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",isbn:"978-1-83968-236-0",printIsbn:"978-1-83968-235-3",pdfIsbn:"978-1-83968-237-7",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"c85e82851e80b40282ff9be99ddf2046",bookSignature:"Dr. Rama Sashank Madhurapantula, Prof. Joseph Orgel P.R.O. and Ph.D. Zvi Loewy",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/8018.jpg",keywords:"Collagen, Proteoglycans, Arthritis, Congenital Diseases, Osteogenesis Imperfecta, Blood Vessels, ECM - Tissue Interfaces, Elasticity, Cartilage Implant, Bone Graft, Angiogenesis, Extracellular Triggers",numberOfDownloads:18,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"July 3rd 2020",dateEndSecondStepPublish:"July 24th 2020",dateEndThirdStepPublish:"September 22nd 2020",dateEndFourthStepPublish:"December 11th 2020",dateEndFifthStepPublish:"February 9th 2021",remainingDaysToSecondStep:"7 months",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:"Most recently, dr. Madhurapantula has been involved with developing microscopy techniques to establish macroscopic stress vs. strain relations in body tissues that present mixed tissue compositions, in conjunction with X-ray diffraction scanning techniques to establish tissue composition.",coeditorOneBiosketch:"Prof. Orgel is a multi-disciplinarian by research and professional practice with international name recognition in the collagen and connective tissue fields and in X-ray diffraction.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"212416",title:"Dr.",name:"Rama Sashank",middleName:null,surname:"Madhurapantula",slug:"rama-sashank-madhurapantula",fullName:"Rama Sashank Madhurapantula",profilePictureURL:"https://mts.intechopen.com/storage/users/212416/images/system/212416.jpg",biography:"Dr. Madhurapantula holds a Ph.D. in Biology from the Illinois Institute of Technology, Chicago, with a focus on the molecular structure and function of type I collagen. Since obtaining his Ph.D., he has worked on various ECM based research projects on understanding the structural aspects of various fibrous tissue assemblies in the human body, in non-disease and disease conditions. He is an expert in the field of in situ X-ray fiber diffraction. Most recently, he has been involved with developing microscopy techniques to establish macroscopic stress vs. strain relations in body tissues that present mixed tissue compositions, in conjunction with X-ray diffraction scanning techniques to establish tissue composition. These datasets together are being used to develop a high definition model of human heart valves with accurate stress-strain finite element models to improve the characteristics of these tissues in the CAVEMAN full human body simulation, which is further utilized in simulated blast and vehicular accident calculations, and to develop a simulated surgery apparatus to train surgeons.",institutionString:"Illinois Institute of Technology",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Illinois Institute of Technology",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:{id:"212413",title:"Prof.",name:"Joseph",middleName:null,surname:"Orgel P.R.O.",slug:"joseph-orgel-p.r.o.",fullName:"Joseph Orgel P.R.O.",profilePictureURL:"https://mts.intechopen.com/storage/users/no_image.jpg",biography:null,institutionString:"Illinois Institute of Technology",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Illinois Institute of Technology",institutionURL:null,country:{name:"United States of America"}}},coeditorTwo:{id:"235950",title:"Ph.D.",name:"Zvi",middleName:null,surname:"Loewy",slug:"zvi-loewy",fullName:"Zvi Loewy",profilePictureURL:"https://mts.intechopen.com/storage/users/235950/images/system/235950.png",biography:"Dr. Zvi Loewy, a senior academic leader and an experienced global pharmaceutical – biotechnology executive leverages a diversified background in big-pharma senior management, biotech startup creation and academia. \nDr. Loewy’s international experience has included leading international research teams; championing the commercial penetration of healthcare products in China; and leading open innovation in the Mid-East. \nDr. Loewy received his education at Rensselaer Polytechnic Institute and at the Albert Einstein College of Medicine. Dr. Loewy is on the faculty of the Touro College of Pharmacy and New York Medical College; is on the boards of the New Jersey Bioscience Incubator; and is an Editor of the Journal of Prosthodontics. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"56773",title:"Iron Deficiency Anemia in Children",doi:"10.5772/intechopen.69774",slug:"iron-deficiency-anemia-in-children",body:'Iron deficiency is the most common micronutrient deficiency worldwide and one of the most important public health problems, affecting approximately 25% of the world’s population according to the World Health Organization (WHO). Iron deficiency is the most common in preschool children and women of childbearing age, particularly in regions of Asia and Africa with poor access to iron-rich foods [1, 2]. There are lower rates of iron deficiency in developed countries such as the United States and other industrialized regions with healthy food rich in nutrients. However, the problem still exists and can have a great impact on mental and physical development, health maintenance, and the quality of life of affected children.
Approximately 8% of toddlers in the United States have iron deficiency, and 2–3% have iron deficiency anemia (IDA) [3]. As age increases, prevalence decreases until adolescence. Sixteen percent of adolescent girls have iron deficiency, and 3% have IDA [4]. Among American females aged 12–15 years, the incidence of iron deficiency was 9% and the incidence of IDA was 2%; in the age group 16–19 years, the incidence was 11 and 3%, respectively [5]. Less than 1% of adolescent males had iron deficiency. Higher incidence of iron deficiency was found in both male and female adolescents in some other countries [6, 7]. The rate of iron deficiency did not decline much during the last 40 years, but there were significant improvements in some subgroups of young children. For example, in children aged 12–24 months, iron deficiency rates declined from 23 to 11% between two study periods [3].
The prevalence of iron deficiency in the United States is higher in children who live in poverty, in low-income families, and in immigrant groups. The highest prevalence was shown in children with African-American and Hispanic origin [3, 8]. Other risk factors associated with higher prevalence of IDA are low birth weight, prematurity, and childhood obesity [3, 8, 9]. These high-risk pediatric subgroups should undergo screening.
Pinhas-Hamiel and co-workers showed that the prevalence of iron deficiency was significantly associated with increased body mass index (BMI) [10]. Obesity was a risk factor in both males and females, but it was about three times higher in girls [10, 11]. It is unclear why obesity is linked to iron deficiency and IDA, but low-quality foods and increased needs comparing to body weight may be connected.
Adolescent athletes, vegetarians, adolescents with chronic illnesses, heavy menstrual blood loss (>80 ml/month), or children who are underweighted or malnourished are at higher risk for iron deficiency and IDA, and they should also have laboratory screening for anemia [12, 13].
In developing countries, where diets do not contain sufficient red meat, IDA is approximately seven times more frequent than in Europe or North America. Despite the fact that there is enough dietary iron in some cases, this is the case because heme iron is absorbed better than nonheme iron. IDA was found in 2/3 of children and adolescents in Nepal and in Sudan [14], and in 48.5% of Egyptian children in 2005 [15]. Parasites like hookworm can worsen iron deficiency due to profound gastrointestinal blood loss.
Neonates have total body iron of 250 mg (80 mg/kg), obtained from maternal sources. In the first 6 months of life, during the period when the infant gets iron-deficient milk diet, this amount decreases to 60 mg/kg. Infants fed with cow’s milk are at greater risk to develop serious IDA because calcium from cow’s milk is competing with iron for absorption. Children should get 0.5 mg more iron than is lost daily in order to maintain a normal body iron of 60 mg/kg.
The prevalence of iron deficiency exceeds 50% in countries with limited food and nutrient sources, such as most countries in Africa, Southeast Asia, and Latin America [16]. The prevalence of anemia ranges from 45 to 65% in children, 20 to 60% in women, and 10 to 35% in men [1]. Half of these cases are presumed to be caused by iron deficiency.
The prevalence of IDA is still high in infancy and preschool children, despite improvements in public health awareness, increased breastfeeding rate, and the presence of iron-fortified foods in diet [17, 18]. All these facts emphasize the importance of constant surveillance and early detection, prevention, and intervention toward iron deficiency in childhood, particularly in high-risk groups. Special attention should be paid to discover and treat iron deficiency during pregnancy and the earliest periods of life, because severe iron deficiency can have a great impact on child’s growth, development, and learning skills.
Iron deficiency is a condition when the body lacks sufficient iron to maintain normal physiological functions. It is defined as decreased total body iron or, in some cases, by serum ferritin level <12 mg/l in children up to 5 years and <15 mg/l in children 5 years and older. Although the serum ferritin level is useful in defining iron deficiency, this definition can be considered only if other conditions that can affect ferritin levels (i.e., inflammation or liver disease) are absent. For children less than 5 years of age with concurrent infection, serum ferritin concentrations <30 mg/l are reflective of depleted iron stores [19].
Anemia is defined as a hemoglobin concentration more than 2 standard deviations below the mean reference value for age- and sex-matched healthy population. WHO hemoglobin thresholds used to define anemia in different age groups are [2]:
children 6 months to 5 years: 11 g/dl;
children 5–12 years: 11.5 g/dl;
children 12–15 years: 12 g/dl;
nonpregnant women: 12 g/dl;
pregnant women: 11 g/dl; and
men ≥15 years: 13 g/dl.
IDA develops when body iron is too low to maintain normal red blood cell (RBC) production. IDA in young children (up to 5 years) is defined as the presence of ferritin level <12 mg/l and hemoglobin level <11 g/dl, in the absence of other conditions that can affect these findings [20].
