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The Double Burden of Malnutrition GCHB 6780 Roger Shrimpton John Mason Lisa Saldanha 30 January 2013 Class 5 : Causes of DBM I (Biology) 1.

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Presentation on theme: "The Double Burden of Malnutrition GCHB 6780 Roger Shrimpton John Mason Lisa Saldanha 30 January 2013 Class 5 : Causes of DBM I (Biology) 1."— Presentation transcript:

1 The Double Burden of Malnutrition GCHB 6780 Roger Shrimpton John Mason Lisa Saldanha 30 January 2013 Class 5 : Causes of DBM I (Biology) 1

2 Content Readings Historical perspective Analytical frameworks Biological/Health Environment – Health transition – Metabolic programming – Energy balance – Genetics Conclusions 2

3 Readings Classes 4-10

4 Jan 23 Class 3 1. Bloom, D.E., Cafiero, E.T., Jané-Llopis, E., Abrahams-Gessel, S., Bloom, L.R., Fathima, S., Feigl, A.B., Gaziano, T., Mowafi, M., Pandya, A., Prettner, K., Rosenberg, L., Seligman, B., Stein, A.Z., & Weinstein, C. (2011). The Global Economic Burden of Noncommunicable Diseases. Geneva: World Economic Forum. (Rocco ) 2. Finkelstein EA, Trogdon JG, Cohen JW, Dietz W. 2009. Annual medical spending attributable to obesity: payer-and-service specific estimates. Health Affairs (Millwood) 28:w822-w831.( Jackie) Jan 24 Class 4 3. Darnton-Hill I, Nishida C and James WPT 2004. A life course approach to diet, nutrition and the prevention of chronic diseases. Public Health Nutrition: 7(1A), 101–12 (Kaitlin) 4. Rowland MG, Rowland SG, Cole TJ. 1988. Impact of infection on the growth of children from 0 to 2 years in an urban West African community. Am J Clin Nutr. 47(1):134-8. (Erin) Readings

5 Jan 30 Class 5 5. WHO 2004. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. A WHO Expert consultation. The Lancet 363:157-63 (Liz) 6. Meas T 2010. Fetal origins of insulin resistance and the metabolic syndrome: A key role for adipose tissue. Diabetes & Metabolism 36:11-20 (Giovana) Feb 04 Class 6 7. Popkin BM 2006. Global nutrition dynamics: the world is shifting rapidly toward a diet linked with noncommunicable diseases. Am J Clin Nutr 84: 289-298 (Theresa) 8. Drenowski A, Darmon N 2005. Food choices and diet costs: an economic analysis. J Nutr 135: 900-904 (Alexandra) Readings

6 Feb 06 Class 7 9. Edwards P and Tsouros A 2006. Promoting physical activity and active living in urban environments: The role of local governments. Copenhagen: WHO Europe. (Rachel) 10. McCormack G, Giles-Corti B, Lange A, Smith T, Martin K, Pikora TJ. 2004. An update of recent evidence of the relationship between objective and self-report measures of the physical environment and physical activity behaviours. J Sci Med Sport. 7(1 Suppl):81-92. (Judy) Feb 13 Class 8 11. World Health Organization.2003. Diet, Nutrition and the Prevention of Chronic Diseases. Report of a joint WHO/FAO expert consultation. Technical Report Series N0 916. pp 54-71. Geneva: WHO. (Steve) 12. Zimmermann MB, Zeder C, Muthayya S, Winichagoon P, Chaouki N, Hurrell RF. 2008. Adiposity in women and children from transition countries predicts decreased iron absorption, iron deficiency and reduced response to iron fortification. Int J Obesity 32(7): 1098-1104 ( Kristine)

7 Feb 18 Class 9 13. Swinburn BA, Caterson I, Seidell JC, James WPT 2004. Diet, nutrition and the prevention of excess weight gain and obesity. Public Health Nutrition: 7(1A), 123– 146 (Anne) 14. Gillespie S, Haddad L. 2001. Attacking the Double Burden of Malnutrition in Asia and the Pacific. ADB Nutrition and Development Series No. 4. Manila: Asian Development Bank. Pp131-146 burden-malnutrition-asia-and-pacific (Rory) Feb 20 Class 10 15. Waters E, de Silva-Sanigorsky A, Hall BJ, Brown T, Campbell KL, Gao Y, Armstrong, R, Prosser L, Summerbell CD. 2011. Interventions for preventing obesity in children. Cochrane Database Syst Rev. 12:CD001871 (Jennifer) 16. Hite AH, Richard, Feinman D, Guzman GE, Satin M, Schoenfeld PA, Wood RJ. 2010 In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee. Nutrition 26:915–924 (Amanda) Readings

