  7. Individuals who were malnourished and on vitamin supplementations
  8. Individuals who regularly used mouthwashes.

Study protocol

A pro forma was designed for the present study so as to have a systematic and methodical recording of all the observations and information.

Clinical parameters

Intraorally, following clinical parameters were recorded by one investigator:

  1. Gingival index (Loe and Silness 1963)[17]
  2. Probing depth of four surfaces of all fully erupted teeth was assessed using William's graduated periodontal probe
  3. Clinical attachment loss (CAL) was assessed on four surfaces of all fully erupted teeth using William's graduated periodontal probe.

Procedure for collection of serum specimen

Two milliliters of blood was collected from the vein present in the antecubital fossa by venipuncture using a 20-gauge needle with 2 ml syringe and centrifuged at 3000 rpm for 15 min and the supernatant serum was immediately transferred to the laboratory for estimation.[18]


Estimation of serum zinc levels

Serum zinc levels were analyzed using zinc kit by colorimetric method.[19] The principle behind this is zinc in an alkaline medium reacts with Nitro-PAPS (pyridylazo-N-propyl-N-sulfopropylamino-Phenol) to form a purple-colored complex. Intensity of the complex formed was directly proportional to the amount of zinc present in the sample. The normal reference range is 60–120 μg/dl.

Estimation of serum magnesium levels

Serum magnesium levels were analyzed using magnesium kit by calmagite method.[20] The principle behind this is, magnesium combines with calmagite in an alkaline medium to form a red-colored complex. Intensity of the color formed is directly proportional to the amount of magnesium present in the sample. The normal reference range is 1.3–2.5 mEq/L.

Both zinc and magnesium reagent kits (Tulip Diagnostics Pvt Ltd, Goa, India) were used and readings were estimated by using semiauto analyzer (Chem-7) (Transasia Bio-medical Private Ltd, India) in the Department of Biochemistry of MIMSR Medical College, Latur.

Statistical analysis

Data were collected by using a structured pro forma. Data were entered into MS excel sheet and analyzed by using SPSS (software package for social statistics) 19.0 version IBM USA. Quantitative data were expressed in terms of Mean and Standard deviation. Qualitative data were expressed in terms of proportions. Unpaired Student's t-test was used to assess whether the mean difference between two groups is significant or not. Means were compared at P < 0.05 which was considered as statistically significant whereas a P < 0.001 was considered as highly significant.

   Results Top

The present study was carried out on 60 individuals in the age group of 30–50 years inclusive of both gender and were divided into 2 groups of 30 individuals each. The groups were as following:

  • Group I: 30 individuals as healthy controls
  • Group II: 30 individuals with CP.

The demographic data of the study population in the control group (Group I) and in CP (Group II) were as follows. In the present study, all CP subjects and healthy controls were in comparable age group (40.53 + 2.46 versus 37.20 + 1.14, respectively). No statistically significant difference was observed in gender-wise distribution in both groups (m/f: 11/19 vs. 12/18). The mean values of GI, PPD, and CAL were lower in healthy participants than those of CP cases. As expected, the mean values of GI (1.93 + 0.38 vs. 0.46 + 0.17), PPD (5.67 + 0.96 vs. 1.40 + 0.50), and CAL (6.13 + 1.01 vs. 0.00 + 0.00) between the study group and control group were statistically highly significant (P < 0.001) [Table 1].
Table 1: Comparing mean levels of clinical periodontal parameters (gingival index, probing pocket depth, clinical attachment loss) in chronic periodontitis cases and healthy control group

Click here to view

The mean serum magnesium levels in CP cases and healthy control group were 1.30 + 0.78 and 1.89 + 0.48, respectively. The mean serum zinc levels in CP cases and healthy control group were 62.10 + 18.76 and 92.51 + 15.64, respectively Unpaired Student's t-test was used for comparison; statistically significant difference was observed in both the groups [Table 2] and [Graph 1], [Graph 2].
Table 2: Comparison of mean serum magnesium and serum zinc levels in chronic periodontitis cases and healthy control group

Click here to view

   Discussion Top

CP is a multifactorial condition caused by complex interactions of dental plaque biofilm with the host immunoinflammatory response. Other than environmental factors, genetics, smoking, and nutritional factors also modify the host response and are responsible for the progression of periodontitis.[21] Balanced diet plays an important role in the maintenance of health of the periodontium and its surrounding structures, in fact the overall health. Nutritional deficiencies are an important risk factors for periodontitis. They mainly affect the proper functioning of the immune system of the body, ultimately resulting in progression of periodontitis.

