Introduction

Childhood obesity is an overweight condition that is caused by deposition of disproportionate fats in the body. This situation is primarily caused by poor feeding habits that result in immediate effects on a child’s health. These effects can be physical, mental, and/or biological. Deficiency of various nutrients can lead to nutritional conditions that are detrimental to children’s wellbeing.

Nonetheless, nutritional problems have significantly increased amongst children worldwide. Iron deficiency is a condition that is closely linked to childhood obesity. Various findings show that sedentary life, high calorie intake, and hereditary factors are the main causes of iron deficiency and obesity. This essay provides critical examination of the evidence of association between iron deficiency and childhood obesity.

Formulation of the Research Problem

Iron deficiency is caused by poor nutrition, starvation, and/or loss of blood among other factors that lead to deprivation of iron. However, other underlying health conditions may also lead to iron deficiency (British Nutrition Foundation, 2005).

Nonetheless, the two conditions are treated differently because the information that is available to show their relatedness is inadequate. Medical practitioners and professionals also fear that combined treatment can pose serious effects to patients who suffer from both conditions. This situation has led to controversial debates about the relationship between iron deficiency and child obesity amongst health practitioners worldwide.

Numerous researchers have inconclusively shown that iron deficiency and childhood obesity are interrelated. According to this claim, the two conditions can occur simultaneously. Various surveys have also shown that obese patients are vulnerable to increased iron deficiency. As a result, they easily succumb to detrimental healthy conditions.

Wenzel, Stults, and Mayer (1962) documented their findings on the relationship between iron deficiency and obesity amongst children following an extensive research to determine predisposing factors of the two conditions amongst obese and normal children. According to the research, there is a relationship between the two conditions. Reduction of iron concentration is evident amongst obese children.

However, this case is not observed in normal children. Nonetheless, this conclusion was unfeasible. However, the study has compelled many health researchers to hypothesise that sedentary life conditions have increased the number of obese patients due decreased physical activity.

Physical inactivity results in reduced myoglobin in the muscles. Eventually, this situation results in iron deficiency. Therefore, there is a need to devise mechanisms that are more robust to establish the association between iron deficiency and childhood obesity

Consumption of excess calories and fats inhibit absorption of various nutrients such as iron and calcium in the body. The occurrence of iron deficiency in obese children is a critical phenomenon that requires immediate attention. Various studies continue to underpin existing knowledge about the relationship between iron deficiency and childhood obesity.

However, there is a need to clarify the relatedness of the two disorders through broad research. A study that was conducted by Yanoff et al. (2007) revealed that there exists a relationship amongst obesity, adipose tissue inflammation, anaemia inflammation, hypoferraemia, and increased serum ferritin. The hepcidin hormone hinders iron uptake in the duodenum. This situation results in utilisation of iron that is stored in the body reserves.

Genetically, nucleotide polymorphisms (SNP) are identified as regulators of hepcidin hormones and iron marker concentration (Benyamin et al., 2009). Some SNPs are associated with iron conditions of the body. Individuals who have low SNP concentration have limited iron markers such as serum iron. Contrarily, these people possess large amount of hepcidins; hence, they always suffer from iron deficiency (Benyamin et al., 2009).

Although iron deficiency is depicted in obese children, only a few studies have been conducted to expound on the mechanisms and factors that contribute to iron deficiency as obesity intensifies. Some studies have also limited their research designs to selection of samples that do not represent the study populations.

For instance, many researchers have suggested weight loss methods such as meal restriction to reduce iron intake. They also advocate for surgical remedies for obesity (Tussing-Humphreys et al., 2010). Therefore, new research is required to establish mechanisms that increase iron intake in obese children in an attempt to curtail iron deficiency problems that are linked to SNP effects on iron conditions

Relevant Approaches to Enhance the Topic

An alternative approach that can used to research more information about the relationship between iron deficiency and obesity is explicit exploration of hepcidin concentration.

