Micronutrient malnutrition

1. Micronutrient malnutrition Vanessa Velazquez-Ruiz, MD Emergency Medicine Global Health Fellow St. Luke’s-Roosevelt Hospital

2. Why talking about micronutrient malnutrition?

3. Micronutrients • Affect a variety of health and disease outcomes: • Child growth and development • Maternal health • Malnutrition and vulnerability to infectious diseases • Estimates of micronutrient malnutrition vary from 20% of the world population (or more than one billion persons) • Dietary deficiencies represents an enormous problem of “hidden hunger”

4. Agenda • Series of lectures • Week #1: Vitamin A and D • Week #2: Iron, Iodine and Zinc deficiencies • Week #3: Obesity and the other spectrum of malnutrition

5. Let’s begin our journey!!!! Fasten your seatbelts and enjoy the ride…

6. Vitamin A

7. Overview • Third most common deficiency in the world • Affects an estimated • 125-130 million preschool age children • And 7 million pregnant women in low-income countries • Prevalent cases of pre school xerophthalmia are believed to number about 5 million • 10% can be considered potentially blinding

8. Leading cause of preventable pediatric blindness in developing world Underlying cause of at least 650,000 early childhood deaths due to diarrhea, measles, malaria and other infectious disease Maternal deficiency may increase risk of maternal morbidity and mortality

9. NEITHER HUMANS or ANIMALS can synthesize or survive without Vitamin A

10. Epidemiology Public Health problem in approx 78 countries • Most widespread across South and Southeast Asia and Sahelian and Sub-Saharan Africa (where food supplies lack preformed vitamin A) • Clusters within counties due to common exposures to poor diet and inadequate care, malnutrition

11. Epidemiology • Age • Corneal xerophthalmia- 2-3y/o • Acute onset of corneal disease may follow recent weaning from breast milk, or s/p illnesses • Gender • Male > Girls • Socioeconomics • Inversely correlates with Vit A deficiency

13. Sources of Vitamin A • Retinol (preformed Vit A): animal products, liver • Beta-carotenes: Provitamin A (converted to Vit A in intestines) • Plant source of retinol from which mammals make 2/3 of their Vit A • Carotenoids: yellow, red fruits/vegetables

14. Vitamin A • Essential in regulating numerous key biologic processes in the body • Morphogenesis • Growth • Nutrition • Vision • Reproduction • Immunity • Cellular differentiation and proliferation

15. Vitamin A deficiency disordersVADDs

16. Main cause of deficiency: Insufficient intake Increase requirements during growth, pregnancy and lactation, infection Change from breast feeding to inadequate complimentary feeding Socio-cultural and economics factors (intra household distribution and gender preferences)

17. Clinical features

18. Xerophthalmia • Three clinical stages: • Retinal dysfunction causing night blindness • Conjunctiva and corneal xerosis • Corneal ulceration and necrosis

19. Night blindness Earliest manifestation Most prevalent stage of xerophthalmia Failure in rod photoreceptors cells in the retina Responsive to Vitamin A supplementation

20. Ask about night blindness A positive history of night blindness is associated with low-to-deficient serum retinol concentrations in preschool aged children and pregnant women Can serve as an indicator of individual and community risk of Vitamin A deficiency

21. Conjuctival xerosis withBitot’s spots Xerosis of the conjunctiva Appears as dry, non-wettable, rough or granular surface (best seen on oblique illumination with hand light) Histological: transformation of normal columnar epithelium with abundant goblet cells to stratified, squamous epithelium that lacks goblet cells.