Minerals have been classified as major minerals (>100 mg/day) or as trace minerals (<100 mg/day). The major minerals are sodium (Na), potassium (K), calcium (Ca), magnesium (Mg), phosphorus (P), and sulfur (S) while the trace minerals are iron (Fe), zinc (Zn), selenium (Se), copper (Cu), iodine (I), fluoride (F), cobalt (Co), chromium (Cr), manganese (Mn), and molybdenum (Mo).[1] Trace elements are imperative for optimum host response. Their consumption in larger quantities or lesser in diet is potentially dangerous to well-being of the periodontium.[21]

The role of zinc in periodontitis is mainly related to its influence on oral mucosa, bone metabolism, and host response. Animal studies have revealed that dietary deficiency of Zn leads to poorer periodontal health. It alters the thickness and keratinization of oral mucosa which becomes more susceptible to infections. Furthermore, deeper periodontal pockets and thicker palatal tissues have been reported in Zn-deficient rats.[9],[22]

Zn deficiency also affects the functioning of immune cells such as monocytes (all functions), natural killer cells (reduced cytotoxicity), neutrophils (reduced phagocytosis), T-cells, and lymphocytes (decreased apoptosis).[23] Furthermore, it increases the secretion of pro-inflammatory cytokines. It is an integral component of antioxidant enzymes and its altered levels result in the generation of oxidative stress. While the deficiency leads to reduced protection of sulfhydryl groups and increased production of reactive oxygen species (ROS), excessive levels may act as pro-oxidant by eliciting a decline in erythrocyte Copper-Zinc-Superoxide dismutase. This enzyme has been localized in the human periodontal ligament where it prevents free radical-induced damage.[24],[25] Therefore, its optimum levels are a prerequisite to maintain the tissues in a healthy state. Zinc acts as an antioxidant to decrease oxidative stress.[26] Potential mechanisms of zinc's antioxidant function may be related to several factors. First, zinc is an essential component of the cell's first lines of defense against ROS, which functions to remove the superoxide anion. The second potential mechanism for zinc's antioxidant effects is the antagonism of redox-active transition metals, such as iron or copper, and the prevention of oxidation of sulfhydryl groups within proteins. A third mechanism by which zinc acts as an antioxidant is through its regulation of metallothionein metabolism.[27] Zinc has a known action on the metalloenzymes, since it participates in their structure, and catalytic and regulatory action.[28] Zinc includes all enzyme classes and many of them participate in a variety of metabolic processes, such as synthesis and/or degradation of lipids, carbohydrates, proteins, and nucleic acids. Zinc is known to be present in appreciable amounts in cell nuclei, nucleoli, chromosomes, ribosomes, and secretory granules.

In the present study, serum zinc levels and serum magnesium levels were significantly altered in Group II as compared to healthy group (Zn = 62.10 + 18.76 μg/dl, Mg = 1.30 + 0.78 mEq/L). Magnesium and zinc are reported to possess antioxidant property. Magnesium is a critical element that catalyzes the enzymatic reactions in all phosphate transfer reactions through the formation of Mg-adenosine triphosphate complexes. Antioxidants catalyze the breakdown of ROS and also have protective cellular functions when blood glucose levels are high.[29] Thus, when the oxidative stress is increased, the magnesium and zinc levels in the body may be depleted as both of them are utilized by the body to their maximum levels to combat the oxidative stress generated. This can be one of the reasons that the serum magnesium as well as serum zinc levels in the present study are significantly lesser in Group II, i.e., CP cases.

The results of the present study for serum zinc levels were in accordance with the studies carried out by Thomas et al.,[18] Thomas et al.[8] Thomas et al. evaluated the serum levels of zinc, copper, and iron in periodontitis cases with and without type 2 diabetes mellitus. The results showed that the serum zinc levels were lowered in CP cases as compared to healthy control group.[8] The authors associated zinc deficiencies and increased levels of copper and iron with increased oxidative stress along with an altered immune response which could lead to various diabetic complications including periodontitis.[8]

On the contrary, studies performed by Pushparani et al.,[5] Pushparani,[30] and Pushparani [31] showed increased serum zinc levels in CP cases as compared to healthy control group. The exact causes for the above observations are not been mentioned.