8 Ashleigh? Chelsea? Look for syllabus, background paper (DBM Draft) and lectures on intranut Readings

9 9 Historical perspective Source: Fogel 2004 1996

10 Historical perspective NUTRITION IS A YOUNG SCIENCE! Recommended daily allowances – 1943 NAS/USA for 8 nutrients – 1989 NAS for 24 nutrients Anthropometric indicators – 1979 used to specify degrees of PEM in International Classification of Diseases – 1995 WHO defines anthropometric indicators and cut-offs for measuring DBM across life course – 2000 Recognition that process of stunting (chronic malnutrition) is largely over by 2 years (Shrimpton et al 2000) – 2005 WHO defines international growth standard for all children (De Onis et al 2006) Nutrition in Development – 2004 Recognition that half of the economic development achieved by the UK in the last century was due to improvements in nutrition (Fogel 2004) – 2004 Recognition that economic development alone reduces MCU only very slowly (Haddad et al 2004) 10

11 Kumanyika S K et al. Circulation 2008;118:428-464 Copyright © American Heart Association Rapidly increasing overweight is a recent phenomenon

12 Overweight is wide spread globally, especially among the richest, and is increasing in most LMICs 12 Subramanian, et al. 2011

13 13 HEALTH Child Malnutrition FOOD Resources & Control Human, Economic & Organisational Natural resources: Inadequate dietary intake Disease Basic causes Immediate causes Underlying causes Education Political and Ideological Superstructure Economic Structure Manifestations CARE Source: UNICEF 1990 Analytical frameworks The UNICEF Conceptual Framework LIMITATIONS LIFECOURSE? OVERNUTRITION?

14 14 Analytical frameworks

15 UK Foresight Project on OBESITY in the UK (2007) Energy balance

16 The Causes of the DBM Four cross cutting themes for analysis of causes of DBM – Biological Health environment – Economic Food environment – The Socio Cultural Environment – The Physical/Built environment 16

17 Biological/Health Environment 17 Infections/Disease (Health Transition) Intrauterine growth retardation (metabolic programming) Metabolic mechanisms in weight control Genetics Medications

18 Biological/Health Environment Infections/Disease 18 Example of the temporal relationship between infection and growth of an individual child in Guatemala. Mata et al. 1976

19 19 Biological/Health Environment Infections/Disease Health transition

20 Biological/Health Environment Infections/Disease There is considerable debate over whether or not obesity is a disease. Opponents argue that obesity is not a disease because it results from a person's chosen lifestyle, eating habits, and environment (i.e. residential location, social circle, economic status). Proponents stress that obesity is a disease because it is caused by genetics, biological factors or illnesses that cause weight gain, and by obesogenic environments. US IRS considers obesity a disease and allows tax deductions for treatment

21 Biological/Health Environment Intrauterine growth 21 Source: Fall 2009

22 22 Biological/Health Environment Intrauterine growth Source: Valdez et al 1994 Among Americans of white and Mexican descent

23 Food supplements offered daily to pregnant women and preschool children aged less than 6 years in rural India, produced the following changes in adolescence fifteen years later: – Less insulin resistance : 20% (3% to 39%; P=0.02) lower HOMA* score; – Less arterial stiffness : 3.3% (1% to 5.7%; P=0.008) lower augmentation index, Source: Kinra et al BMJ 2008 * HOMA = Homeostasis model assessment of insulin resistance 23 Biological/Health Environment Intrauterine growth

24 Nutrition supplementation in during pregnancy and early child hood (=<72m ) in Guatemala was associated with the following changes in adulthood: – a lower fasting glucose level (7.0 mg/dl, 95% confidence interval (CI): 0.5, 13.5) for exposure at ages 36–72 months; – lower systolic blood pressure (3.0 mmHg, 95% CI: 0.4, 5.6) for exposure at ages 24–60 months; – and a lower triglyceride level (sex-adjusted; 22.2 mg/dl, 95% CI: 0.4, 44.1) and higher high density lipoprotein cholesterol level (males only; 4.7 mg/dl, 95% CI: 1.5, 7.9) for exposure from conception to age 36 months. Source: Stein et al 2006 24 Biological/Health Environment Intrauterine growth

