Post on 03-Jan-2016
description
Micronutrient malnutrition II
Vanessa Velazquez-Ruiz, MDEmergency Medicine Global Health Fellow
St. Luke’s-Roosevelt Hospital
Today schedule….
Zinc Deficiency
Iodine deficiency
Are you ready!!!!!!
Lets begin the second part of our journey
Zinc Deficiency
Common but overlooked problem in developing countries
Important role in biological processes
Gene expression
Cell development
Replication
Immune function
Growth and development
Overview
Intakes of zinc are commonly lower than recommended
Adaptation mechanisms preclude the development of severe deficiencies
Many consequences to adaptation states to low zinc levels
Overview
Probably affects a quarter or a third of pre school children and their mothers
Lack of simple quantitative markers for zinc deficiency
Overall, 20.5% of the world population is at risk of zinc deficiency
Estimated to be responsible for 800,000 deaths/year from diarrhea, malaria, pneumonia in children under five
One of the ten largest contributors to the burden of disease in developing countries
Zn deficiency in world crops: major areas of reported problems (adapted from Alloway, 2008a
Overview
Incidence and prevalence have not been defined
Lack of sensitive, practical, accepted indicators for zinc deficiency
Population-based surveys have not been done
Marginal deficiency is not characterized as a specific syndrome
Severe clinical deficiency is not seen owing to adaptation or death
Risk factors for zinc deficiency
Insufficient dietary intake (low protein diet)
High phytate and/or fiber intake (vegetarians)
Diarrheal disease
Malabsorption syndromes
Parasitosis
Hot, humid climate
Lactation
Rapid multiplicative cell growth (pregnancy, infancy, adolescence)
Genetic disease (acrodermatitis enteropatthica, Sickel cell anemia)
Close geographical linkage between soil zinc deficiency and human zinc deficiency
Zinc Metabolism
Zinc absorption
Absorbed at all levels of the small intestine
Intestine must recover zinc from both diet and endogenous sources
Total body zinc content maintained with absorption of 5mg/day
Zinc Storage
No specific organ for storage
60% striated muscle
20% in bone
5% in blood and liver
3% in the skin and GI tract
Zinc excretion
Mostly in feces
Through urine
In tropical countries, sweat losses can be considerable
Turnover of skin, hair and nails
Menstrual blood and semen
Lactation (2-3mg per day in the first several weeks)
Sources of zinc
Animal products, seafood, cereals Oysters and shellfish
Absorption impaired by phytates and fiber.
Protein acts as anti-phytate
Clinical presentation
Severe deficiency
Growth retardation
Impaired immune system
Skin lesions in extremities and perioral area
Hypogonadism
Anorexia
Cognitive dysfunction
Alopecia
Mild to moderate
Increases susceptibility to infection
Growth retardation
Failure to thrive
Impaired taste (hypogeusia)
During pregnancy
Birth defects
Spontaneous abortions
Fetal growth retardation
Low birth weight
Preterm delivery
Increase complications during delivery
Impairs estrogen-dependent gene expression in the uterus (via zinc-finger protein)
Lack of estrogen impairs the conversion of uterus from passive state to one capable of concerted contractions with sufficient force to expel fetus
Zinc and diarrheal disease
Strong evidence that supplements improves the prognosis (reduces severity and duration) of children treated for diarrheal disease
Zinc supplement + oral rehydration treatments been explored
UNICEF recommends packs of ten tablets of 20mg Zinc/daily for tx of diarrhea
Zinc and respiratory diseases
Regular zinc supplements have shown to prevent respiratory diseases in children with lower birth weights
Pool analysis of randomized controlled trails showed reduction of pneumonia by 41% in preschool children supplemented with zinc
One trial in Bangladesh showed reduced duration of severe pneumonia by 30% with zinc as adjunct therapy
Zinc and malaria
Gambia: 32% fewer clinic visits for malaria due to Plasmodium falciparum in young children supplemented with Zinc
69% reduction for malaria episodes accompanied by high levels of parasitemia (>10,0000 parasites/μL)
Zinc and HIV
Low serum Zinc identifies in 29% of hospitalized AIDS patients
Some studies showed that low zinc levels may reflect HIV replication and the possibility that Zinc may enhance viral replication, however,
Daily zinc supplementation for 30 days has proven to reduce infectious disease morbidity in AIDS patients in other studies
http://www.zincsaveskids.org/
http://www.youtube.com/watch?v=vN_qQPxPK3Q
Assessment
Plasma and Serum Zinc concentration
Circulating zinc less than 0.2% of total body
Cut-off values to assess risk of zinc deficiency Below 10.71 μmol/L for fasting sample and less
then 9.95μmol/L for non fasting
Dietary assessment
Food intake distributions of a population
Analysis of local staple foods
Recall of an individual for food consumed
Weighed food records by research assistants
24-hr dietary recall
Local food composition tables if available
Other
Hair zinc concentrations
Diminished taste acuity (hypogeusia)
Composite index for predicting the national risk of zinc deficiency- uses a combination of stunting rates and adequacy of zinc in the national supple
Replacement and treatment
Table 1: Recommended Dietary Allowances (RDAs) for
Zinc Age Male FemalePregnancy Lactation
0–6 months 2 mg* 2 mg*
7–12 months 3 mg 3 mg
1–3 years 3 mg 3 mg
4–8 years 5 mg 5 mg
9–13 years 8 mg 8 mg
14–18 years 11 mg 9 mg 12 mg 13 mg
19+ years 11 mg 8 mg 11 mg 12 mg
* Adequate Intake (AI)
Recommended nutrient intakes (RNIs) for dietary zinc (mg/day) to meet the normative storage requirements from
diets differing in zinc bio-availability
Treatment
To combat zinc deficiency, five intervention strategies can be used:
Supplementation using medicines
Food fortification through the incorporation of zinc additives in food
Dietary modification/diversification
Genetic biofortification through plant breeding
Agronomic biofortification through zinc fertilization.