The terms “iron deficiency” and “IDA” are often used in the same context. However, iron deficiency without anemia is three times as common as IDA. If iron requirements are below iron intake, total body iron reduces gradually. Hemoglobin levels are initially normal, reflecting the stage when iron deficiency exists in the absence of anemia. At that point, ferritin level and transferrin saturation are reduced. As total body iron decreases and iron stores are exhausted, hemoglobin levels drop below normal values. Thus, iron deficiency is defined as reduced body iron but hemoglobin levels are still above the cut-off value for anemia. Worsening of that condition leads to iron-deficient erythropoiesis and finally to development of IDA.
Iron is an essential micronutrient in the human body. It plays an important role in many metabolic processes, such as oxygen transport, electron transport, and DNA synthesis. Iron is a component of many cellular proteins and enzymes. Heme proteins, hemoglobin and myoglobin, contain about 3/4 of total body iron. The rest of body iron is stored in ferritin and hemosiderin, and about 3% is part of enzyme systems, such as catalase and cytochromes [21]. Iron is mostly recycled from senescent RBCs by macrophages. Only a small proportion of total body iron enters and leaves the body on a daily basis. Consequently, mechanisms that affect intestinal absorption and intercellular iron transport have great impact on iron balance. The serum iron concentration is regulated by absorptive cells in the proximal small intestine, which can regulate iron absorption to compensate for iron body loss. There are three different pathways of iron uptake in the small intestine: the heme pathway and two specific pathways for ferric and ferrous iron, respectively.
Enterocytes absorb heme iron and nonheme iron noncompetitively. Dietary iron contains both chemical forms of iron. Heme iron is mainly found as ferrous iron (Fe2+), while the most part of nonheme dietary iron is ferric iron (Fe3+). When heme enters the enterocyte, it is degraded by heme oxygenase with release of iron. It passes the basolateral membrane of the enterocyte and competes with nonheme iron to bind transferrin in the plasma. The way of nonheme iron transport in the body is still not known. The concentration of iron in the enterocytes depends on the body’s needs for iron. Individuals who are iron-deficient have a small amount of iron in enterocytes, while those who have sufficient body iron have higher amounts of iron in the absorptive intestinal cells. Iron in the enterocyte regulates absorption by either up-regulation of receptors or saturation of an iron-binding protein, or both. Iron that is delivered to other nonintestinal cells in the body is bound to transferrin. There are two pathways through which transferrin iron can be delivered into nonintestinal cells: classical transferrin receptor pathway and the pathway independent of the transferrin receptor.
In adults, only 5% of total body iron requirements is from different food sources. This amount is the same as iron loss, which is mainly from the gastrointestinal tract. The majority (95%) of iron comes from the breakdown of old RBCs. In children, approximately 30% of iron comes from diet, probably due to fast growth in pediatric age [21, 22].
There are three major factors that can influence intestinal iron absorption: iron stores in ferritin and transferrin, erythropoietic rate, and bioavailability of iron in foods. When iron stores decrease, receptors in the intestinal mucosa increase in order to raise iron uptake. Iron absorption also increases when there is increased or ineffective erythropoiesis.
During the intrauterine period, the only source of iron is the iron that is crossing through the placenta. The majority of healthy infants have iron stores of about 80 mg/kg, and 2/3 of total iron is bound in hemoglobin molecules. Normal hemoglobin concentration is 15–17 g/dl. Healthy infants have enough body iron for the first 5–6 months of life [22, 23]. There are some conditions that can reduce iron stores at birth or can act through other mechanisms, thus increasing the risk for developing IDA during the first months of life. These conditions are maternal iron deficiency, prematurity, administration of erythropoietin for anemia of prematurity, fetal-maternal hemorrhage, twin-twin transfusion syndrome, other perinatal hemorrhagic events, and insufficient intake of dietary iron during early infancy. Delayed clamping of the umbilical cord (approximately 120–180 seconds after delivery) can improve the amount of iron and significantly reduce the risk of IDA [24].
Deficiency of iron during pregnancy increases the risk of iron deficiency in the infancy. A study of Kumar et al. showed that iron in the cord blood sample was in correlation with mother’s hemoglobin and ferritin levels [25]. The content of iron in breast milk was reduced in mothers with severe anemia, but it was normal in mothers with mild or moderate anemia. It is recommended to implement iron supplementation during pregnancy in the populations with high prevalence of maternal IDA. It is also important to provide different kinds of iron-fortified foods for pregnant women who are at risk to develop IDA [26].
Prematurity is one of the risk factors for IDA because premature infants have smaller total blood volume at birth compared to healthy term infants, decreased ferritin concentrations, poor gastrointestinal absorption, and increased blood loss through phlebotomies [27]. Iron is mostly accumulated during the third trimester of gestation that is shorter in preterm infants. There is also increased risk for iron deficiency after use of erythropoietin for the prevention and the treatment of the anemia of prematurity [23].
Chronic fetal-maternal hemorrhage and twin-twin transfusion syndrome (TTTS) can reduce iron stores and cause anemia in term or premature infants. A small amount of fetal blood (<0.1 ml) is commonly found in maternal circulation. Causes of increased loss of fetal blood into the maternal circulation are seen as a result of trauma, placental abruption, or may be spontaneous and idiopathic. Manifestations of fetal-maternal hemorrhage depend on the amount and the rapidity of blood loss [28]. TTTS is a rare complication of monochorionic twins (or higher multiple gestations). It is the result of blood transfusion from one twin (donor) to another twin (recipient) through placental vascular anastomoses. The donor twin is smaller and often anemic, and the recipient twin is often plethoric with hemoglobin differences greater than 5 g/dl. Advanced stages of TTTS have 60–100% mortality rate, and fetuses who survive are at risk of severe cardiac, neurologic, and developmental disorders [29].
Feeding and all dietary aspects are very important in early infancy and childhood because they can greatly impact development of IDA. There are many dietary factors that can affect iron metabolism. The most common factors are poor iron intake, decreased iron absorption, consumption of unmodified cow’s milk before 12 months of age, and occult intestinal blood loss due to cow’s milk protein-induced colitis [30].
Poor iron intake in infancy usually occurs when babies are fed with infant formulas or transitional foods which are not fortified with iron. In the study from Chile, the prevalence of IDA was higher in infants fed with the formula without iron (20%), much lower in those fed with iron-fortified formula (0.6%), and medium in infants fed with human milk (15%) [31]. In another study, an increased prevalence of IDA in infancy was observed in infants fed with nonformula cow’s milk > 600 ml or more daily or > 6 breast feeds per day [32]. The amount of iron in human milk is highest during the first month of life, but gradually decreases in the following period. This amount varies among individuals. Maternal diet does not affect iron amount in the human milk.
Intestinal iron absorption depends on the form of iron in the foods. Dietary sources of heme iron, such as fish, meat, and poultry, have higher bioavailability of iron compared to nonheme sources of iron, such as fruits, vegetables, and grains. There are also various components of food that influence intestinal iron absorption. Vitamin C increases iron absorption from bread, cereals, fruits, and vegetables (nonheme iron) but has little effect on the absorption of heme iron. IDA is a common problem in children who follow a vegetarian diet. Intestinal absorption of ferrous and ferric iron is inhibited by tannins in different kinds of teas, foods rich in phosphates, oxalates, carbonates, and phytates (seeds and grains). Purified heme is absorbed poorly because heme polymerizes into macromolecules. Globin prevents the formation of insoluble heme polymers so that it remains available for absorption. Peptides from the degraded globin bind to iron and prevent iron polymerization and precipitation. Different forms of iron can be absorbed better when given together (i.e., spinach with meat).
One of the most important risk factors for IDA is early introduction of unmodified (nonformula) cow’s milk. It increases the risk for intestinal blood loss in infants compared with the formula or breast feeding, mainly due to colitis [33]. Daily intake of 720 ml or more of cow’s milk in preschool children is associated with increased risk for iron deficiency. The reasons are low concentration of iron in cow’s milk, low bioavailability of iron, and possibly increased intestinal blood loss [34]. Sutcliffe et al. reported increased risk for iron deficiency in children with continued bottle-feeding compared with children with cup-feeding in the age of 2–3 years, mainly due to the greater volumes of cow’s milk in bottle-feeding [35].
Dietary iron is absorbed mainly throughout duodenum. Gastrointestinal malabsorption of iron occurs in diseases that affect this portion of the intestine, including celiac disease, Crohn disease, giardiasis, and resection of the proximal small intestine. In children, anemia secondary to iron, folic acid, and vitamin B12 malabsorption is a common complication of celiac disease, and further screening with tissue transglutaminase antibodies has been strongly recommended [36]. Conditions that cause gastrointestinal blood loss are also associated with iron deficiency. These include cow’s milk protein-induced colitis, inflammatory bowel disease (IBD), duodenal/gastric ulcers, and chronic use of nonsteroidal anti-inflammatory drugs or aspirin. Iron deficiency occurs in about 60–80% of patients with IBD. Anemia of chronic disease, vitamin B12 deficiency, folic acid deficiency, and hemolysis contribute to the development of anemia in patients with IBD [37, 38].
Routine screening for IDA should be obtained in children 6–24 months of age. Screening consists of reviewing risk factors during any possible occasion or visit (risk assessment), and laboratory testing (laboratory screening) at least once during the mentioned period. Screening is recommended at all times for all infants and children who have any risk factor (malnutrition, low birth weight, prematurity, signs and symptoms of IDA, or living in the area with high prevalence of iron deficiency).
