Obesity is a public health emergency
BMJ 2019; 366 doi: https://doi.org/10.1136/bmj.l5463 (Published 13 September 2019) Cite this as: BMJ 2019;366:l5463
All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
The Theme of the 20th Anniversary of the Oxford Round Table which I attended in 2008 was on Obesity as a Persisting Health Problem with the expression of much distress and discomfort that, in spite of ‘Technological Advances’ in Diagnosis, Therapy/ Available Drugs, Clinical Management, Prevention and Research on Obesity, it remained a Public Health Scourge! Now in 2019, Obesity remains not only as a ‘Public Health Challenge’ but also a ‘Public Health Emergency’ [1]! Several Reports have re-affirmed Obesity still persisting as a possible ‘Epidemic Health Challenge’ [2-4]. The ‘Approaches’ to tackling the ‘Obesity Challenge’ have disposed ‘Multi-faceted Interventions’ [5-9]. These include, among several others: Individual Interventions of Healthy Eating with ChooseMyPlate/ MyFoodPlate/ FoodPyramid Websites and Increased Healthy Physical Activities. Others include Healthy Living/ Lifestyle, Healthy Weight Reduction (Not ‘Dieting’!), Regular Tips for Parents, Community Programmes and State/ Government Efforts and Programmes.
A more ‘Programmatically Apt Intervention Strategy’ should dispose a ‘Productive Harvest’ from the ‘Triple-A Process’ on Obesity as a ‘Public Health Challenge’ [10]. Interventions that do not have a nexus with the ‘Triple-A Process Harvests’ are not likely to be promising, successful and impactful! Still enmeshed in the ‘Obesity Aetiology Conversation’, some have questioned whether Obesity should be regarded as a ‘Disease’ [11]. Others have questioned the roles of ‘Individual Choices’, ‘Energy Consumption-Expenditure Imbalance’ or ‘Environmental Factors’ including the ‘Food Environment’ [12-14]. There have been attempts to investigate the ‘Gene-Environment Interaction’ in the ‘Obesity Aetiology Conversation’ with ‘Genetic Predisposition’ to the ‘Apple-Pear Shape Dichotomy’ and the ‘Obesity Development and Manifestation’ [15-17].
‘Interventions’ to address the ‘Persisting Obesity Challenge’ have focused on the ‘Aetiology’, ‘Diagnosis’, ‘Drugs and Management’, ‘Prevention’ and ‘Obesity Research’ [18,19]. Diagnostic Screening includes Waist Circumference, Waist/ Hip Ratio, Screening for Overweight and Body Mass Index Measurements. Pharmacological Interventions/ Anti-Obesity Medications include, among others: Orlistat, Lorcaserin, Bupropion, Sibutramine, Phentermine, Sertraline and Fluoxetin. Surgical Interventions involve Gastric Bypass Operations/ Bariatric Surgeries (Roux-en-Y Operation as a Case-in-Point!). Treating other ‘Components’ of the ‘Metabolic Syndrome’ is also productive in the Management of Obesity!
The Developmental Origins of Health and Disease Hypothesis (DOHAD Hypothesis) and the Foetal Origins of Adult Diseases Hypothesis (FOAD Hypothesis) have been explored as the possible ‘Programmatic Pillars’ for the ‘Obesity Challenge Interventions’20-23. With these ‘Obesity Programmatic Interventions’, the ‘Obesity Health Challenge’ has remained an unacceptable ‘Public Health Difficulty’ [1-4,20-23]. Obesity is one of the ‘Components’ of the ‘Metabolic Syndrome’ which are captured by the Acronym ‘DOHIDIMS’: ‘Diabetes, Obesity, Hypertension, Ischaemic Heart Disease, Dyslipidaemia, Insulin Resistance Syndrome in the Metabolic Syndrome’ [24,25] ! The ‘O’ of the ‘DOHIDIMS’ can also represent ‘Others’ which may include Cancers and Infant Microbiome-induced Neurobehavioural Disorders [1,14,25] !. Concerning the ‘Obesity Health Challenge’ and unearthing the ‘Aetiology’ and ‘Prevention’, much attention and resources have not been proportionately focused on the ‘Role/ Contribution’ of ‘Exclusive and Optimal Breastfeeding (EBF-OBF)’! This may be regarded as the ‘Obesity Interventional Inequity’ which needs to be addressed by greater ‘Attention and Resources’ being deployed and focused on the ‘EBF-OBF Dyad’ as a Child Survival Intervention! This is the justification for the ‘Pre-FOAD Hypothesis’ as a ‘Panacea’ for the ‘Interventional Inequity’! I had similarly made this same point which was highlighted for ‘Programmatic Expedience and Impact’ concerning Diabetes, a ‘Component’ of the ‘Metabolic Syndrome’, when I attended the 2013 International Diabetes Federation (IDF)-organized World Diabetes Congress in Melbourne, Australia!