The results of the present study for serum magnesium levels were in accordance with the studies carried out by Pushparani et al.[5] and Agrawal et al.[27] considering CP and healthy control groups only. In their study, they observed that concentration of magnesium decreased slightly but was nonsignificant in CP cases. They found that as the disease progresses, magnesium levels were decreased. Pushparani et al.[5] evaluated serum zinc and magnesium concentrations in type 2 diabetes mellitus patients with periodontitis. The researchers observed that as the disease progresses with CP, the magnesium level was found to be decreased more significantly, indicating that the diabetic individuals who develop periodontitis are more prone to diabetic complications.


  1. This study is limited by its cross-sectional design; the association of magnesium and zinc with CP cannot be proved with confidence. Several years of follow-up is necessary to detect long-term effects of magnesium and zinc on chronic diseases such as CP
  2. For more appropriate conclusions, studies with larger sample size should be carried out.

   Conclusion Top

The mean serum magnesium and serum zinc levels were significantly altered in CP cases as compared to healthy controls. The levels were found to be significantly less in diseased individuals. This study has also depicted that altered serum magnesium and zinc levels in CP cases emphasis on inflammatory nature of periodontal diseases and possible systemic effects of periodontal infection on biological molecules of the body.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Schifferle RE. Periodontal disease and nutrition: Separating the evidence from current fads. Periodontol 2000 2009;50:78-89.  Back to cited text no. 1
Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ, et al. Dietary Vitamin C and the risk for periodontal disease. J Periodontol 2000;71:1215-23.  Back to cited text no. 2
Petersen PE, Ogawa H. Strengthening the prevention of periodontal disease: The WHO approach. J Periodontol 2005;76:2187-93.  Back to cited text no. 3
Bathla S. Effects of systemic factors over the periodontium. In: Periodontics Revisited. 1st ed. New Delhi: JPBMP; 2011. p. 107-10.  Back to cited text no. 4
Pushparani DS, Anandan SN, Theagarayan P. Serum zinc and magnesium concentrations in type 2 diabetes mellitus with periodontitis. J Indian Soc Periodontol 2014;18:187-93.  Back to cited text no. 5
[PUBMED]  [Full text]  
Yamaguchi M, Weitzmann MN. Zinc stimulates osteoblastogenesis and suppresses osteoclastogenesis by antagonizing NF-jB activation. Mol Cell Biochem 2011;355:179-86.  Back to cited text no. 6
Paolisso G, Barbagallo M. Hypertension, diabetes mellitus and insulin resistance. The role of intracellular magnesium. Am J Hypertens 1997;10:346-55.  Back to cited text no. 7
Thomas B, Gautam A, Prasad BR, Kumari S. Evaluation of micronutrient (zinc, copper and iron) levels in periodontitis patients with and without diabetes mellitus type 2: A biochemical study. Indian J Dent Res 2013;24:468-73.  Back to cited text no. 8
[PUBMED]  [Full text]  
Orbak R, Kara C, Ozbek E, Tezel A, Demir T. Effects of zinc deficiency on oral and periodontal diseases in rats. J Periodontal Res 2007;42:138-43.  Back to cited text no. 9
Hans CP, Sialy R, Bansal D. Magnesium deficiency and diabetes mellitus 2. Curr Sci 2002;83:1456-63.  Back to cited text no. 10
Corica F, Corsonello A, Ientile R, Cucinotta D, Di Benedetto A, Perticone F, et al. Serum ionized magnesium levels in relation to metabolic syndrome in type 2 diabetic patients. J Am Coll Nutr 2006;25:210-5.  Back to cited text no. 11
Guerrero-Romero F, Rodriguez-Moran M. Low serum magnesium levels and metabolic syndrome. Acta Diabetol 2002;39:209-13.  Back to cited text no. 12
Staudte H, Kranz S, Völpel A, Schütze J, Sigusch BW. Comparison of nutrient intake between patients with periodontitis and healthy subjects. Quintessence Int 2012;43:907-16.  Back to cited text no. 13
Meisel P, Schwahn C, Luedemann J, John U, Kroemer HK, Kocher T, et al. Magnesium deficiency is associated with periodontal disease. J Dent Res 2005;84:937-41.  Back to cited text no. 14