Review of risk factors in all children is recommended at 4, 15, 18, 24, and 30 months, at 3 years, and once yearly afterward. This is currently the most important and valuable screening tool, more useful than laboratory testing of hemoglobin. Risk assessment consists of focused dietary history. The most vulnerable groups are children with the history of prematurity or low birth weight, infants using low-iron formula, nonformula cow’s milk, soy milk or goat’s milk before 12 months of age, infants having less than two iron-rich meals daily after 6 months of age, preschool children drinking more than 600 ml milk per day, or having less than three iron-rich meals daily.
American Academy of Pediatrics (AAP) suggests laboratory testing as the screening tool for iron deficiency at 1 year of age [30]. Universal laboratory screening is recommended for all children 9–12 months of age. Additional laboratory screening is recommended for children with risk factors for iron deficiency and IDA. There are two groups of children that should undertake additional laboratory screening:
children with high risk for iron deficiency—repeated laboratory testing at 15–18 months of age or when some risk is identified; and
children with special health needs (chronic diseases, inflammatory disorders, restricted diets)—repeated laboratory testing in the period of early childhood (2–5 years of age).
Laboratory screening in most cases includes complete blood count, which includes hemoglobin, hematocrit, mean corpuscular volume (MCV), and red blood cell distribution width (RDW). The minimum laboratory screening is measurement of hemoglobin with the normal value greater than 11 g/dl.
Laboratory testing of serum ferritin at the time of the first screening is the major diagnostic tool in children with risk factors for iron deficiency and IDA [30]. Ferritin levels should be always evaluated carefully because ferritin is nonspecifically elevated in a wide variety of inflammatory conditions. A C-reactive protein can help to validate the results of serum ferritin levels. Other screening measurements that can be taken into account as a different approach for iron deficiency include reticulocyte hemoglobin concentration and combination of soluble transferrin receptor and hemoglobin [39].
It is recommended by AAP to perform risk assessment once a year during the period of adolescence. Adolescents with risk factors (those with a history of IDA, low-iron diet, or girls with heavy menstrual bleeding) should have laboratory testing for anemia [40]. Considering different opinions on screening recommendations in adolescents, each physician should personally decide about the screening process based on the risk factors. Laboratory testing should be done every 5 years starting from age 13 in girls, and at least once during the rapid growth period in boys. Children with any risk factor (increased physical activity, special diets, obesity, malnutrition, chronic illnesses, and heavy menstrual bleeding in girls) should be monitored more frequently [12].
There is some controversy on routine screening for iron deficiency in areas with low rates of iron deficiency and IDA (i.e., United States). Studies provide little evidence that routine screening or iron treatment improves child’s growth and neurodevelopmental outcome. On the other hand, routine screening is recommended because of the important health benefits. Besides, a physician should not decide about screening program only based on symptoms and risk factors in a child. Those who favor screening for iron deficiency in the adolescent period list high prevalence of anemia in that population and adverse consequences of iron deficiency [41]. The screening tests are generally minimally invasive (blood sample), and therapy for IDA is safe.
Many recommendations for prevention of iron deficiency and IDA have been published, and the most commonly used are those provided by WHO and AAP. Widely used approaches include iron-fortified foods in a diet, iron-rich formulas, introduction of cow’s milk in a diet from 12 months of age, screening for iron deficiency, and iron prophylaxis in infants [30].
It is important to emphasize that only a fraction of dietary iron is absorbed from food, depending on bioavailability (dietary iron absorption). Human milk contains only 0.3–1.0 mg/l of iron, but the bioavailability of iron is 50%, while milk formulas contain 12 mg/l of iron with bioavailability of iron 4–6% only [42]. As mentioned above, dietary iron has two main forms: heme and nonheme iron. Plants and iron-fortified foods contain nonheme iron only, whereas meat, seafood, and poultry contain both heme and nonheme iron. Heme iron has higher bioavailability than nonheme iron. The bioavailability of iron is approximately 14–18% from mixed diets, and 5–12% from vegetarian diets. Daily iron requirements vary depending on age and gender. Requirements for iron are 0.6 mg/day in healthy infants and 0.8 mg/day in preadolescent children. Adult males need 1 mg/day of iron, and adult females need 1.5 mg/day [43]. The recommended dietary iron for healthy full-term infants (from birth to 12 months of age) is 1 mg/kg/day (maximum 15 mg); for premature infants 2–4 mg/kg/day (maximum 15 mg); for toddlers 1–3 years of age 7 mg/day; for children aged 4–8 years 10 mg/day; for children aged 9–13 years 8 mg/day; for adolescent boys aged 14–18 years 11 mg/day, and for adolescent girls aged 14–18 years 15 mg/day [43]. Boys have increased requirements during pubertal growth because of expanding blood volume and increase in hemoglobin concentration. Increased requirements in girls during puberty are mostly due to menstrual blood loss, although the loss differs in various individuals. Besides, adolescent girls more often have a tendency to eat food that contains less iron and to avoid high iron-containing foods, contributing to iron deficiency [44].
Infants who are not breastfed, obtain sufficient amount of iron from iron-fortified formula. Breastfed infants should receive an additional source of iron (as iron supplement or complementary food) in these doses:
Full-term breastfed infants should receive an iron supplement from the age of 4 months (1 mg/kg/day, maximum 15 mg) until the infant has sufficient iron-rich complementary foods in a diet.
Premature breastfed infants should receive an iron supplement starting from the age of 2 weeks (2–4 mg/kg/day, maximum 15 mg) throughout the first year of life (as supplements or iron-fortified formula).
Supplementation of iron is necessary to meet requirements in infants from populations with high rates of iron deficiency and IDA. In a prospective randomized trial of early versus late iron supplementation in low-birth-weight infants, infants who received early iron supplementation (started when feedings reached 100 ml/kg/day) had lower risk of infection and lower number of blood transfusions compared to infants who received late supplementation (started at 61 days of age) [45]. In a study from India that included breastfed infants at the age of 4–6 months, oral iron supplementation resulted in better growth, especially in infants who had anemia or were otherwise nutritionally deficient [46].
Prevention of iron deficiency and IDA varies by geographical region, age group, and other conditions. In countries with high prevalence of IDA, comprehensive strategies and interventions for high-risk groups are implemented, in particular for young children, adolescent girls, women in reproductive age, and pregnant and breastfeeding women. In some regions, food fortification with iron, control of helminth infection, and control of malaria are effective approaches to prevent IDA [17].
The optimal way to reach iron requirements is an improvement of food quality. In countries with low prevalence of iron deficiency, recommended dietary intake should assure expected iron requirements. Exclusive breastfeeding is recommended for the first 4–6 months of life. Preterm breastfed infants should receive an iron supplement from 2 weeks of age. Additional source of iron should be given to infants starting at 4 months of age, first as an iron supplement, followed by iron-fortified foods (two or more meals/day meet the expected requirements for iron). Partially breastfed and nonbreastfed infants should consume exclusively iron-fortified formulas [47].
Starting from the age of 6 months, infants should receive one feeding rich in vitamin C (green vegetables, fruits, and juices) daily. After 6 months of age, meat should be introduced in a diet. Heme iron (meat and fish) is more bioavailable than nonheme iron (vegetables and cereals). Combining heme foods with nonheme foods also increases the absorption of iron [48]. Moreover, consumption of meat meets many requirements besides iron.
Infants should not be given nonformula cow’s milk until the age of 12 months. The higher concentration of calcium in cow’s milk inhibits absorption of iron. Children aged 1–5 years should drink less than 600 ml of milk daily. Besides, they should take enough iron-containing foods to fulfill daily iron requirements. Children, who do not eat at least 2 or 3 iron-rich foods every day, may have inadequate iron intake and may need iron supplementation [49].
IDA is the final stage of iron deficiency, and the first one that can recover with iron supplementation. Iron deficiency without anemia may also be associated with some clinical signs and symptoms, such as fatigue, cognitive dysfunction, or decreased energy.
The most common presentation of IDA in an asymptomatic infant or a child, who is well-nourished and otherwise healthy, is mild-to-moderate microcytic and hypochromic anemia. Slowly progressive paleness may sometimes be missed, but anemia also produces nonspecific pallor of the mucous membranes. Signs of epithelial tissues that may be associated with IDA are koilonychia, glossitis, and angular stomatitis. Severe form of IDA is much rare and is presented with poor feeding, irritability, lethargy, tachypnea, and cardiomegaly. Growth is impaired in children with severe IDA, and splenomegaly may be present.
Symptoms of IDA are presented by many body systems and functions of the affected child: impaired psychomotor and/or mental development, effects on immunity and susceptibility to infection, decreased exercise capacity, weakness, pica and/or pagophagia, headache, irritability, beeturia, and restless leg syndrome in older children. Some of these symptoms may lead to long-term consequences. Iron deficiency significantly contributes to thrombotic risk. In cases of severe IDA, some children may experience acute life-threatening conditions, including hypotension, tachycardia, tachypnea, respiratory distress, and congestive heart failure. The presence of one or more of these findings requires immediate hospital admission and prompt treatment. Severe IDA may rarely be associated with increased intracranial pressure, clinical signs of pseudotumor cerebri, or papilledema. All these symptoms resolve with iron supplementation [50].