This approach entails assessment of processes such as iron uptake, protein, and haem iron intake in a restricted dieting with reference to the SNPs of obese children. This research aims at examining the evidences of association between iron deficiency and childhood obesity through the following criteria.

  1. Examination of hepcidin concentration in a given sample of children
  2. Systematic review of the relationship between iron deficiency and obesity
  3. Investigation of the influence of SNP on iron concentration in children

Existing Literature on Iron Deficiency and Childhood Obesity

Numerous studies indicate that iron deficiency is more prevalent amongst obese children. However, most of the studies are speculative; hence, the association between obesity and iron deficiency has remained unclear amongst many scholars, medical practitioners, and professionals.

Nonetheless, a recent research that was conducted by the International Obesity Task Force (IOTF) shows that childhood obesity is most common in westernised countries (Lobstein & Jackson, 2004). According to the IOTF criteria, about 10-percent of children whose age lies between 5 and 17 years are overweight.

About 3-percent of these overweight children are obese (Lobstein & Jackson, 2004). Between 5 to 20-percent are occurrences in Africa and Asia. However, Europe accounts for 20-percent while American and the Middle East countries account for over 30-percent (Lobstein & Jackson, 2004).

Current Information about Obesity and Iron Deficiency in Children

A lot of information shows that obesity is related to over-nutrition that results in overweight. On the other hand, under-nutrition results in anemia that is links to inadequate intake of nutritional requirements such as iron.

It is evident that overweight individuals lack iron due to intake of foods that have insufficient iron content, impartial, and/or decreased absorption of iron in the body, and dilutional hypoferremia.

Various clinical reports show that most of the obese patients develop inflammations due to hepcidin hormones. These inflammations disrupt iron absorption in the body; hence, lead to iron deficiency (Wang et al., 2007).

Nutrition

Human health is directly related to nutrition and human development. Nutrition enables the body to acquire essential nutrients in correct proportions. This process enhances various developmental stages that range from infancy, childhood, adolescence, and adult to old age. Several organisations that include the World Health Organisation (WHO) have confirmed that nutrition is as important as right life itself and other freedoms.

Besides provision of satiety when food is eaten in times of hunger, it enables the body to gain protection by fighting against illnesses (World Health Organisation, 2008). Therefore, individuals need to feed on adequate food that is regarded as balanced diet to supply the body with the required nutrients.

Iron Deficiency in Children

Anaemia is a global problem that is caused by deficiency of iron in the body (World Health Organisation, 2008). Iron deficiency has increasingly become a trending health issue in both developed and developing nations.

Iron and vitamin B12 are vital for production of erythrocytes that promote transportation of oxygen throughout the body. Foods such as meat, dried fruits, grains, spinach, and soya beans among others are rich in iron (British Nutrition Foundation, 2005).

According to the World Health Organisation (2008), iron prevalence is highest amongst preschool children and expectant mothers in developing nations. The number of children who are obese is approximately 40-percent in industrialised nations.

An Australian study revealed that about 20-percent of young girls whose age lies between 14 and 18 years were either anaemic or had lower iron content in their bodies (Ahmed, Coyne, Dobson, & McClintock, 2008). Another report that was released by WHO revealed that anaemia is also common amongst young girls who experience early pregnancy (National Health and Medical Research Council, 2006).

Iron deficiency has negative influence on children’s growth, behaviour, and cognitive development. It is also responsible for deterioration of physical activity, work performance, and functioning of the immune system (World Health Organisation, 2008).

In addition, iron deficiency causes cognitive problems. A recent research reveals that impairment of cognitive performance in children is mainly caused by iron deficiency (Perez et al., 2005). Maternal iron deficiency can affect both the health of prospective mothers and foetus. In this case, the mother faces a high risk of experiencing pre-term delivery, post-partum depression, and impending poor mother-child interaction (Perez et al., 2005).

Children who are born of iron deficient mothers are susceptible to fat deposition metabolism syndrome, cardiovascular problems, and delayed cognitive development. Therefore, it is crucial to maintain proper regulation of iron in the bodies of expectant mothers (Perez et al., 2005).