The ‘Pre-FOAD Hypothesis’ has its ‘Starting Locus’ from EBF which, with integration with ‘Optimal Implementation’ of the ‘Child Survival Interventions (CSI)’ and optimizing the benefits of the ‘Two Growth Spurts’ (During the Period of EBF and Pre-Pubertal), assures that the ‘Girl Child’ grows and develops into the ‘Female Adult’ with the ‘Optimal Pre-Pregnancy Maternal Phenotype’ and the capacity, through ‘Developmental Plasticity’ and ‘Intrauterine Body Programming’, to give birth to Newborns with the ‘Optimal Body Composition’ that will be ‘Anti-Obesiogenic’ and protect against ‘Adult Disease Induction (ADI)’ and the development of the ‘DOHIDIMS Components’ [24,25] ! A further ‘Developmental Benefit’ of the ‘Pre-FOAD Hypothesis’ through the ‘EBF-OBF Practice’ is the assurance of the establishment of the desired ‘Infant Microbiome’ which, with the appropriate ‘Firmicutes: Bacteroidetes Ratio’ favours the development of the ‘Pear-shaped Body’ and ‘Protection against Obesity’ [15-17,25,26] ! Increased Firmicutes in the ‘Infant Microbiome’ favours a predisposition to Obesity. The evaluation of the ‘Personal Microbiomics’, as part of the ‘Personal Metabolomics’, with the ‘OMICS Technology’ using ‘High-Throughput Data’ is valuable in addressing the ‘Obesity Epidemic’! In this era, ‘P6M’ is the way to go for more impactful care: ‘Predictive Promotive Preventive Proactive Precision Personalized Medicine’!! ‘EBF-OBF is a low-cost high-impact ‘Intervention Strategy’ for the ‘Obesity Health Challenge and Epidemic’. EBF has been canvassed as the ‘Mother of ALL Child Survival Interventions (CSI)’; The CSI are captured by the Acronym ‘GOBIF3E2TH’ which represents the following: Growth Monitoring (Now with ‘and Promotion’), Oral Rehydration Therapy, Breastfeeding (EBF-OBF), Immunization, Family Planning, Food Supplementation, Female Education, Environmental Sanitation, Essential Drugs Programme, Treatment of Common Childhood Conditions and Health Education [27] ! Addressing the ‘Pre-FOAD Hypothesis’ definitely holds some promise towards a ‘Sustainable Panacea’ to eclipse the current ‘Interventional Inequity’ in the persisting ‘Obesity Epidemic’ in addition to possibly impacting positively on the other ‘Components’ of the ‘Metabolic Syndrome’/ ‘DOHIDIMS’!
REFERENCES
1. Ayton A, Ibrahim A. Obesity is a public health emergency. BMJ 2019; 366:l5463 of 13th September 2019.
2. Rodgers A, Woodward A, Swinburn B, Dietz WH. Prevalence trends tell us what did not precipitate the US Obesity epidemic. Lancet Public Health 2018; 3:e162-163. PMID 29501260
3. Finucane MM, Stevens GA, Cowan MJ, Global burden of Metabolic Risk Factors of Chronic Diseases Collaborating Group (Body Mass Index). National, regional and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants. Lancet 2011; 377:557-67.
4. Skinner AC, Ravabakht SN, Skelton JA, Perrin EM, Armstrong SC. Prevalence of obesity and severe obesity in US children, 1999-2016. Pediatrics 2018; 141:e20173459.
5. Hill JO, Peters JC. Environmental contributors to the Obesity epidemic. Science 1998; 280:1371-1374.
6. World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: WHO; 1998.
7. Jeffrey RW. Public health strategies for obesity treatment and prevention. Am J Health Behav 2001; 25:252-259.
8. Campbell K, Waters E, O’Meara S, Summerbell C. Interventions for preventing obesity in Children. Cochrane Library, Issue 2. CD001871. Oxford: Update Software; 2002.