Impaired psychomotor and/or mental development is common in infants with iron deficiency, and neurocognitive impairment in adolescents with IDA [51–53]. Negative impact on social and emotional behavior may appear and can lead to the development of attention deficit hyperactivity disorder (ADHD) [54]. Mood swings are frequent. Children with iron deficiency get tired easier and faster, and play less compared to healthy children. Numerous randomized trials performed on different pediatric age groups showed that iron supplementation prevented or corrected neurodevelopmental delay. These studies were mostly performed in low- or middle-income countries [55–57]. In the study from Costa Rica, iron deficiency and IDA were more frequent in infants fed with nonfortified- iron formula. In these infants, psychomotor development declined at the age 9 and 12 months. There were not any significant changes in mental development and behavior [58]. Some other studies demonstrated that psychomotor impairment might not completely recover after treatment of moderate-to-severe IDA [56, 59–62]. Children who had iron deficiency at the inclusion in the study continued to have lower cognitive scores when tested at school age and in adolescence compared to children with good iron balance and no iron deficiency [59]. Children who were treated for iron deficiency during infancy had lower scores on electrophysiological tests on recognition memory at 10 years of age, comparing with children without iron deficiency during infancy. Behavioral tests showed similar results in these two groups [61].
The biologic basis of neurodevelopmental disorders is not fully understood. Iron deficiency decreases expression of dopamine receptors, disrupts function of several enzymes in the nervous system with subsequent alterations in brain energy, and decreases myelin formation. Myelination disruption or impairment can be associated with constant changes in transmission through auditory and visual systems. In a study from Chile, auditory brainstem responses (ABR) and visual evoked potentials (VEP) were measured in two groups of 4-year-old children: children who were treated for IDA in infancy and non-anemic children who also received iron supplementation [63]. Subtle auditory and visual dysfunction was demonstrated with longer VEP and ABR latencies in children who had IDA in infancy compared with control group.
The relationship between IDA and febrile seizures (FS) has been examined in several studies with conflicting results. Studies that suggest positive correlation between iron deficiency and FS aim that the possible mechanism is iron-dependent metabolism of some neurotransmitters [64, 65]. Other studies found no association between iron deficiency and FS [66]. Zehetner et al. showed that iron supplementation for 16 weeks in dosage 5 mg/kg/day reduced the severity and frequency of breath-holding spells in children with IDA [67].
Iron deficiency and IDA have numerous effects on immune system and susceptibility to infection. Iron deficiency in children can induce defective functions of leukocytes and lymphocytes, and defective production of interleukin (IL)-2 and IL-6 [68, 69]. On the contrary, iron overload can increase the risk of infections with specific types of bacteria. Accumulation of iron in immune cells interferes with their antibacterial activity, and some bacteria grow well in an iron-rich environment. Besides, iron-binding proteins transferrin and lactoferrin have bacteriostatic effects, and these effects are lost when these proteins are saturated with iron [70].
Since both iron deficiency and iron excess can compromise cellular function, the levels of iron that cells are exposed to should be regulated precisely. In populations with high prevalence of iron deficiency and IDA, iron supplementation has different effects on susceptibility to infection and immunity. Low iron status may protect against malaria infection, but malaria in turn is linked with anemia, and changes in iron metabolism during a malaria infection may modulate susceptibility to co-infections [71]. Recent study of Zlotkin and coworkers showed that iron supplementation did not increase the risk of malaria infection [72].
Iron is an essential cofactor in aerobic metabolism. In IDA muscles are forced to depend on anaerobic metabolism more than they do in healthy nonanemic individuals. Iron deficiency leads to decreased exercise capacity in children, especially adolescent athletes. IDA is associated with decreased work capacity [73, 74].
Pica refers to unusual appetite for substances that are not food. In children, pica is often associated with iron deficiency and IDA [75]. The most common form of pica is starch or clay ingestion. Both substances decrease absorption of dietary iron. Pagophagia is a particular form of pica characterized by repetitive and compulsive ingestion of ice, freezer frost, or iced drinks. Some children prefer cold vegetables instead of ice. Pagophagia is very common in iron deficiency without anemia and is present in a half of patients with IDA. It responds to iron supplementation very fast, earlier than hemoglobin recovery [76]. The mechanism through which iron deficiency causes pagophagia is unclear. Biochemical processes involving the central nervous system might elucidate the underlying mechanism. Pica is not specific for iron deficiency. It can be found in children with developmental disabilities, such as intellectual disability or autism. It is also described in children after brain injury [77].
Both iron deficiency and overload have been associated with an increased thrombotic risk in experimental and clinical studies. It has been reported that IDA is associated with cerebral vein thrombosis [78]. In Canadian study, children with arterial or venous stroke who were previously healthy, had ten times more chance to have IDA than children without stroke [79]. The mechanism of this association is complex. It may be related to reactive thrombocytosis that is often finding in IDA. Iron deficiency may contribute to a hypercoagulable state by affecting blood flow patterns. Besides, IDA with hypoxia could precipitate situations of increased metabolic stress (i.e., infections) in particularly vulnerable areas of the brain supplied by end arteries [80].
Beeturia is defined as pink or red urine after the ingestion of beets. It is most common in individuals with iron deficiency [81]. This manifestation is caused by increased intestinal absorption and increased excretion of the red pigment betalaine (betanin). The pigment is decolorized by ferric ions, and urine excretion of betalaine is increased in iron deficiency.
This syndrome is a common sleep-related movement disorder characterized with uncomfortable urge to move legs. It occurs usually in the evenings, during periods of inactivity and rest, and is occasionally relieved by movement. Restless leg syndrome is associated with iron deficiency and is often improved by iron supplementation. The brain iron insufficiency has been documented by independently replicated cerebrospinal fluid and brain imaging studies for individuals without IDA [82].
Detailed history and physical examination are essential in diagnosis of any disease. Detailed history from the parents is very important in diagnosing iron deficiency and anemia, especially about prenatal period and dietary habits including time of introducing solid foods.
Presumptive diagnosis of IDA is made by a combination of risk assessment and laboratory testing of hemoglobin level (<11 g/dl). In infants younger than 6 months, lower values of hemoglobin are observed because of physiological anemia, but hemoglobin values under 9 g/dl demand further evaluation in order to investigate if there is any accompanying factor. Other findings like low mean corpuscular volume (MCV) or high red cell distribution width (RDW) help to determine diagnosis. For a definite confirmation, additional steps are needed:
Estimate risk factors for lead poisoning and measure blood lead level if it is indicated [30, 83].
If there is no evidence of lead toxicity, and the most likely is dietary deficiency, apply empirical trial of oral iron supplementation*
For infants and toddlers less than 24 months of age with anemia—move directly to empirical trial because IDA is the most probable cause of anemia in this age group.
For children 24 months of age and older—besides hemoglobin, hematocrit, MCV, and RDW, evaluate reticulocyte count, peripheral blood smear, and stool for occult blood before starting empirical trial.
In children with severe anemia, complicated medical history, and with signs and symptoms atypical for IDA, additional testing should be performed before starting treatment.
These additional steps are necessary because anemia is not sensitive or specific for iron deficiency. Two-thirds of children with iron deficiency in the United States are not anemic, namely 9% have iron deficiency and 3% are anemic. The prevalence of anemia is much higher in countries with higher rates of iron deficiency. On the other hand, two-thirds of anemic toddlers have some other cause of anemia apart from iron deficiency [30]. Evaluation for iron deficiency in adolescence should also include serum ferritin levels. IDA in adolescent is identified by hemoglobin concentration below 11 g/dl combined with low serum ferritin (<12 ng/ml).
In infants and toddlers up to 24 months of age who have mild microcytic anemia with presumptive diagnosis of IDA based on screening results, the strategy of choice is therapeutic trial of iron [51]. The recommended dosage is 3 mg/kg of elemental iron, once or twice daily, best between meals (daily dosage 3–6 mg/kg). Ferrous sulfate is the convenient and most commonly used form of iron. If there is increase of hemoglobin concentration greater than 1 g/dl after 4 weeks of treatment, the diagnosis of iron deficiency is confirmed. In this case, iron supplementation and monitoring of the child with laboratory tests should be continued for at least several months, after hemoglobin levels reach normal range according to age.
IDA is less common in older children than in infants. Additional evaluation, besides complete blood count, MCV, and RDW, is suggested in children older than 2 years before starting iron treatment. This evaluation includes reticulocyte count, peripheral blood smear, and stool for occult blood. If results support the diagnosis of IDA, iron supplementation should be started. Additional evaluation is required only if there is no response to the treatment.
Basic laboratory testing in diagnosing IDA is complete blood count, including hemoglobin, hematocrit, MCV, and RDW. More detailed evaluation is needed for children with complicated medical histories, severe forms of anemia (hemoglobin <7 g/dl) or presence of features that are not typical for IDA. In these cases, several other tests should be performed: serum iron, serum ferritin, total iron-binding capacity (TIBC), transferrin saturation, and stools for the presence of occult blood. These tests, although nonspecific for IDA, can support the diagnosis of IDA in majority of cases. Low serum iron and ferritin levels with an elevated TIBC are diagnostic for iron deficiency.
