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The Double Burden of Malnutrition

GCHB 6780

Roger ShrimptonJohn Mason

Lisa Saldanha

30 January 2013Class 5 : Causes of DBM I (Biology)

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Content• Readings• Historical perspective• Analytical frameworks• Biological/Health Environment

– Health transition– Metabolic programming– Energy balance– Genetics

• Conclusions

Readings

Classes 4-10

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 http://www.who.int/nutrition/publications/public_health_nut2.pdf (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

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 http://www.who.int/nutrition/publications/bmi_asia_strategies.pdf (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

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. http://www.euro.who.int/__data/assets/pdf_file/0009/98424/E89498.pdf (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. http://whqlibdoc.who.int/trs/WHO_TRS_916.pdf (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)

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 http://www.who.int/nutrition/publications/public_health_nut3.pdf (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 http://beta.adb.org/publications/attacking-double-burden-malnutrition-asia-and-pacifichttp://www.adb.org/documents/books/nutrition/malnutrition/prelim.pdf (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

• Ashleigh?• Chelsea?

Look for syllabus, background paper (DBM Draft) and lectures on intranut

Readings

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Historical perspective

Source: Fogel 2004

1996

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Historical perspectiveNUTRITION 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)

Kumanyika S K et al. Circulation 2008;118:428-464

Copyright © American Heart Association

Rapidly increasing overweight is a recent phenomenon

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Overweight is wide spread globally, especially among the richest, and is increasing in most LMICs

Subramanian, et al . 2011

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HEALTH

Child Malnutrition

FOOD

Resources & ControlHuman, 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?

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Analytical frameworks

Analytical frameworks

UK Foresight Project on OBESITY in the UK (2007)

Energy balance

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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

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Biological/Health Environment

• Infections/Disease (Health Transition)• Intrauterine growth retardation

(metabolic programming)• Metabolic mechanisms in weight control• Genetics• Medications

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Biological/Health EnvironmentInfections/Disease

Example of the temporal relationship between infection and growth of an individual child in Guatemala. Mata et al. 1976

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Biological/Health EnvironmentInfections/Disease

Health transition

Biological/Health EnvironmentInfections/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

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Biological/Health Environment Intrauterine growth

Source: Fall 2009

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Biological/Health Environment Intrauterine growth

Source: Valdez et al 1994

Among Americans of white and Mexican descent

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• 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

Biological/Health Environment Intrauterine growth

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• 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

Biological/Health Environment Intrauterine growth

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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

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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

Opie L H Circulation 2007;115:e32-e35

Copyright © American Heart Association

Biological/Health Environment(Metabolism)

Plus: LEPTIN and Grehlin!

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

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

880 122 4 6 8 10 14 16 18 20 22 24

Month

Bod

yw

eig

ht

(kg

) Control

Sibutramine

Weight loss Weight maintenance

Same diet and exercise for both sibutramine and controlSource: James WPT, et al, 2000

Biological/Health Environment (appetite)

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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 O’Rahilly 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.

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Biological/Health Environment Genetics

Source: Brooks et al 1995

BUT!Birth weight related to weight of recipient mother not of donor

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Biological/Health Environment Genetics

Source: Godfrey et al 1997

BUT!Thinness of baby at birth relates to birth weight of mother but not father

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

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Biological/Health Environment

Source: Pijl H, Meinders AE. Bodyweight changes as an adverse effect of drug treatment. Drug Safety 1996;14:329-342.

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Conclusions1. Obesity and diet related NCDs are replacing infectious diseases as

major causes of death2. Constrained maternal and child nutrition increases the risks of diet

related NCDs (metabolic syndrome) later in the life course3. 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.