9. Crawford D. Population strategies to prevent obesity. BMJ 2002; 325 (7367):728-729.
10. UNICEF. Triple-A Process in Nutrition Programme Assessment. UNICEF 1996
11. Wilding JPH, Mooney V, Pile R. Should obesity be recognized as a disease? BMJ 2019;N366:l4258.
12. de Macedo K, de Freitas JS, da Silva Torres IL. The influence of palatable diets in reward system activation: a mini review. Adv Pharmacol Sci 2016; PMID 27087806
13. Brandvist M, Bjorngaard JH, Odegard RA, Asvold BO, Sund ER, Vie GA. Quantifying the impact of genes on BMI during the Obesity epidemic: longitudinal findings from the HUNT Study. BMJ 2019; 366:l4067.
14. Small DM, DiFeliceantonio AG. Processed foods and food reward. Science 2019; 363:346-7.
15. Padgett J, Biro FM. Different shapes in different cultures: Body dissatisfaction, overweight and obesity in African American and Caucasian females. J Pediatr Adolesc Gynecol 2003; 16:349-354.
16. Play up your shape. People Style Watch 2011; 126-138.
17. Thoma ME, Hediger ML, Sundaram R et al. Comparing Apples and Pears: Women’s Perception of their Body Size and Shape. J Women’s Health (Larchmt) 2012; 21 (10):1074-1081.
18. Reilly JJ, Wilson ML, Summerbell CD, Wilson DC. Obesity: diagnosis, prevention and treatment; evidence-based answers to common questions. Arch Dis Childh 2002; 86:392-394
19. Orzano AJ Scott JG. Diagnosis and treatment of obesity in adults: an applied evidence-based review. J Am Board Fam Pract 2004;17 (5):359-69
20. Barker DJ. The developmental origins of adult disease. J Am Coll Nutr 2004; 23:588S95S
21. Armitage JA, Poston L, Taylor PD. Developmental origins of obesity and the metabolic syndrome: the role of maternal obesity. Front Horm Res 2008; 36:73-84
22. Calkins K, Devasker SU. Foetal origins of adult disease. Curr Probl Pediatr Adolesc Health Care 2011; 41 (6):158-176
23. World Health Organization. Launch of the Healthy Life Trajectories Initiative (HeLTI): an International DOHaD Research Collaboration. WHO; Geneva; 2017
24. Eregie CO. Programming the End from before the Beginning: Juxtaposing Technology with the ‘TEA Triad’. 106th Inaugural Lecture, University of Benin, Benin City, Nigeria. University of Benin Press; 17th December 2009.
25. Eregie CO. Breastmilk, Breastmilk Substitutes (Including Infant Formula) and Infant Microbiome: Still more Justification for the Prohibition of Advertisement of Breastmilk Substitutes (BMS). https://www.bmj.com/content/364/bmj.l1279/rr-6 of 4th April 2019.
26. Koleva PT, Bridgman SL, Kozyrskyi AL. The Infant Gut Microbiome: Evidence for Obesity Risk and Dietary Intervention. Nutrients 2015; 7 (4):2237-2260
27. Eregie CO. UNICEF Consultancy Report. 1996 World Breastfeeding Week Celebration. UNICEF Nigeria, Lagos; 1996
Professor Charles Osayande Eregie,
MBBS, FWACP, FMCPaed, FRCPCH (UK), Cert. ORT (Oxford), MSc (Religious Education),
Professor of Child Health and Neonatology, University of Benin, Benin City, Nigeria,
Consultant Paediatrician and Neonatologist, University of Benin Teaching Hospital, Benin City, Nigeria,
UNICEF-Trained BFHI Master Trainer,
ICDC-Trained in Code Implementation,
*Technical Expert/ Consultant on the FMOH-UNICEF-NAFDAC Code Implementation Project in Nigeria,
*No Competing Interests.
Competing interests: No competing interests
Dear Sir,
To Dr. Agnes Ayton's question (BMJ 21 September 2019) “Is obesity a consequence of individual choices or a disease affecting the population?” one may reply “Nutrition`s the thing - specifically, a surfeit of bad advice ushered in by the 1977 USA Dietary Guidelines directing us to avoid butter and animal fats generally, all of which came to be replaced by carbohydrates”.