Complete blood count shows the severity of anemia. Increased RDW is the first laboratory sign of iron deficiency [51, 84]. RDW is high in IDA because there is a wide variation in RBC size. MCV and mean corpuscular hemoglobin concentration (MCHC) are low. Platelet count is often elevated, and it normalizes after iron treatment. Peripheral blood smear is an important workup in patients with anemia. The first finding of IDA on peripheral smear is anisocytosis. Besides, RBCs are hypochromic and microcytic.
In infants and small children, iron deficiency is usually identified by a serum ferritin concentration <12 ng/ml. Diagnosis of IDA is based on the combination of hemoglobin concentration below 11 g/dl and serum ferritin levels below 12 ng/ml. However, when examining the results, it must be taken into consideration that ferritin is an acute-phase reactant. Elevated serum ferritin levels have been associated with a wide range of conditions including inflammation, infection, chronic disease, and malignancy [85].
Free erythrocyte protoporphyrin (FEP), soluble transferrin receptor (sTfR), and reticulocyte hemoglobin content (CHr) are very useful and reliable laboratory tests to support the diagnosis of iron deficiency. FEP is a precursor of heme that normally occurs in very low concentration in RBCs. Elevated FEP values thus indicate early impairment of iron status and provide information about gradual changes in the iron supply. The sTfR refers to the cleaved extracellular portion of the transferrin receptor 1 that is released into serum. Iron deficiency causes overexpression of transferrin receptor and sTfR levels. The sTfR is regarded as a more stable marker of iron levels in an inflammatory state. CHr is a measure of early iron-deficient erythropoiesis. Reticulocyte hemoglobin content decreases earlier than hemoglobin content of RBC because normal life span of RBC is 120 days [86]. It has been shown that CHr measurement is more reliable and accurate laboratory test for the diagnosis of iron deficiency than hemoglobin level <11 g/dl, resulting in detection of greater number of patients with iron deficiency comparing to hemoglobin. On the other hand, greater number of falsely identified patients with iron deficiency was detected also by CHr, which is, although more sensitive, less specific than hemoglobin [87]. Serum transferrin receptor is found on reticulocytes and increased number of transferrin receptors is observed in IDA.
Some other types of anemia and other conditions that can be confused with IDA are mild hereditary anemias (alpha or beta thalassemia traits), mild anemia after recent infection or immunization, anemia of chronic disease, and combined nutritional anemias (malabsorption with vitamin B12 or folate deficiency). If the child does not respond to iron supplementation nor has some predisposing factor, other conditions should be considered.
For the successful treatment of IDA in infants and children, it is necessary to determine the appropriate dose and scheduling of oral iron therapy, apply dietary modifications together with iron supplementation, and follow-up the response to treatment.
Suggested dose for oral supplementation for infants and children with IDA is 3–6 mg/kg/day of elemental iron. Ferrous sulfate is generally recommended in a dose of 3 mg/kg of iron once or twice daily (maximum total daily dose, 150 mg of elemental iron). Elemental iron constitutes 20% of ferrous sulfate. Ferrous fumarate and ferrous gluconate are other forms of oral iron salts with different content of elemental iron. The iron supplement should be given between meals and preferably with juice because absorption of ferrous sulfate is increased when it is given with juice rather than with milk or other fluids. For maximum absorption of iron, administration 30–45 minutes before meal or 2 hours after meal is highly recommended.
The same doses of oral iron supplementation are recommended as a therapeutic trial for infants and young children with mild microcytic anemia and presumptive diagnosis of IDA [51]. Treatment should result in an increase of hemoglobin concentration greater than 1 g/dl within 4 weeks [30].
Side effects of oral iron preparations are gastrointestinal intolerance in higher doses, gray staining of teeth and gums (especially when given as a liquid preparation), effects on immune system, and susceptibility to infection.
Dietary changes are necessary not only to prevent iron deficiency but also to add oral iron therapy. Following dietary changes are recommended for infants and children with proven or suspected IDA:
Infants should not be fed with unmodified cow’s milk or low-iron formula. If infants are not breastfed or are partially breastfed, they should be fed with iron-fortified formula. Infants fed with cow’s milk may have iron deficiency as a result of intestinal blood loss due to cow’s milk protein-induced colitis. Lack of iron fortification in unmodified cow’s milk contributes to iron deficiency state.
When iron deficiency is detected or suspected in a child older than 12 months, intake of cow’s milk should be limited to 600 ml/day. Higher intake of cow’s milk has been associated with higher risk for iron deficiency in several studies [34, 88]. Discontinuing bottle-feeding is also recommended because it generally helps in limiting milk intake [89]. If IDA is persistent and stool is positive for blood, all milk products should be stopped. In these cases, child should receive appropriate amount of calcium in a diet (calcium-rich foods).
Parents should be advised to modify child’s diet in order to increase iron consumption. Infants 6 months and older should have appropriate intake of iron from complementary foods. Diet should contain cereals fortified with iron, food rich in vitamin C, and pureed meat.
Follow-up assessment is necessary to confirm that anemia has been caused by iron deficiency and the treatment was administered at correct dosage and timing. After 4 weeks of therapy, complete blood count should be done. It is recommended to perform evaluation when child is healthy and without viral infection that may cause acute decrease in hemoglobin.
If hemoglobin has increased at least by 1 g/dl after 4 weeks of oral iron supplementation, therapy should be continued, and hemoglobin re-evaluated every 2–3 months until hemoglobin reaches the normal value. Iron therapy should be continued additional 2–3 months to replace iron storage pools. Discontinuation of the treatment can lead to the recurrence of IDA.
If the appropriate response is missing after 4 weeks of treatment, additional evaluation of anemia is recommended. Possible causes of persistent or recurrent IDA are ineffective treatment, blood loss, malabsorption, or incorrect diagnosis. Parents should be asked whether the iron preparation has been given at the appropriate dosage and timing, whether suggested dietary modifications have been done, and if there were any intercurrent illnesses that could transiently decrease hemoglobin level. If the patient had no intercurrent illness and has been taking iron supplement in an appropriate dosage and timing, it is suggested to proceed with the following evaluation:
Evaluation for the type of anemia—Measuring of serum ferritin level, hemoglobin electrophoresis, vitamin B12, and folate can rule out the thalassemia trait, chronic disease anemia, and mixed nutritional deficiency. These conditions may imitate or complicate IDA. Very rare genetic mutations may interfere with iron transport and cause anemia similar to IDA, but without response to iron supplementation [90].
Evaluation for gastrointestinal blood loss—Stool should be tested for occult blood in a few separate samples. If the results are positive, it is recommended to assess further investigation for common causes of gastrointestinal blood loss, including cow’s milk protein-induced colitis, celiac disease, and inflammatory bowel disease.
Parenteral iron therapy is reserved for patients with severe forms of anemia who are intolerant to oral preparations, have poor response to oral supplementation, poor compliance, or malabsorption. Children with chronic gastrointestinal diseases as inflammatory bowel disease may require parenteral iron therapy because they often do not tolerate oral supplementation.
Most commonly used form of iron for parenteral use in children is low molecular weight iron dextran. It produces mild infusion reactions in less than 1% of patients and serious adverse effects are very rare [91]. Recently, ferric carboxymaltose administered as a short intravenous infusion without a test dose proved to be safe and highly effective in children and adolescents with IDA refractory to oral iron therapy [92]. Evaluation of treatment is usually performed at 4–12 weeks after the initial infusion.
Blood transfusion is rarely required in children with IDA. Transfusions are not considered necessary even with hemoglobin levels 4–5 g/dl, if the child is otherwise well. Blood transfusion should be administered only when there is an urgent need to restore oxygen-carrying capacity, i.e., in severe decompensated anemia. IDA develops gradually and over periods long enough to allow compensatory mechanisms to maintain intravascular volume. Consequently, there is a real risk of fluid overload with transfusion, and these patients should receive transfusion with caution. Standard of practice recommends slow transfusion of packed RBC volume of 5 ml/kg over 4 hours to avoid complications [93].
Iron deficiency is the most common nutritional deficiency in the world, affecting more than a quarter of the global population. Iron plays an essential role in many physiological functions, including oxygen binding and transport, cell growth and differentiation, gene regulation, enzyme reactions, and neurotransmitter synthesis. Iron deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases compensatory. During later stages, deficiency impairs erythropoiesis, ultimately causing anemia.
Iron deficiency and IDA have many systemic effects, and the most concerning are diminished mental, motor, and behavioral functioning that might not be completely reversible after treatment with iron. Therefore, intervention should focus on primary prevention, which includes breastfeeding, fortification of foods with iron, use of iron-rich formulas when breastmilk is insufficient, and avoiding cow’s milk before 1 year of age. Routine laboratory screening is recommended for all children 9–12 months of age. Risk assessment, consisting of focused dietary history, presents the most valuable screening tool, and additional laboratory screening is recommended for children with risk factors for iron deficiency and IDA.
Treatment starts with establishing the diagnosis. The main therapeutic principles are detection of the condition that causes iron deficiency, correction of underlying etiology, iron supplementation, dietary modifications, and education of families. Oral iron is the first-line therapy, giving in appropriate dose and scheduling. Adequate follow-up assessment for response is also important. If the appropriate response is missing, further evaluation should be obtained to rule out conditions that might simulate or complicate IDA.