Iodine deficiency
Overview
Iodine is an essential constituent of the thyroid hormones (T4, T3)
Deficiency can lead to Goiter or cretinism depending on the severity
The ongoing global health effort to eliminate iodine deficiency through iodization of salt presents one of the largest public health efforts
By 1990, there were 1,572 million people worldwide consuming inadequate amounts of iodine
Iodine deficiency is the leading cause of mental retardation in the world
Problem is global, with mountainous regions and large river deltas the most well-known areas of endemic deficiencies
Epidemiology
Mountainous areas, high altitude and alluvial plains
Leaching of iodine form the soil due to erosion and heavy rain, deforestation, overgrazing lead to loss of iodine form soil and water
WHO Region Proportion of population with UI Population with < 100 µg/L (%)
UI < 100 µg/L (millions)
Africa 42.6260.3Americas 9.8 75.1South East Asia 39.8 624Europe 56.9435.5Eastern Mediterranean 54.1228.5Western Pacific 24 365.3Total 35.21988.7
192 WHO Members States Based on population estimates for the year 2002 (United Nations, Population Division, World Population Prospects: The 2002 Revision)
WHO 2003
Risk factors
Residency in an area where soil and water are poor in iodine
Ingestion of substances known as “goitrogens”( found in vegetables and fiber) that can interfere with metabolism
Cabbage, sweet potato, brussel sprouts, turnips
Cassava containing high concentration of thiocyanates
Role of iodine in biological functions
Metabolism
Growth and development
Synthesis of growth hormone
Normal bone cell growth and development
Brain development
Early growth and differentiation of the brain and nervous systems in the fetus
Immune function
Sources of Iodine
Seafood and seaweed
Crops grown on iodine rich soil
Iodized salt
Drinking water (less than 10%)
WHO recommended dietary requirements
Spectrum of iodine deficiency disorders
Fetus
Abortions
Stillbirths
Congenital anomalies
Increase perinatal mortality
Neurological cretinism: mental deficiency, deaf-mutism, spastic diplegia, squint
Myxoedematous cretinism: dwarfism, mental deficiency
Spectrum of iodine deficiency disorders
Neonate
Neonatal goiter
Neonatal hypothyroidism
Spectrum of iodine deficiency disorders
Child and adolescent
Goiter
Juvenile hypothyroidism
Retarded physical development
Spectrum of iodine deficiency disorders
Adult
Goiter
Hypothyroidism
Impaired mental function
Iodine-induce hyperthyroidism
Goiter
Enlargement of thyroid gland in response to insufficient iodine intake
Low iodine -> decrease T4 -> increase production of TSH -> stimulates hyperplasia of the thyroid -> increase uptake of iodine -> Goiter
Definition by palpation: enlargement of the thyroid such that lateral lobes are larger than the terminal phalanx of the thumb of the person who is being examined
Goiter Severity of goiter correlates with severity of the
deficiency
In areas of endemic goiter , the daily intake is less the 100 μg/day
Cretinism
Usually found where the prevalence of endemic goiter is more than 30%
Characterized by mental retardation
Two extreme types of cretinism:
Neurological
Myxoedematouse
Myxoedematous cretinism (hypothyroid cretinism): severe growth retardation, mental retardation not severe, coarse, dry skin, husky voice.
Neurological cretinism: stature is normal, mental retardation is severe, deaf-mutism, cerebral diplegia
Assessment of iodine status
Urinary iodine
Most useful/reliable indicator I status
24hr or random (30 samples) urine collection
Related to recent dietary I intake
Adequate 100-200 μg/L
Mild deficiency 50-99μg/L
Moderate Deficiency 20-49μg/L
Severe Deficiency Less than 20μ/L
Assessment of iodine status
Thyroid size (goiter surveys)
Palpation
Ultrasound (more reliable)
“Total Goiter Rate”, schoolchildren
Grade 0 No palpable or visible goiter
Grade 1 Palpable mass but not visible when neck in normal position
Grade 2 Visible, palpable swelling of the neck
Classification for Goiter
Mild 5-19.9
Moderate 20-30
Severe >30
Goiter by palpation or by thyroid volume by US (>97% of percentile)
*School-children
TSH screening programs
For early detection of congenital hypothyroidism
Useful epidemiology information, not cost effective
The degree of iodine deficiency can be evaluated on the basis of the frequency of neonatal blood TSH above the cutoff point of 3μU/ml
Mild deficiency TSH 3-19.9
Moderate deficiency TSH 20-40
Severe deficiency TSH > 40
Prevention
Iodized salt: “Universal salt iodization” (150μg of I/day)
Oral iodide oil
Adult : 1ml (480mg)
0.5ml (240mg)
Iodized oil injections
Prevention
Other:
Iodization of drinking and irrigation water
Iodine saturated silicon matrices placed in wells and hand pumps
Fortification of food
Conclusion
Iodine deficiency is the leading cause of preventable mental retardation
Great progress in providing access to iodized salt
WHO/UNICEF/ICCIDD report in 1999, from 5 billion people living in counties with iodine deficiencies, 68% now have access to iodized salt.
From 130 counties, 104 have intersectoral coordination and 98 have legislations about iodized salt
Much work needs to be done…
To be Continued…Stay tune for more on micronutrient deficiencies
next week… same channel, same time
Thanks
Any questions…
References
WHO website