23. Bitot’s spots: gray-yellow patches of keratinized cells and saprophytic bacilli that aggregate on temporal limbus (lesions are bubbly, foamy or cheesy like)

24. Corneal xerosis Corneal xerosis (“drying”) presents as superficial punctuate erosions that lend a hazy, non-wettable, irregular appearance to the cornea Usually both eyes Severe xerosis, cornea becomes edematous with dry granular appearance (“peel of an orange”) Vitamin A successfully treats corneal xerosis

26. Corneal Ulceration Appearance: Round or oval, shallow or deep, sharply demarcated and often peripheral to the visual axis Only one eye Vit A will heal lesion leaving a stromal scar or leukoma

28. Corneal Necrosis Keratomalacia (“corneal melting or softening”) Initially opaque localized lesions that can cover and blind the cornea Treatment with Vit A leaves a densely scarred cornea

29. Conjunctival xerosis and localized corneal necrosis in a severely malnourished 2-year-old Indonesian boy. Same eye 2 months after Vitamin A therapy

31. Poor Growth Experimental Vitamin A depletion in animals causes a deceleration in weight gain to a “plateau” as hepatic retinol reserves becomes exhausted Corneal xerophthalmia is associated with severe linear growth stunting and acute wasting malnutrition Recovery from xerophthalmia has been associated with gain in weight

32. Infection Predisposes individuals to severe infection Higher mortality rates in children and pregnant women Vit A maintains epithelial barrier function and regulates cellular and antibody-mediated immunity

33. Treatment • Children with any stages of xerophthalmia • High potency Vit A at presentation, the next day and 1-4 weeks later (WHO recommendations) • Children at high risk Vit A deficiency: measles, diarrhea, respiratory diseases, severe malnutrition • High dose supplementation: single dose if no supplement in 1-4 mo

34. Replacement • q4-6 months • Infants 50K IU PO • Infants 6-12mo: 100K IU PO • Mothers: 200K IU PO w/in 8 wks delivery (WHO recommendation) • Pregnant or women of reproductive age: small doses 10K IU/d or 25K IU wkly

35. Prevention Dietary diversification Fortification Supplementation

36. Dietary diversification Increase intake from available and accessible foods Nutrition education Social marketing Community garden programs Measures to improve food security

37. Fortification • Taking advantages of existing consumption patterns of fortifiable foods to carry Vitamin A into the diets • Examples: • Vitamin A fortification of sugar in Guatemala • Vitamin A fortified monosodium glutamate in Southeast Asia

38. Supplementation • Encompassing community based efforts to provide Vit A supplements to high-risk groups • Preschool-aged children • Mothers within 6-8weeks after childbirth • UNICEF procures and distributes over 400 million Vit A supplements to nearly 80 countries • Integrating vitamin A delivery with immunization services during each of three routine contacts in the first 6 months of life

41. Nutritional Ricketsand Vitamin D deficiency

43. Overview Resurgence in the prevalence of Rickets In developing countries, not only associated with effects on bone growth and mineral homeostasis but also with infant and child mortality when accompanying lower-respiratory tract infections

44. Definition Disease of the growing bones from a failure or delay in the calcification of newly formed cartilage at the growth plates of long bones and failure of mineralization of newly formed osteoid (osteomalacia) Bones no longer able to maintain normal shapes

45. Causes of Rickets • Calciopenic rickets • Phosphopenic rickets • Primary defect of mineralization * Nutritional Rickets is a form of calciopenic rickets and is classically associated with Vitamin D deficiency

46. Effects of Vitamin D deficiency • Active Rickets • Impaired Calcium homeostasis • Consequent to impaired dietary calcium absorption or inadequate intake • Vit D (or more specifically 1,25-(OH)2D) controls the absorption of Calcium • ↓serum Ca → induce ↑ PTH secretion → osteoclasts ↑ resorb bone → demineralization of bone & cartilage at sites of rapid growth & remodeling

47. Effects of Vitamin D deficiency • Predisposition to lower respiratory tract infections by • Effects on immune system • Muscle weakness and hypotonia • Effects of rickets and osteomalacia on rigidity and support provided by the ribs during respiration

48. Effects of Vitamin D deficiency • During pregnancy and early infancy • Poor maternal weight gain • Higher incidence of maternal hypocalcaemia, poor neonatal bone mineralization and fractures, and reduced longitudinal growth • Increase risk of DM type 1, multiple sclerosis and bipolar disorder

49. Sources of Vitamin D • Diet • Fortified food products • Fish oils, egg yolks, mushrooms • Animal products (fatty parts, liver) • Vit D in diet: cholecalciferol or ergocalficerol

50. Via skin synthesis under the influence of UV-B radiation