WHO | World Health Organization |
IDA | Iron deficiency anemia |
BMI | Body mass index |
RBC | Red blood cells |
TTTS | Twin-twin transfusion syndrome |
IBD | Inflammatory bowel disease |
AAP | American Academy of Pediatrics |
MCV | Mean corpuscular volume |
RDW | Red blood cell distribution width |
ADHD | Attention deficit hyperactivity disorder |
ABR | Auditory brainstem response |
VEP | Visual evoked potential |
FS | Febrile seizures |
IL | Interleukin |
TIBC | Total iron-binding capacity |
MCHC | Mean corpuscular hemoglobin concentration |
FEP | Free erythrocyte protoporphyrin |
sTfR | Soluble transferrin receptor |
CHr | Reticulocyte hemoglobin content |
According to Tannahill [1], health promotion is an umbrella term covering overlapping fields of health education, prevention and attempts to protect public health through social engineering, legislations, fiscal measures and institutional policies which entail the combination of the best in terms of both theory and practice from a wide range of expert groups (educationists, behavioral scientists, medical practitioners) and non-professionals including the communities involved. For him, health promotion stems largely from a new focus for health services that recognize some basic facts: many contemporary health problems are preventable or avoidable through lifestyle change; modern technology is a bundle of mixed blessings bringing both benefits and risks to health; medical technology is at the phase of diminishing returns (losing efficacy and connection to ordinary people); such non-medical factors as better nutrition, improved living conditions and public health measures have contributed to both health and longevity even more than medical measures; that doctors can cause as well as cure disease; and increasing public desire to attain better or improved quality of life and at the same time demystifying and demedicalising the attainment (achievement) of good health [1].
For the World Health Organization (WHO), health promotion is essentially about engendering a context in which the health and well-being of whole populations or groups are owned mainly by the people concerned, i.e., enabling citizens of local communities to achieve political control and determination of their health [2, 3]. Therefore, health promotion goes beyond mere healthcare but puts health on the policymaking agenda in all sectors and at all levels, directing policymakers to be cognisant or conscious of the health consequences of their decisions and accept responsibilities for health.
Health promotion can be seen as the whole process of enabling or empowering people to increase control over and improve their overall health. It focuses on creating awareness of health issues, engendering behaviour modification consistent with prevention and attitudes to ill health and motivating increased usage of available health facilities. In the pursuit of good health (physical, mental and social well-being), individuals and groups through health promotion are enabled to identify and realize aspirations, satisfy needs and change or cope with the environment in manners consistent with complete good health.
Health promotion is expected to contribute to programme impact by enabling prevention of disease, reduction of the risk factors or behaviors associated with given diseases, promoting and fostering lifestyles and conditions that are conducive to good health and enabling increasing use of available health facilities. Therefore, health promotion creates both the awareness and conscientisation that leads to disease prevention, control of health situations and usage of health services and facilities. It implies individual and collective control and participation in health focusing on behavioral change, socio-economic lifestyles and the physical environment.
Without doubt the WHO’s Ottawa Charter definition of health promotion is very comprehensive and encompasses the core values and guiding objectives of health promotions [3]. It summarily sees health promotion as the process of enabling people to increase control over and improve their health. In line with the above definition, Macdonald and Davies [4] contend that it calls attention to the critical role of the concepts of process and control as the real essence of health promotion. For them, “the key concepts in this definition are ‘process’ and ‘control’, and therefore effectiveness and quality assurance in health promotion must focus on enablement and empowerment. If the activity under consideration is not enabling and empowering it is not health promotion” [4], p. 6.
As the burgeoning literature on health promotion over the years indicate it is a community-driven (inspired), multifaceted and multidisciplinary area of concern that also involves critical sociopolitical, economic and environmental elements and dynamics (see [4, 5, 6, 7, 8, 9, 10]).
It is important to also understand that even though one can make a distinction between public health and health promotion, in reality both are interconnected and hardly practically separable. In other words, public health is built on health promotion and health promotion is imperative for public health delivery. As has been argued, public health “is synonymous with health promotion in that it aims to implement co-ordinated community action to produce a healthier society” [11], p. 315.
There is no gainsaying the fact that health promotion nowadays has an overwhelming sociopolitical component that is really definitive. In fact, as has been posited, “health promotion activities are by their nature inherently politically based and driven, thus making it impossible to divorce them from the political arena” [11], p. 314. Health promotion becomes a dynamic area of interface between public policy institutions (the state and its agencies), the public (community/people) and the professionals (ranging from the media professionals, public health advocates, social workers to medical practitioners).
The chapter depended on the desk review of extant literature and documents for its information. The main exclusionary criteria in this regard were materials not related to health promotion and materials published before 1984, which were considered extreme-dated. The inclusive criteria were determined by such concepts as public health, public health in Africa, health promotion, health education and awareness and theories and models in health promotion. Such prominent Internet information sites like the WHO, American Public Health Association (APHA), Health Resources and Services Administration (HRSA) and the Universitats Bibliothek Leipzig (UBL) Online Resources were utilized in gathering materials for the chapter.
There is no gainsaying the fact that effective and result-oriented health promotion practice depends on sound theory [12]. In other words, theory becomes very informative of health promotion practice and activities. In recognition of the above, one would examine briefly the main theories that have implicated health promotion globally. It is important, however, to state here that the choice of a theory or model to guide health promotion should be determined largely by the specific nature of the health issue being addressed, the community or population in view and the sociopolitical context in question. This is because theories and models are simply used in practice in order to plan health programmes, explain and understand health behaviour as well as underpin the identification of appropriate intervention and implement such intervention in ways that are both effective and sustainable.
Despite a plethora of theories and models utilized in health promotion, I will only focus on five of the most popular and commonly used. These are ecological models of health promotion, the Health Belief Model (HBM), Stages of Change Model or the Trans-theoretical Model, Theory of Reasoned Action or Planned Behaviour and the Social Cognitive Theory.
As the name implies, these models focus on the interaction of people with their physical and sociocultural environments. The approach thus recognizes that there are multiple levels of influence on health and health behaviour especially the health seeking behaviour and choices that people make. The ecological models are anchored on five overriding influences which determine and guide health behaviour and response to health issues [13, 14, 15, 16]. These influences are intrapersonal or individual factors (these impact on individual behaviour, e.g., beliefs, knowledge, attitude, etc.); interpersonal factors (these are produced through living with and interacting with other people, e.g., family, friends and social groups/networks; these other people can function as both the source of solidarity and support as well as sources of barriers and constraints to health-promoting behaviour of the individual, e.g., dwelling among chronic smokers or having intense interaction with them may expose one to the dangers of either smoking or the influence of second-hand smoke); community factors (these make reference to social norms that are shared by groups or communities, and such norms whether formal or informal can influence health behaviour and health seeking behaviour of the individual and group members, e.g., relationship between institutions, groups and organizations); institutional factors (policies, rules, regulations and institutional structures that may constrain or even promote healthy behaviour in a given society, e.g., the workplace and voluntary organizations to which the individual belongs are prime examples); public policy factors (policies at different level of governance that regulate, structure or support actions and practices targeted at health outcomes like disease prevention policies and structures enabling early detection, control or response and management of health crisis in the society; these stem from the position of the government and are critical in achieving the goals of public health delivery) (Figure 1).
Ecological models of health promotion (simplified).
As the above pyramid, suggests the individual, interpersonal and community factors are at the base. These factors therefore exert more influence and pressure over the individual’s health behaviour than the institutional and public policy factors as these are more important. In other words, the institutional and public policy factors are literally far from the individual and do not exert as much pressure on his behaviour as those factors that are very close to him both spatially and otherwise. In an age of increasing pessimism in government, people are much driven by interpersonal and community factors than what comes from a typical further off entity.
Given the above, it is obvious that the ecological approach is very pertinent in the understanding of the range of factors that influence people’s health. Its main strength is that it can provide what is called a complete perspective on factors that affect health behaviour and response to health issues especially the role of social and cultural factors or normative patterns on health in the society. It is perhaps very well suited to health intervention and practice in developing societies with an overbearing influence of sociocultural factors on behaviour, attitudes and practice of the people.
This is a theoretical model that has been found useful in guiding both health promotion and strategies for disease prevention. As the name suggests, it focuses on individual beliefs about specific health conditions which predict or direct individual health behaviour [17, 18]. The specific components of this belief that influence health behaviour include perceived susceptibility to the disease; perceived severity of the disease in question; perceived benefits of action (positive benefits of such action) as well as cues to action (awareness of factors that engender action); self-efficacy (belief that action would lead to success); and perceived barriers or obstacles to action (especially if such obstacles are seen as daunting or insurmountable or otherwise).
In the utilization of the HBM in health promotion, there are five main action-related segments that would help in identifying key decision-making points and thus facilitate the utilization of knowledge in guiding health intervention. These are: collection of information (through needs assessments; rapid rural appraisal, etc. in order to determine those at risk of the disease or affliction and specify which population or component of the population to be targeted in the intervention); conveying in unambiguous and clear terms the likely consequences of the health issue in question and its associated risk behaviors in order to facilitate a clear apprehension of its severity; communication (getting information to the target population on the recommended steps to take and the perceived or likely benefits of the recommended action); provision of needed assistance (help the people in both the identification of and reduction of barriers or constraints to action); and demonstration (actions and activities that enable skill development and support aimed at enhancing self-efficacy and increased chances of successful behaviour modification targeted at the health issue in question) (Figure 2).