In physiological terms, the blight`s insulin resistance (IR) admirably investigated by the late Professor Gerald Reaven.
Over the decades since, this dietary shift has ignited a world-wide epidemic of Type II diabetes - as ever greater numbers slip into Insulin Resistance. In the same issue of the BMJ we learn from the Pioneer 100 Wellness Project that, of 109 subjects undergoing routine checks, 59 were identified to have diabetes or pre-diabetes.
The burden - financial and in morbidity - of this nutritional shift may eventually come to exceed most other calamities befalling man over the ages.
Time for a paradigm shift?
Dr. Georges S. Kaye
London
gsk@georgeskaye.com.
Competing interests: No competing interests
FURTHER INTERVENTION ON OBESITY AS A PUBLIC HEALTH EMERGENCY: A ROLE FOR THE CUMULATIVE GROWTH SCORE (CGS) OF EXCLUSIVELY BREASTFED INFANTS IN THE ‘Pre-FOAD HYPOTHESIS’ APPROACH
Obesity has been recognized as a ‘Public Health Challenge’ and, indeed lately, as a ‘Public Health Emergency’1-5! It has, in fact, assumed ‘Epidemic Proportions’ as a ‘Public Health Problem’ as gleaned from several Reports of various ‘Interventions’ to address the ‘Obesity Health Scourge’ but disappointingly with unsatisfactory ‘Outcomes’ and the resultant persisting ‘Public Health Challenges’ with Obesity6-10. The ‘Interventions’ include Individual/ Personal Activities and Actions, Institutional Efforts and Programmes, Community/ Government Initiatives and Research Undertakings. The ‘Approaches/ Obesity Interventions’ have variously explored ‘Energy Balance Management’ through Individual Healthy Eating and Increased Healthy Physical Activities. Institutional and Government/ Community ‘Programmatic Diagnostic Screening Initiatives’ have also focused on Anthropometric Measurements: Body Weight, Waist Circumference, Waist/ Hip Ratio, Body Fat Composition and Body Mass Index. These are geared towards achieving Healthy Weight Reduction Goals. Efforts have been heightened towards ‘Obesity Research’ to identify and investigate useful ‘Anti-Obesity Drugs’ for ‘Pharmacological Interventions’11,12. Various ‘Gastric Bypass Procedures’/ ‘Bariatric Surgeries’ have also been undertaken as part of the ‘Comprehensive Obesity Intervention Programmes’! Additionally, ‘Obesity Research Endeavours’ have investigated the ‘Aetiological Contributions’ of ‘Gene-Environment Interaction’ and ‘Developmental Stresses and Plasticity’ to the ‘Obesity Scourge’ through improved understanding of the ‘Developmental Origins of Health and Disease Hypothesis (DOHAD Hypothesis)’ and the ‘Foetal Origins of Adult Diseases Hypothesis (FOAD Hypothesis)’13-16. Explored in these endeavours are various complex and possibly interacting and intriguing ‘Obesity Spheres’: Genetic, Metabolic, Behavioural, Cultural, Environmental and ‘Gene-Environment Interaction’/ ‘Genomics’! In spite of these ‘Obesity Interventions’, the ‘Obesity Scourge’ persists as a ‘Public Health Challenge’ and this is the rationale undergirding the conceptualization of the ‘Interventional Inequity’5!!
The ‘Obesity Interventions’ have deployed ‘Exploratory Resources’ and ‘Focused Attention’ to the ‘Aetiological’, ‘Diagnostic’, ‘Therapeutic’, ‘Preventive’ and ‘Prognostic’ Issues in Obesity. Disproportionately less ‘Attention and Resources’ within the ‘Obesity Research Armory’, unearthing the ‘Aetiological Issues’, have been directed to ‘Breastfeeding’ (‘Exclusive Breastfeeding (EBF)’ and ‘Optimal Breastfeeding (OBF)’, the ‘Starting Locus’ of the ‘Pre-FOAD Hypothesis’! This is the ‘Obesity Interventional Inequity’ which the ‘Pre-FOAD Hypothesis’ seeks to address and rectify5,17,18! This is also better appreciated from the perspectives of the ‘Three Hits Hypothesis’ regarding ‘Developmental Plasticity’, ‘Intrauterine Body Programming’, ‘Postnatal Body Programming’ and the predisposition to Obesity19,20. There are the ‘Genetic’, ‘Intrauterine’ and ‘Postnatal’ ‘Contributors’ as ‘Hits’! Concerning ‘Postnatal Evaluation’ for ‘Optimal Promotive Care’ of Exclusively Breastfed Infants, several Nomograms have been reported to assure ‘Anti-Obesiogenic Promotive Care’21-24. The ‘New Growth Standards’ were an imperative for the proper ‘Growth Monitoring and Promotion’ of Exclusively Breastfed Infants giving the peculiar growth of Breastfed Infants in the era of the Baby-Friendly Hospital Initiative (BFHI). ‘Growth Monitoring and Promotion (GMP)’ is an integral ‘Component’ of the ‘Child Survival Interventions (CSI)’25!!