Willershausen B, Ross A, Försch M, Willershausen I, Mohaupt P, Callaway A, et al. The influence of micronutrients on oral and general health. Eur J Med Res 2011;16:514-8.  Back to cited text no. 15
Loe H, Theilade E, Jensen S. Experimental gingivitis in man. J Periodontol 1965;36:177-87.  Back to cited text no. 16
Loe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontologica Scandinavica 1963;21:533-51.  Back to cited text no. 17
Thomas B, Kumari S, Ramitha K, Ashwini Kumari MB. Comparative evaluation of micronutrient status in the serum of diabetes mellitus patients and healthy individuals with periodontitis. J Indian Soc Periodontol 2010;14:46-9.  Back to cited text no. 18
[PUBMED]  [Full text]  
Zinc Kit [Kit Insert]. Goa (India): Crest Biosystems. A Division of Coral Clinical Systems; 2013.  Back to cited text no. 19
Magnesium Kit [Kit insert]. Goa (India): Crest Biosystems. A Division of Coral Clinical Systems; 2013.  Back to cited text no. 20
Gaur S, Agnihotri R. Trace mineral micronutrients and chronic periodontitis – A review. Biol Trace Elem Res 2017;176:225-38.  Back to cited text no. 21
Seyedmajidi SA, Seyedmajidi M, Moghadamnia A. Effect of zinc-deficient diet on oral tissues and periodontal indices in rats. Int J Mol Cell Med 2014;3:81-7.  Back to cited text no. 22
Meunier N, O'Connor JM, Maiani G, Cashman KD, Secker DL, Ferry M, et al. Importance of zinc in the elderly: The ZENITH study. Eur J Clin Nutr 2005;59 Suppl 2:S1-4.  Back to cited text no. 23
Bettger WJ. Zinc and selenium, site specific vs. general antioxidant. Can J Physiol Pharmacol 1993;71:721-4.  Back to cited text no. 24
Jacoby BH, Davis WL. The electron microscopic immunolocalization of a copper-zinc superoxide dismutase in association with collagen fibers of periodontal soft tissues. J Periodontol 1991;62:413-20.  Back to cited text no. 25
Torzewski M, Suriyaphol P, Paprotka K, Spath L, Ochsenhirt V, Schmitt A, et al. Enzymatic modification of low-density lipoprotein in the arterial wall: A new role for plasmin and matrix metalloproteinases in atherogenesis. Arterioscler Thromb Vasc Biol 2004;24:2130-6.  Back to cited text no. 26
Agrawal P, Arora S, Singh B, Manamalli A, Dolia PB. Association of macrovascular complications of type 2 diabetes mellitus with serum magnesium levels. Diabetes Metab Syndr Clin Res Rev 2011;5:41-4.  Back to cited text no. 27
Klotz LO, Kröncke KD, Buchczyk DP, Sies H. Role of copper, zinc, selenium and tellurium in the cellular defense against oxidative and nitrosative stress. J Nutr 2003;133:1448-51.  Back to cited text no. 28
Anderson RA, Roussel AM, Zouari N, Mahjoub S, Matheau JM, Kerkeni A. Potential antioxidant effects of zinc and chromium supplementation in people with type 2 diabetes mellitus. J Am Coll Nutr 2001;20:212-8.  Back to cited text no. 29
Pushparani DS. Influence of serum zinc on calcium, iron and magnesium levels in type 2 diabetes mellitus with periodontitis. Int J PharmTech Res 2015;8:112-9.  Back to cited text no. 30
Pushparani DS. Low serum zinc and increased acid phosphatase activity in type 2 diabetes mellitus with periodontitis subjects. Biochem Pharmacol (Los Angel) 2015;4:162.  Back to cited text no. 31


  [Table 1], [Table 2]

This article has been cited by
1 Inflammatory Responses in Periodontitis with or Without Rheumatoid Arthritis Alter Salivary Metallothionein and Zinc
Jazli Aziz, Rathna Devi Vaithilingam, Zamri Radzi, Mohammad Tariqur Rahman
Biological Trace Element Research. 2022;
[Pubmed] | [DOI]
2 Dysregulation of metallothionein and zinc aggravates periodontal diseases
Jazli Aziz,Mohammad Tariqur Rahman,Rathna Devi Vaithilingam
Journal of Trace Elements in Medicine and Biology. 2021; 66: 126754
[Pubmed] | [DOI]
3 Micronutrients and bioactive compounds in oral inflammatory diseases
Kiranjit Kaur,Dean Sculley,Janet Wallace,Alexandria Turner,Celeste Ferraris,Martin Veysey,Mark Lucock,Emma L. Beckett
Journal of Nutrition & Intermediary Metabolism. 2019; : 100105
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
    Materials and Me...
    Article Tables

 Article Access Statistics
    PDF Downloaded282    
    Comments [Add]    
    Cited by others 3    

Recommend this journal