25 Biological/Health Environment Metabolism 1 Obesity is fundamentally a problem of energy balance, and as such, it can only develop when energy (food) intake is in excess of total energy expenditure it is a universal observation that Basal Metabolic Rate (BMR) is raised not suppressed in obese people because they have a greater lean body mass (LBM) than their lean counterparts, and because LBM is the major determinant of BMR Differences between intake and expenditure are primarily buffered by changes in the amount of lipid deposited in the specialized fuel storage organ, white adipose tissue (or white fat). There is also brown adipose tissue, which is specialized for heat production by non-shivering thermogenesis. Source: Trayhurn 2007 25

26 Biological/Health Environment Metabolism 2 Adipose tissue is now recognized as the source of key hormones which play an important role in the regulation of energy balance – particularly leptin – and a diverse range of protein factors and signals termed adipokines, which are involved in overall metabolic regulation. A number of inflammation-related proteins are released by white adipocytes, as well as adiponectin, and these include cytokines, chemokines and acute phase proteins. The current view is that the inflammatory state of obesity plays a key causal role in the development of type 2 diabetes and the metabolic syndrome associated with obesity. Source: Trayhurn 2007 26

27 Opie L H Circulation 2007;115:e32-e35 Copyright © American Heart Association Biological/Health Environment(Metabolism) Plus: LEPTIN and Grehlin!

28 Kg decades Biological/Health Environment (appetite) Commonly weight increases a kilo a year during adulthood – passive obesity Snacking of ultra-processed foods seems to fool appetite mechanisms +100Kcal a day can add up to gradual increments over time

29 STORM Mean bodyweight changes during weight loss and weight maintenance phases in 600 European subjects over 2 years 104 102 100 98 96 94 92 90 88 012246810141618202224 Month Bodyweight (kg) Control Sibutramine Weight loss Weight maintenance Same diet and exercise for both sibutramine and control Source: James WPT, et al, 2000 Biological/Health Environment (appetite)

30 Biological/Health Environment Genetics It has been suggested that there are genetic factors which enable individuals to efficiently collect and process food to deposit fat during periods of food abundance, which has been called the thrifty genotype Multiple studies of families, adoptees, twins and, most powerfully, adopted twins have all confirmed that heritable factors are likely to be responsible for 45–75% of the inter- individual variation in BMI. (Farooqi and ORahilly 2007) These heritable factors are likely to be multiple and are likely to operate through the full range of potential mechanisms, including energy intake, energy expenditure and the partitioning of nutrients between fat and lean tissue. 30

31 Biological/Health Environment Genetics 31 Source: Brooks et al 1995 BUT! Birth weight related to weight of recipient mother not of donor

32 Biological/Health Environment Genetics 32 Source: Godfrey et al 1997 BUT! Thinness of baby at birth relates to birth weight of mother but not father

33 Medications That Can Cause Weight Gain Psychotropic medications – Tricyclic antidepressants – Monoamine oxidase inhibitors – Specific SSRIs – Atypical antipsychotics – Lithium – Specific anticonvulsants (valproic acid) -adrenergic receptor blockers – Propanolol Diabetes medications – Insulin – Sulfonylureas – Thiazolidinediones Highly active antiretroviral therapy Tamoxifen Steroid Hormones – Glucocorticoids – Progestational steriods 33/26 Biological/Health Environment Source: Pijl H, Meinders AE. Bodyweight changes as an adverse effect of drug treatment. Drug Safety 1996;14:329-342.

34 Conclusions 34 1.Obesity and diet related NCDs are replacing infectious diseases as major causes of death 2.Constrained maternal and child nutrition increases the risks of diet related NCDs (metabolic syndrome) later in the life course 3.Obesity is a disease because it is caused by genetics, biological factors or illnesses that cause weight gain, and by obesogenic environments. 4.It seems that obesity in the modern world is a natural biological response to a changed environment and that innate body-weight regulatory mechanisms have been overwhelmed by energy-dense diets and sedentary lifestyles 5.Although personal choice is an important component of obesity control, much has to be done to create an environment that facilitates the right choices. 6.Once created the obese state is very difficult to revert, and visceral fat seems to play a key role in this.

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