In developing Countries with poor ‘Health Records’ and ‘Low Average Adult Female Literacy Levels’, and where many parents may not accurately recall the ‘Birth Dates’ of their Infants as may also be observed in the ‘Camps of Motherless Babies’ especially among ‘Internally Displaced Persons (IDPs)’, ‘Immigration/ Refugees Camps’ and ‘Rehabilitation/ Settlement Camps’, the ‘Postnatal Age (PNA)’ may not be readily available or accurately documented. The ‘Accurate Postnatal Age’ of the Infants is a necessity for the proper use of the ‘New Nomograms’ developed specifically for Exclusively Breastfed Infants21-24! The ‘Cumulative Growth Score (CGS)’ was developed and reported for the ‘Estimation of Postnatal Age (PNA)’ among Exclusively Breastfed Infants26!! The ‘Cumulative Growth Score (CGS)’ is a ‘Composite Score’ computed from the ‘Postnatal Score (PNS)’ assigned to each of the four ‘Anthropometric Parameters and Measurements’ for Exclusively Breastfed Infants: weight, head circumference, mid-arm circumference and length. With the Cumulative Growth Score (CGS), the Postnatal Age (PNA) is estimated with reasonable accuracy and the Exclusively Breastfed Infants are enabled to benefit from the ‘Pre-FOAD Hypothesis’ Approach with the ‘Coupling’ of the ‘EBF-OBF Dyad’ and the ‘Child Survival Interventions (CSI)’/ ‘GOBIF3E2TH’25! This amplifies the relevance of the ‘Postnatal Component’ of the ‘Three Hits Hypothesis’19,20! This is the ‘Thrust’ and ‘Subsumption’ within the ‘Pre-FOAD Hypothesis’ as an ‘Antidote’ to the ‘Interventional Inequity’ towards the rational deployment of appropriate and adequate ‘Obesity Armory Components’ to manage and control the possible ‘Obesity Epidemic’. Here is the compelling role for the ‘Cumulative Growth Score ((CGS)’ in the accurate Estimation of the ‘Postnatal Age (PNA)’ of Exclusively Breastfed Infants! The relevant Tables (Including the Definitions of the Postnatal Scores (PNS)) and the Figure (Chart for Computing Postnatal Age (PNA) from the Cumulative Growth Score (CGS)) are accessible from the ‘Award-winning Poster Presentation’ at the 19th Annual International Conference of the Academy of Breastfeeding Medicine held in November 2014 in Cleveland, Ohio, United States of America26!!
REFERENCES
1. Rodgers A, Woodward A, Swinburn B, Dietz WH. Prevalence trends tell us what did not precipitate the US Obesity epidemic. Lancet Public Health 2018; 3:e162-163. PMID 29501260
2. Finucane MM, Stevens GA, Cowan MJ, Global burden of Metabolic Risk Factors of Chronic Diseases Collaborating Group (Body Mass Index). National, regional and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants. Lancet 2011; 377:557-67.
3. Skinner AC, Ravabakht SN, Skelton JA, Perrin EM, Armstrong SC. Prevalence of obesity and severe obesity in US children, 1999-2016. Pediatrics 2018; 141:e20173459.
4. Ayton A, Ibrahim A. Obesity is a public health emergency. BMJ 2019; 366:l5463 of 13th September 2019.
5. Eregie CO. Obesity as a Public Health Emergency: A Look at the ‘Pre-FOAD Hypothesis’ as a Panacea for the ‘Interventional Inequity’. https://www.bmj.com/content/366/bmj.l5463/rr-0 of 4th October 2019.