Assessment of Iron

Many clinicians conduct thorough assessment of iron in patients. Assessment criteria include check-ups on the levels of haemoglobin, serum iron, saturation of transferring, iron total binding capacity, and serum ferritin to indicate the iron content in the body of a patient (Wians, Urban, Keffer, & Kroft, 2001).

However, complication arises when level of iron in the body of the patient is too insufficient to support clinical assessment. In this case, a need to seek the attention of a physician arises. Iron deficiency can occur when the body experiences exhaustion of iron that is available in the reserves, a situation that results in reduction of serum ferritin.

This condition is referred to as stage I iron deficiency. After the iron in the reserves is depleted, stage I progresses to stage II iron deficiency. This situation results in erythropoiesis that reduces serum iron and transfer concentration; hence, it results in imbalance of iron in the body (Wians et al., 2001).

Pathomechanisms in Relation to Obesity

Obesity is directly linked to adipose tissues, which are fat deposit localities. Adipose tissues of obese children contain macrophage and cytokines. In the adipose tissues, adipokines transform to obese phenotype (Mather & Goldberg, 2014).

Adiponekines produce adiponectin, which are responsible for activation of insulin and prevention of inflammatory conditions. Concentrations are decreased as obesity increases (Mather & Goldberg, 2014). This situation results in increased insulin resistance in the body of the patient.

Leptin, an enzyme that is responsible for fullness, is absent in obese children. Absence of leptin causes obese children to develop unending eating habits. This situation leads to increased and/or abnormal production of resisting hormones that enhance inflammation of the adipose tissue.

This condition results further enhances obesity (DePaoli, 2014). Eventually, increased inflammation of adipose tissues generates serious consequences in the liver. As a result, regulation of iron homeostasis is disrupted. This situation leads to iron deficiency in the body of the child.

Poor Metabolism of Iron in Obese Patients

Studies have shown that obese children experience improper metabolism of iron due to the inability of the intestines to absorb iron (Zimmermann et al., 2008). The bodies of such children are characterised by low absorption of iron because of obesity.

Therefore, decreased iron absorption that leads to deficiency of iron amongst the obese children is highly linked to overweightness. Inflammatory conditions that are observed in the obese children result in higher concentration of hepcidin hormone that is crucial for iron metabolism. However, high amount of hepcidins inhibit functionality of duodenum to enhance absorption of iron. This situation results in deficiency of iron (del Giudice et al., 2009).

Presence of erythroid, an erythropoietin precursor, enables production of blood. However, the presence of inflammatory cytokines can lead to interference of erythropoietin production due to inhibition of response by the erythroids. In most cases, this state of affairs leads to anaemic conditions in obese patients (Sonnweber et al., 2012).

Obese children have substantial fat deposits in their bodies. Iron absorption mechanisms perform poorly in the presence of fat deposits. As a result, iron absorption in the duodenum can be hindered. Eventually, iron deficiency occurs (Sonnweber, et al., 2012).

Iron Deficiency and Obesity due to Inflammatory Cases

There are two cases of inflammations. The first case usually occurs in the adipose tissues of obese patients. The second case is related to anaemia. It is known as anaemia of inflammation. In both cases inflammation, hypoferraemia, and serum concentration are examined (del Giudice et al., 2009). Numerous researchers allude that both cases are similar.

This conclusion is contradictive because two different mechanisms that occur under different processes cannot be similar irrespective of the fact that they generate same results. A study that was conducted by Yanoff et al. (2007) reveals that serum hepcidins in obese children generates the differences between the two conditions. Hepticidin elevation is one of the differences that occur.

However, the scales of elevation differ in both cases. Researchers have noted that hepcidin concentration is higher in obese children than in normal children (Yanoff et al., 2007). Analysis of these differences indicates that anaemia inflammation and obesity are characterised by unequal iron levels.

Patients with anaemic inflammation experience iron deficiencies because there is redistribution of iron into other cells within their bodies (Tussing-Humphreys et al., 2010). Furthermore, there is continual use of iron that is stored in the bodies of obese patients. The liver metabolises large amounts of iron as compared to the duodenum (Yanoff et al., 2007).