Health belief model (HBM).
In Africa, the HBM has been very useful in understanding people’s response and behaviour to HIV/AIDS and other chronic diseases. Being a society very flushed with beliefs, the degree of responsiveness to a health situation is often the direct product of a set of beliefs held by the individual and/or by his immediate community.
This model is focused on examining and explaining the individual’s readiness to change his behaviour and sees such change as occurring or happening in successive stages. It therefore adopts a quasi-evolutionary framing of behaviour change in which behaviour change, sustenance and termination are encompassed in six stages. These stages are pre-contemplation (existence of no intention to take any action by the individual); contemplation (thinking about taking action and ruminating on plans to do this soon); preparation (signifies intention to take action and includes the possibility that some steps or preliminary steps to action have been taken already); action (discernible change in behaviour for a brief period of time); maintenance (sustenance of the action taken; behaviour change that is maintained in the long run or long-term behaviour change); and termination (the expressed and discernible desire never to return to prior negative behaviour by the individual concerned).
The above stages are very important in planning behaviour change or modification and recognize that behaviour change is both gradual and takes time. What is needed from the health promoter is that at each of these stages specific interventions or programmes are devised to help the individual progress to the next stage. Also, the recognition that the model may in reality be cyclical rather than lineal, i.e., individuals may progress to the next stage or even regress to previous or lower stages, is important in planning health promotion interventions utilizing this model. It also calls attention to understanding that there are individual differences in the adoption of change, i.e., some people may be swift in behaviour modification, while others may take longer time; but each needs support in order to pull through.
The main contention of this theory is that an individual’s health behaviour is usually determined by his intention to exhibit or display a given behaviour. Therefore, the intention to exhibit a given behaviour (or behaviour intention) is predicated upon or predicted by two main factors, viz. personal attitude to the behaviour in question and subjective or personal norms (an individual’s social and environmental context and the perception the individual has over that behaviour) related to that behaviour.
The basic assumption here is that both positive attitudes and positive subjective norms will generate greater perceived control of behaviour and increase the chances of intentions towards changes in behaviour. The theory generally provides information that can be used in predicting people’s health behaviour and thus in planning and driving through health interventions. It anchors in recognizing the predictors of behaviour-oriented action and the need for supportive social and environmental contexts that facilitate and sustain desirable health behaviour.
This theory combines both the cognition of the individual and the social context of the individual in offering explanation and understanding of health behaviour and response. It seeks to describe the influence of the experience of the individual, his perception of the actions of other people near him and the factors in the person’s immediate environment on health behaviour of the individual. It moves from this general perspective to provide opportunities for social support (defined as conducive to healthy behaviour) and reinforcements that generate behaviour change or modification. In this sense, the SCT depends on the idea of reciprocal determinism which denotes the continuing or uninterrupted interaction among the person’s characteristics, his behaviour and the social context or environment in which the behaviour takes place.
However, the best way to appreciate the SCT is to examine the main components the theory isolates as related to behaviour change at the individual level. These are self-efficacy (belief in one’s ability to control and execute behaviour within a given context); behaviour capability (thorough comprehension of behaviour and the ability to exhibit or perform it); expectations (outcomes or outputs of the behaviour change in question); expectancies (the assignation of value to the above outcome of behaviour and which is important in sustaining the behaviour); self- control (the regulation and monitoring of behaviour of the individual); observational learning (the act of watching others performing the desired behaviour and the outcomes therein as well as modeling that behaviour in question); and reinforcements (incentives and rewards seen as eliciting, encouraging and sustaining behaviour change in the individual) [19].
The three components as the above diagram shows reinforce each other and in the process condition and determine behaviour of the individual even in the context of health as well as choices made therein (Figure 3). The SCT is very pertinent in contexts where desirable health outcomes can be achieved by behaviour modification or change. For instance, certain chronic diseases or health conditions can be tackled through healthy lifestyles and dieting that reduce risk factors and chances of individuals succumbing to such conditions. Therefore, the theory can help frame intervention programmes in this area that focus on changing people’s behaviour and in the process achieve desirable health outcomes.
Illustration of the social cognitive theory (SCT).
Theories and perspectives or models as already indicated are critical in providing explanations of a problem or issue (broadening our understanding and perspective as it were) and also very important in the effort to tackle a given problem or issue in the society especially by way of developing and implementing programmes and interventions. Perhaps, the above underscores why some scholars [20, 21, 22] would highlight the difference between the so-called theories of the problem and theories of action, meaning that while the former aids our apprehension of a given issue or social reality, the latter is important in terms of taking actions or evolving activities to tackle the issue in question.
Health promotion generally implicates a huge element of politics and power dynamics in the sense that only political will and cognition can build discernible changes in health. Lobbying and advocacy are critical tools of health promotion and function within the political arena. The sociopolitical contexts and influences are especially recognizable in the public health sector in the developing world where political will and doggedness are often necessary to drive through even the most salutary change or innovation in the health sector. Also, political forces are equally dominant in the provision of crucial health infrastructure and facilities as well as the reasonable funding demanded by any effective public health system. As Harrison opines health promotion “requires concerted, sophisticated and integrated political action to bring about change and requires professionals concerned with public health to engage with the politics of systems and organizations” [5], 165.
Therefore, health promotion seeks to empower and transform communities by getting them involved in activities that influence public health especially through agenda setting, lobbying and advocacy, consciousness raising and social education [11, 22]. All these are accomplished on terms that are either defined or strictly affected by the socio-economic realities of the people themselves. By its emphasis on the community, health promotion has a heavy sociological frame that prioritizes the values of society as well as mobilization and solidarity in the quest for good and sustainable health. It thus makes assumption that individual members of the society would give equal weight to their own health and the health of their neighbors. In other words, it is often anchored on the uncanny assumption that the health of the individual member of a given society is intertwined with the health of the community as a collective. This means the reference point of health promotion is that one’s health is as good as the health of the members of the community or society as a whole, i.e., common health destiny. Therefore, such things as community empowerment, community competence and overwhelming sense of community are all apprehended as contributing to the health of the communities [23].
Traditionally there are five approaches utilized in health promotion. These are medical (the focus here is to make people free from medically defined diseases and afflictions; it is mainly anchored on prevention strategies and the role of the medical practitioner or expert in ensuring that the patients comply with recommendations); behavioural change (behaviour modification approach that recognizes that people’s behaviour and lifestyles can be changed in order to enable them attain good health, i.e., facilitate adoption of healthy lifestyle); educational (provision of information and knowledge that enable understanding of health issues and build awareness for informed decision-making and choice among people); client-centred (in this situation health practitioners work with clients in order to identify what they know about a given disease and take appropriate action; emphasis on perceiving the client as equal and building the clients self-empowerment that enable them make good choices and control their health outcomes); and societal change (the focus here is on the society or community rather than the individual and seeks to change or modify both the physical and social environments in order to make them consistent with or conducive to good health).
The conventional health promotion methods (modes of operationalizing health promotion and achieving its goals) include health education (the conscious and systematic effort at providing education or knowledge to people on particular and general aspects of health; it is about enabling people through proper and right knowledge on what to do and how to do it; it is empowering and improving people’s capacity to act with regard to their health issues and conditions), information, communication (the above three are often captured in the popular acronym IEC), social mobilization, mediation, community theater and advocacy and lobbying. However, while these methods are okay in differing contexts, a decision on the specific medium to use should be guided by both environment (community conditions) and the nature of the health issue involved. The use of more than one method in any given case is highly recommended especially in Africa where there are broad inequalities in access to social goods and the media. The increasing use of social media especially among young Africans calls attention to their deployment equally in core health promotion. Social media platforms like WhatsApp and blogs can be very potent in this regard.
There is an undeniable need to give high priority to health promotion research in Africa. Such research should aim at enabling a realistic and focused achievement of the goals of health promotion. Broadly, health promotion aims inter alia at:
The prevention of communicable and non-communicable diseases
The reduction of risk factors associated with diseases
The fostering of lifestyles and conditions in the general population that are consistent with overall well-being or good health
The effective/maximal utilization of existing health services and stimulating demand for others where/when necessary
According to the WHO [24] Health Promotion Strategy for the African Region, the contributions of health promotion to the achievement of health objectives include increasing individual knowledge and skills especially through IEC; strengthening community action through the use of social mobilization; enabling the emergence of environments supportive and protective of health by making optimal use of mediation and negotiation; enabling the development of public policies, legislation and fiscal controls which enhance and support health and overall development using advocacy and lobbying; and making prevention and consumer needs the core focus of health services delivery. All these can be positively influenced by research and studies which evaluate the effectiveness of what has been done as well as explore new strategies suitable to the socio-environmental context in question.
However, while research is very critical to achieving the goals of health promotion, it should be concise and focus essentially on the priority health programmes which have been identified by the WHO for the continent. Some of such programmes include the Global Fund for Malaria, HIV/AIDS and Tuberculosis, Immunization, Mental Health, the Tobacco Free Initiative and Reproductive Health as well as the fight against recurrent scourge of Ebola, etc. Such research should focus on identifying effective health promotion approaches and communication media to embody and convey the outcomes to communities through community participation; the extent or effectiveness of these means and seeking to still improve overall programme effectiveness and sustainability. Therefore, health promotion research should focus on ascertaining goals/outcomes of health promotion (to guide policy), provide reliable conditions associated with these outcomes or goals, precisely define the changes intended and delineate reliable mechanisms and indicators of M and E of health promotion strategies in specific country/community contexts.