6. Hill JO, Peters JC. Environmental contributors to the Obesity epidemic. Science 1998; 280:1371-1374.
7. World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: WHO; 1998.
8. Jeffrey RW. Public health strategies for obesity treatment and prevention. Am J Health Behav 2001; 25:252-259.
9. Campbell K, Waters E, O’Meara S, Summerbell C. Interventions for preventing obesity in Children. Cochrane Library, Issue 2. CD001871. Oxford: Update Software; 2002.
10. Crawford D. Population strategies to prevent obesity. BMJ 2002; 325 (7367):728-729.
11. Reilly JJ, Wilson ML, Summerbell CD, Wilson DC. Obesity: diagnosis, prevention and treatment; evidence-based answers to common questions. Arch Dis Childh 2002; 86:392-394
12. Orzano AJ Scott JG. Diagnosis and treatment of obesity in adults: an applied evidence-based review. J Am Board Fam Pract 2004;17 (5):359-69
13. Barker DJ. The developmental origins of adult disease. J Am Coll Nutr 2004; 23:588S95S
14. Armitage JA, Poston L, Taylor PD. Developmental origins of obesity and the metabolic syndrome: the role of maternal obesity. Front Horm Res 2008; 36:73-84
15. Calkins K, Devasker SU. Foetal origins of adult disease. Curr Probl Pediatr Adolesc Health Care 2011; 41 (6):158-176
16. World Health Organization. Launch of the Healthy Life Trajectories Initiative (HeLTI): an International DOHaD Research Collaboration. WHO; Geneva; 2017
17. Eregie CO. Programming the End from before the Beginning: Juxtaposing Technology with the ‘TEA Triad’. 106th Inaugural Lecture, University of Benin, Benin City, Nigeria. University of Benin Press; 17th December 2009.
18. Eregie CO. Breastmilk, Breastmilk Substitutes (Including Infant Formula) and Infant Microbiome: Still more Justification for the Prohibition of Advertisement of Breastmilk Substitutes (BMS). https://www.bmj.com/content/364/bmj.l1279/rr-6 of 4th April 2019.
19. Loos RJF. Recent progress in the genetics of common obesity. Br J Clin Pharmacol 2009; 68 (6): 811-829
20. Li X, Zhang M, Pan X, Xu Z, Sun M. ‘Three Hits’ Hypothesis for Developmental Origins of Health and Disease in View of Cardiovascular Abnormalities. Birth Defects Res 2017; 109 (10):744-757
21. Eregie CO. A normative growth standard of upper arm measurements for exclusively breastfed infants. E Afr Med J 2000; 77:5-7.
22. Eregie CO. Exclusive breastfeeding and infant growth studies: Reference standards of head circumference, length and mid-arm circumference/ head circumference ratios for the first six months of life. J Trop Pediatr 2001; 47:329-334.
23. Garza C, de Onis M. The WHO Multicentre Growth Reference Study Group. Rationale for developing a new international growth reference. Food Nutr Bull 2004; 25 (1 Suppl): S5-S14.
24. de Onis M, Garza C, Onyango A, Martorell R (eds.). WHO Growth Standards. Acta Paediatr 2006; 95:1-104.
25. Eregie CO. UNICEF Consultancy Report. 1996 World Breastfeeding Week Celebration. UNICEF Nigeria, Lagos; 1996
26. Eregie CO. Clinical Evaluation of Exclusively Breastfed Infants: The Value of a Cumulative Growth Score (CGS) for the Estimation of Postnatal Age (PNA). Breastfeeding Medicine 2014; 9 (Suppl 1):S-9.
Professor Charles Osayande Eregie,
MBBS, FWACP, FMCPaed, FRCPCH (UK), Cert. ORT (Oxford), MSc (Religious Education),
Professor of Child Health and Neonatology, University of Benin, Benin City, Nigeria,
Consultant Paediatrician and Neonatologist, University of Benin Teaching Hospital, Benin City, Nigeria,
UNICEF-Trained BFHI Master Trainer,
ICDC-Trained in Code Implementation,
*Technical Expert/ Consultant on the FMOH-UNICEF-NAFDAC Code Implementation Project in Nigeria,
*No Competing Interests.
Competing interests: No competing interests