High amounts of hepcidins in obese patients prevent the duodenum from absorption of iron. Instead, these hormones enhance utilisation of iron that is stored in the reserves. Unregulated utilisation of iron results in its depletion. As a result, the obese child experiences iron deficiency.

Although there are many differences that are realised between anaemic inflammatory and obesity, some researchers claim that no hepcidin hormones are found in abdominal subcutaneous adipose tissues of both obese and normal patients (del Giudice et al., 2009). Therefore, there is a need to initiate further research on iron deficiency in relation to obesity to clarify on the already existing information.

Three Studies that have been selected on the Topic

A critical analysis of the following studies enabled the researcher to understand the concepts and relationships between iron deficiency and childhood obesity.

The relationship between Obesity and Hypoferraemia in Adult (Cross-section vs. Longitudinal vs. Randomised Trial Control vs. Case Controlled )

The samples used for this study were recruited on the following criteria. Firstly, the study involved non-expectant mothers and lactating participants who had 18 years and above. The study considered a BMI index of 30Kg/m2 or above (Cheng et al., 2012).

The ranges of the ages and BMI were not given. Study hypotheses were acceptable if the mean age and BMI were found to be greater than 18 years and 30 kg/m2 respectively. In addition, the researcher only accepted participants who underwent bariatric surgery and showed reduction in weight. Those who had attended the bariatric surgery before the research were not accepted.

Several study designs were applied in this study. For instance, 12 participants who were not included in the bariatric surgery were categorised into various groups.

7 of the participants were subjected to cross-sectional study design, 2 participants were case-controlled, and 3 participants were subjected to longitudinal intervention. Out of 19 bariatric surgeries, 3 surgeries were cross-sectional, 11 surgeries were longitudinal, 3 surgeries were retrospective, and 2 surgeries were randomly controlled trials.

Both qualitative and quantitative techniques were applied. For example, use of physical examination that involved actual measurements of anthropometric values and chemical analysis was crucial for this experiment. Qualitatively, the study involved recording of general health descriptions of participants. Individuals who were not under medication were perceived as healthy (Harbour & Miller, 2001).

However, there are confusions that arose in the course of the study, especially during assessment of methodology that was being used. For example, most of the participants were unable to meet three out of five quality items.

Most of the bariatric surgeries were substandard and only 5-percent of these met at least three quality items (Tussing-Humphreys et al., 2010). Mix-ups were also realised in demographic information such as age, gender, menopausal status, and ethnicity among other factors.

Some participants were excluded due to complications such as anaemia and high or low ferritin. This situation resulted in biased outcome. Biomarkers were used to assess iron statuses of the participants. Their use led to underestimation of iron deficiency due to presence of concentrated serum ferritin in obese participants.

The study was characterised by heterogeneous selection criteria and laboratory procedures (Cortese & Angriman, 2014). As a result, meta-analysis of obtaining mean differences became unsatisfactory. Therefore, the results lacked authenticity (Cheng et al., 2013).

Iron, Hepcidin Inflammatory Status of Obese, and Overweight in Young Women (Cross-Sectional Study Design)

This study entailed a cross-sectional design that involved analyses of iron, anaemic inflammatory, and Hepcidin hormone statuses of obese and overweight young women. According to the study, the group of healthy women whose age lied between 14 and18 years had a BMI measure of ≥27.5 kg/m2 (Cheng et al., 2012).

Conceptualisation of the study designs was realised through inclusion and exclusion procedures that used various databases. The researcher collected data through selection of the best samples that comprised 54-percent of the study population. Biochemical analyses were accomplished using Enzyme-Linked Immunosorbent Assay (ELISA).

Study samples were analysed through biochemical analysis in a bid to generate plots and interpretations. The results were approved through critical peer appraisal. The study evidenced that there were higher haemoglobin and ferritin concentrations in obese individuals than in the health participants. The researchers also alluded that an alteration of iron biomarkers in obese population results from inflammations related to obesity (Cheng et al., 2012).