The importance of research is essentially derived from the fact that it calls attention to the need for verification and evidence-based activities in health promotion. These are without doubt the ways of knowing if real empowerment and enabling has been achieved in the process. Thus,
Health promotion is about enabling people to improve their health; and secondly, evidence relevant to health promotion should bear directly on factors that support or prevent enablement and empowerment (determinants of health) activities that support enablement and empowerment (health promotion) and assessing whether these activities have been successful (evaluation of health promotion). [25], p. 357
The above clearly suggest that health promotion should be anchored on evidence or should rest on experience and reality regarding what works or what is possible and effective in any context. In this manner, “evidence-based health promotion involves explicit application of quality research evidence when making decisions” [26], p. 126. Research is even more foundational in health promotion since health promotion efforts need to be anchored on agreed definitions and values of health promotion. As Seedhouse contends the failure to be explicit about definitions and values generates conceptual confusion in research as well as sloppy practice [27].
The evaluation of health promotion which should be a core research activity may be based on the three main forms of evidence/knowledge associated with health promotion [28]: instrumental (controlling social and physical environments), interactive (understanding of diseases/health issues; lived experiences; solidarity) and critical (reflection and action; raising consciousness regarding causes and means of overcoming them). These three evidences are anchored on the given scientific/philosophical traditions, viz. instrumental (positivism, quantitative, experimental, scientific knowledge), interactive (constructivist, naturalistic, ethnographic/qualitative knowledge) and critical (materialist, structural and feminist theory).
There is also an overwhelming need for health promotion research to be aware of the difference between health promotion outcomes and health outcomes. Health outcomes crudely imply the consequences or benefits of healthcare delivery (e.g., reduction of mortality rate) related to a disease (which may be the case in spite of an increment in number of those affected by the disease). But health promotion outcomes signify the form of control and attitudinal re-orientation groups and individuals adopt in facing a given disease which may impact on the number of people affected by the disease and improve attitudes and behaviour towards those affected by the disease. Health promotion outcomes can be seen directly through community members’ perception and interpretations of a given health issue which makes the achievement of control possible.
Health promotion research should utilize both quantitative and qualitative methods. In addition to complementing quantitative methods in health promotion research, qualitative research enables the researcher reach the heart of issues in engagement with community members. In Africa, where a good percentage of the population are still domiciled in the rural areas, qualitative approach offers the possibility of profound insights into the why and how of health behaviors which may not be possible or easily achieved with the quantitative or traditional biomedical approaches. As a result, “the increasing popularity of qualitative methods is as a result of perceived failure of traditional methods to provide insights into the determinants – both structural and personal – of whether people pursue or do not pursue health-promoting actions” [25], p. 359.
It is important to recognize that in spite of apparent good intentions, health promotion can actually generate negative or counterproductive effects when not well managed. Thus, “negative outcomes occur where professionally paternalistic and disempowering health policy decisions force health-related outcomes that are irrelevant to sustained community development and are not based on or resourced according to the social reality of the community” [11], p. 315. The above sentiments caution one against embarking on health promotion activities and initiatives that are not anchored on the health realities of the community concerned. Often, overzealous health professionals unintentionally betray the health priorities of communities by assuming knowledge of all there is to know about the health situations and needs of the people.
Perhaps a critical shortfall of some health promotion activities and processes is the adoption of what can be termed the pathogenic paradigm which over-relies on risk instead of emphasizing protective mechanisms. This essentially entails a focus on the failure of communities and individuals to avoid disease or their apparent susceptibility to diseases instead of seeking to unleash their potential and capacity to engender and sustain good health and development. It is an approach that relies too much on health practitioners and experts and hardly gives voice to the people and their own knowledge cum realities.
Generally health promotion in Africa suffers from some of the debilitating challenges which confront the practice of health promotion broadly in many countries in the continent. These challenges, among others, include:
Poor definition and rudimentary elaboration of expected health outcomes
Ambiguous elaboration of factors and conditions to be targeted in health promotions
Ambiguity of health promotion policies and guidelines
Lack of capacity (or inadequate capacity) to develop, implement and evaluate health promotion programmes
A general context of inadequate investment in health promotion
Underdeveloped sectoral collaboration
Low political will and commitment to health promotion programmes as well as institutional corruption and resource mismanagement
The above challenges have implications for research in health promotions in the continent. There is no gainsaying the need for health promotion to be evidence based because essentially it is the only way to make it responsive to the health needs and interests of the people.
Health promotion combines varied but complementary indicators like legislation, health finance including fiscal measures and taxation, gender inclusiveness, mapping of priorities and organizational change. In spite of their differences, these issues are in reality intertwined or systematically connected in the sense that, for the public health system to function well and optimally, there should be a synergy between these indicators. Briefly:
This revolves around having the political will to make and drive through policies and laws that improve and sustain healthcare delivery. It also involves public health sector governance and leadership which aim at ensuring that only competent and qualified people lead the sector and that activities are governed by a democratic and free process which place emphasis on human rights, dignity and self-worth of all stakeholders.
Without doubt efficient health promotion and by implication the entire health delivery system cannot function without finance. In fact, the extent and impact of health promotion depend to a significant extent on the availability of funds. The problem of finance is especially critical in developing nations in Africa where political corruption and competing needs whittle down whatever gets to health from the yearly appropriation of government. However, there is a need to understand that a lot needs to be done in terms of the fiscal policies in these nations in order to achieve the desire for good health and improved life expectancy. In other words, the process of fiscal policymaking and budgetary allocation should prioritize health promotion and health delivery in these countries.
There is no gainsaying the fact that the health system as a whole is dynamic especially so in Africa where apart from battling known ailments new ones (or novel presentation of the old ailments) spring up now and then. The above entails that the health system calls for dynamic organizational setting that is robust enough to deal with changes while making improvements in the system. There is apparently no denying the fact that health promotion as a critical component of health delivery would benefit from organizational change. This is particularly so in the face of the reality that health promotion in most of the continent is still below the expectation. This is not to deny that health promotion has worked well in specific instances like the HIV/AID scourge and maternal health. However, such grab and slash system which focuses on only one of such delimited issues in the system cannot be seen as either robust or effective in the long run.
There is an obvious need to ‘en-gender’ health promotion as a very critical issue in Africa. This would entail ensuring that those involved in health promotion ensure that in all key phases of health promotion (planning, implementation and evaluation) women and men should be equal partners and collaborators. Gender, in this case, while calling attention to the needs of women, should also ensure that the men are not left behind even in approaching health issues traditionally seen as the concerns of women. Typical example here is in the area of family planning or reproductive health which demands the active collaboration or participation of both men and women to achieve desired results.
For the WHO [24], the priority interventions in Africa in respect of health promotions include capacity building, development of plans, incorporation of health promotion components in non-health sectors and strengthening of priority programmes using health promotion interventions. These essentially mean pursuing health promotion through capacity building, action planning, advocacy and multisectoral orientation. They are also in tune with relating to the determinants of health promotion in the continent. These include socio-economic conditions and physical (environment), biological, and behavioral lifestyles which impact on health in Africa. Countries can be encouraged to map out their priorities taking into consideration such factors as disease and financial burdens, threats, intervention tools and agencies, acuity, management capabilities, persistent challenges, etc.
Generally, there is a need for stepping up health promotion research in Africa in the areas of family and reproductive health targeting such issues as VVF, antenatal care, diabetes, cardiovascular issues, new disease forms/resurgence of old diseases (including Ebola), etc. especially in terms of communicating with those who are marginal to the formal sector of the society or who are less privileged by virtue of education, economic opportunities or physical/mental challenges, etc. in both urban and rural contexts. Health promotion can profit from an acute awareness of the fact that what works in one socio-geographical setting may not work in another since no two societies are exactly the same. This would entail designing programmes that even where the general principles or goals remain the same embody recognition of the socio-geographical peculiarities of the society/community concerned.
Given the usual paucity of funds in the continent, it makes sense that to minimize cost and save time, there should be incorporation of both needs assessment and evaluation into ongoing health promotion activities. This approach offers a smart way of pursuing health promotion goals without elaborate budget.
In spite of country differences and specific structural challenges, there is a need to build a culture of sharing and documenting outcomes and evidences of health promotion between different countries and organizations. This is a step towards achieving the desirable goal of multinational coordination especially for infectious diseases and epidemics. Equally, African nations need to invest more in capacity building for media and theater practitioners in both private and public sectors on health promotion. There is no gainsaying the media’s crucial role in health information dissemination. Actually, health promotion is largely media driven and should be programmed as such.
In addition to media practitioners, there should be health programme or intervention specific to health promotion capacity building for different cadres of public sector workers. Such capacity building or training should be anchored on acute awareness of current research trends and best practices globally. There should also be increased attention to the need for specific health promotion for under-represented health issues and priority to non-communicable diseases should be targeted. It should also improve capacity on how to incorporate methods of targeting members of the society marginal or vulnerable within each country context.
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