However, I contradict this conclusion based on the researchers’ inability to acquire sufficient data to guarantee a successful study. Furthermore, the researchers did not elaborate on the methods that they used to come up with measurements of cytokine that were available in adipose tissues of the participants’ bodies. Conclusions are not based on mere assumptions.

Although the researcher elaborates on the quality of methodology, there are still unanswered questions about the number of reviewers who assessed the processes through epidemiological checklists. These items change with time.

The probability of obtaining exact information and accurate anthropometric measures through administration of questionnaires is low. Biasness was also inevitable since cross-sectional designs are applied in situations where an item within a group of sample develops abnormality after selection. In this case, it is uncertain whether the questionnaire caused biasness based on ethnicity or other discriminating traits.

A Candidate Gene Approach to Identifying Differential Iron Responses of Overweight and Obese children to an Energy-Restricted Haem Iron-Rich Diet (Longitudinal Research Design)

The research involved a longitudinal study of children who followed monitored diets in an attempt to reduce their obese conditions and were still suffering from iron deficiency. The longitudinal approach was used to examine genetic polymorphism that occurs due to iron metabolism (Barker, Langenberg, & Wareham, 2012).

A sample of obese children with high-protein and high haem iron verses children with low-protein and low-haem iron were examined for a period of 12 months. Participants with heterozygous or homozygous T allele had lower serum iron and higher Hepcidin than participants who had homozygous alternative C allele at the base level (Knutson, 2009).

Individuals who had T allele heterozygote and homozygote did not maintain healthy serum iron and protein levels. An iron-lowering effect was confirmed in T allele in both serum iron and Hepcidin at the baseline. Therefore, the longitudinal study provides an appropriate approach to examine the relationship between iron deficiency and childhood obesity since it is based on procedural experiments.

In-depth understanding of genes also requires longitudinal examination. For instance, some participants had both copies of T allele. However, when they were subjected to higher-protein, higher iron (HPHI) diet, they showed lower serum iron and transferring saturation in 12 months than those who were given low-protein, low-haem iron diets (LPLI) (Traglia et al., 2011).

However, longitudinal studies have various limitations such as absence of clinical rationale. In addition, such studies focus on genetic analysis. In this case, the participants were so few to guarantee substantial chemical variations.

Methodology

Literature Search

A review of literature will be conducted on previous examinations of the evidence of association between iron deficiency and childhood obesity. Information will be obtained through systematic analysis, observation, and snowballing processes that include sources such as journals and internet academic tools.

Furthermore, information will be received from professionals such as nutritionists, paediatrics, and doctors in health facilities and relevant organisations that deal with nutritional health.

According to the initial search, a correlation framework that gives a brief summary of the relationship between iron deficiency and childhood obesity will be designed. Various key terms that will be relevant to this topic are iron deficiency, obesity, childhood, overweight, and adipose tissue inflammatory conditions.

Study Design

Both randomly controlled trial technique and systematic analysis design will be used to collect data (Habour & Miller, 2001). A review will cover broader area of the topic. However, it will not be exclusively limited to qualitative and quantitative techniques. It will analyse the evidences of the relationship between iron deficiency and childhood obesity.

The study will review most of current assessment techniques and will combine both systematic and randomly controlled trial techniques; hence, the study design will be unique (Habour & Miller, 2001). The research will focus on measurement of both specific repercussions and literary publications with a view of providing up-to-date information that will enhance understanding of iron deficiency in childhood obesity.

Current Ethical Issues that Regulate Research

The study will be registered under a relevant authority. In addition, the ethics committee of the health service of the area under study and the university’s ethics committee will approve the study. An informed consent form will be administered to participants to append their signatures.

The sample researches that are elaborated above followed the same criteria. For example, some of the researchers had registered their studies with the Australian New Zealand Clinical Trials Registry. The studies had also complied with certain ethical standards of Health Service Ethics Committee and ethics of other institutions that were involved.

Other Research Designs and Contribution

Cross-sectional design

Cross-sectional study design is a descriptive approach to research that assumes the form of a survey. This method enables a researcher to describe characteristic of specific subgroups; hence, it is appropriate for the study (Habour & Miller, 2001).

It focuses on a given group of samples. Furthermore, it can be used to investigate the relationship between a given risk factor and its outcome. Therefore, it is can be used to identify the prevalence of iron deficiency amongst obese children.

Cross-sectional design serves as an essential to method to generate hypotheses for future use. The design technique is also inexpensive (Habour & Miller, 2001). Assessment of outcome and risk factors are also easier. Last yet importantly, this study design eases understanding of disease aetiology; thus, it enhances public health planning.

Epistemological Appreciation of Quantitative and Qualitative Designs Used

The epistemological position of the qualitative design is majorly theoretical. At the outset, demographic data such as gender, age, and history of health are passed to the researcher by word of mouth (Stacy & Miles, 2007). These are fictions because parents can fail to notice certain abnormal conditions of their children that can warrant medication.

Therefore, this method only provides information that is based on assumptions. Most researches that pertain to health are based on minimal practice since they are expensive to undertake.

This situation implies that there is lack of understanding of the significance of qualitative research. Therefore, a quantitative design is a sure way of obtaining facts since biochemical laboratory procedures provide real results whilst minimising errors (Stacy & Miles, 2007).

Conclusion

In the light of this essay, many researchers have endeavoured to establish the relationship between iron deficiency and obesity. In spite of the different ideologies that have been used to study the relationship between the two conditions, no single research has ever established a harmonious conclusion.

Many research methods encounter difficulties that hinder realisation of the association between the two conditions. For instance, although the longitudinal approach provides realistic results, it lacks clinical rationale. However, longitudinal studies have various limitations such as absence of clinical rationale.

Its focus on genetic analysis does not guarantee substantial chemical variations that can be used to evaluate how iron deficiency relates to childhood obesity. Different approaches have also been applied in research to provide deeper understanding not only in separate study of obesity and iron deficiency but also to conduct collective examination of the two conditions.

However, there is a need to focus on longitudinal research. As aforementioned, this research design is a combination of two research designs that include randomised controlled technique and systematic analysis design. It provides knowledge-based research that is required in this topic.

However, researchers can also use cross-sectional examination design since it enables examination of the relationships between relevant risk factors and outcomes. As a result, it is suitable for examination of commonness of iron deficiency amongst obese children.

Reference List

Ahmed, F., Coyne, T., Dobson, A., & McClintock, C. (2008). Iron status among Australian adults: findings of a population based study in Queensland, Australia. Asia Pacific Journal of Clinical Nutrition, 17(1), 40-7.

Barker, A., Langenberg, C., & Wareham, N. (2012). Genetic determinants of glucose homeostasis. Genetics of Metabolism and Diabetes, Best Practice & Research Clinical Endocrinology & Metabolism, 26(2), 159-70.

Benyamin, B., Ferreira, M., Willemsen, G., Gordon, S., Middelberg, R., McEvoy, B.,…Hottenga, J. (2009). Common variants in TMPRSS6 are associated with iron status and erythrocyte volume. Nature Genetics, 41(11), 1173-5.

British Nutrition Foundation. (2005). Nutrient requirements and recommendations.

Cortese, S., & Angriman, M. (2014). Attention-deficit/hyperactivity disorder, iron deficiency, and obesity: is there a link? Postgraduate Medicine, 126(4), 155-70.

Cheng, H., Griffin, J., Bryant, C., Rooney, K., Steinbeck, K., & O’Connor, H. (2013). Impact of diet and weight loss on iron and zinc status in overweight and obese young women. Asian Pacific Journal of Clinical Nutrition, 22(4), 574-82.

del Giudice, E., Santoro, N., Amato, A., Brienza, C., Calabro, P., Wiegerinck, T.,…Cirillo, G. (2009). Hepcidin in obese children as a potential mediator of the association between obesity and iron deficiency. Journal of Clinical Endocrinology and Metabolism, 94(12), 5102-7.

DePaoli, A. (2014). Leptin in common obesity and associated disorders of metabolism. Journal of Endocrinol, 223(1), 71-81.

Harbour, R., & Miller, J. (2001). A new system for grading recommendations in evidence based guidelines. BMJ Journals, 323(7308), 334-6.

Knutson, D. (2009). Into the matrix: regulation of the iron regulatory hormone hepcidin by matriptase-2. Nutrition Reviews, 67(5), 284.

Lobstein, T., & Jackson-Leach, R. (2007). Child overweight and obesity in the USA: prevalence rates according to IOTF definitions. International Journal of Pediatric Obesity, 2(1), 62-4.

Mather, J., & Goldberg, R. (2014). Clinical use of adiponectin as a marker of metabolic dysregulation. Best Practice and Research. Clinical Endocrinology Metabolism, 28(1), 107-17.

National Health and Medical Research Council. (2006). Nutrient reference values for Australia and New Zealand including recommended dietary intakes. Canberra: Commonwealth of Australia.

Perez, E., Hendricks, M., Beard, J., Murray-Kolb, L., Berg, A., Tomlinson, M.,…Irlam, J. (2005). Mother-Infant Interactions and Infant Development Are Altered by Maternal Iron Deficiency Anemia. Journal of Nutrition, 135(4), 850-5.

Sonnweber, T., Ress, C., Nairz, M., Theurl, I., Schroll, A., Murphy, T.,…Wroblewski, V. (2012). High-fat diet causes iron deficiency via hepcidin-independent reduction of duodenal iron absorption. The Journal of Nutritional Biochemistry, 23(10), 1600-8.

Stacy, C., & Miles, L. (2007). Justifying Knowledge, Justifying Method, Taking Action: Epistemologies, Methodologies, and Methods in Qualitative Research.

Traglia, M., Girelli, D., Biino, G., Campostrini, N., Corbella, M., Sala, C.,…Masciullo, C. (2011). Association of HFE and TMPRSS6 genetic variants with iron and erythrocyte parameters is only in part dependent on serum hepcidin concentrations. Journal of Medical Genetics, 48(9), 629-34.

Tussing-Humphreys, L., Nemeth, E., Fantuzzi, G., Freels, S., Holterman, A., Ayloo, S.,…Vitello, J. (2010). Decreased serum hepcidins and improved functional iron status 6 months after restrictive bariatric surgery. Obesity, 18(10), 2010-6.

Wang, Y., Lam, K., Kraegen, E., Sweeney, G., Zhang, J., Tso, A.,…Chow, W. (2007). Lipocalin-2 is an inflammatory marker closely associated with obesity, insulin resistance, and hyperglycemia in humans. American Association for Clinical Chemistry, 53(7), 34-41.

Wenzel, J., Stults, B., & Mayer, J. (1962).Hypoferraemia in obese adolescents. Lancet, 2(7251), 327-8.

Wians, H., Urban, E., Keffer, H., & Kroft, S. (2001). Discriminating between iron deficiency anemia and anemia of chronic disease using traditional indices of iron status vs transferring receptor concentration. American Journal of Clinical Pathology, 115(1), 112-8.

World Health Organisation. (2008).Worldwide prevalence of anaemia 1993-2005: WHO global database on anaemia. Geneva: World Health Organisation.

Yanoff, L., Menzie, C., Denkinger, B., Sebring, N., McHugh, T., Remaley, A., & Yanovski, J. (2007). Inflammation and iron deficiency in the hypoferremia of obesity. International Journal of Obesity, 31(9), 1412-9.

Zimmermann, B., Zeder, C., Muthayya, S., Winichagoon, P., Chaouki, N., Aeberli, I., & Hurrell, F. (2008). Adiposity in women and children from transition countries predicts decreased iron absorption, iron deficiency and a reduced response to iron fortification. International Journal of Obesity, 32(7), 1098–1104.

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