MALNUTRITION and DISABILITY
Dr Ingrid Bucens, Vientiane, May 2011.
E
33% (mod) stunted
emerging global priority
More difficult to measure
23% screen positive for ‘significant disability’
39% ‘not fulfilling developmental potential’
Layout of talk
1. MN – definitions, prevalence, consequences
2. Links between malnutrition and disability
3. Interventions for prevention and treatment
of malnutrition related disability
4. Programmatic issues.
Malnutrition – Classifications
• Macronutrient (‘Protein-energy’) vs micronutrient
• Degree - mild/moderate/severe
– How far anthropometric measures deviate from normal
• Rapidity of onset and duration
– Acute (wasting +/– oedema)
– Chronic (stunting)
• Timing of onset / age group affected
– In-utero
– Childhood
– Adult (life-long)
Recognising Childhood Malnutrition
TYPE
ANTHROPOMETRIC
MEASURE
APPEARANCE
UNDERWEIGHT
WFA < -2SD
Skinny
WASTING
WFH <- 2SD
Very skinny
WASTING +
OEDEMA
(WFH) OEDEMA
Swollen, skin and
hair abnormalities
STUNTING
(Chronic MN)
HFA < -2SD
Short (+/- skinny)
MACRONUTRIENT (protein - energy) deficiency
May not look abnormal
May not look abnormal
unless lined up against
same age peers.
Recognising Malnutrition in
Mothers and Babies
• MOTHERS
– LOW BMI
• < 18.5kg/m2
– MUAC
• <20-25cm
– SHORT
• Height < 145cm
• Chronic undernutrition.
• BABIES
– LBW (< 2.5kg)
• ‘Mixed bag’ - Preterm + SGA
– SGA (IUGR + others)
Recognising
MICRONUTRIENT deficiencies
-
IRON
-
-
- Anaemia
- Mucous membranes, nail
changes
-
FOLIC ACID
- Anaemia
-
IODINE
- Endemic regions
(mountains,
non-iodinised salt)
- Goitre
ZINC
-
Skin rash + persistent diarrhoea
(acrodermatitis enteropathica)
VITAMIN A
-
Night blindness (not so easy to
recognise in children)
Prevalence
• 33% stunting
– Some regions ~ 50%
• 10-19% mothers low BMI
• 11% babies IUGR
• 10% wasting
– S Asia ~ 16%
– Kwashiorkor less common
– Severe wasting 3.5%
• 45% children <5 yrs have
anaemia ~ half due to
iron deficiency
HUGE NUMBERS OF MOTHERS, BABIES AND CHILDREN AFFECTED
BY MALNUTRITION IN LOW AND MIDDLE INCOME COUNTRIES.
CONSEQUENCES of Malnutrition
• Individual (death,
disease, disability)
– DEATH
– INFECTIONS
• +/- death / disability
– GROWTH FAILURE
– ADULT HEALTH OUTCOMES
• ‘Barker’
– DISABILITIES
• Families / Generations
– Growth
– Reproductive health
• Maternal complications
and death
• Small size at birth ,
disability outcomes
– Educational / Economic
• Societal
– Economic
• Burden of treatment
• Loss of productivity
– DALYS
SIZE OF THE BURDEN
Global deaths and disease burden measured in DALYS, in children
< 5 yrs, attributed to nutritional status measures in 2004
21.4
21.2
Lancet (2008) Maternal and Child Undernutrition Series, 1st paper.
THE LINKS TO DISABILITY
1. Common risk factors / root causes
a.
b.
Psychosocial
Biological
2. Disability is a cause of MN.
3. MN is a cause of disability.
4. Overlap of intervention strategies.
Link 1:- Common multiple risks
• The common milieu of MN and disability
– WHO ‘The Critical Link’
• Common mechanisms (CARING) are important
for healthy physical growth and psychological
development.
• Children in low resource contexts (POVERTY) are
often exposed to multiple, cumulative risks
which compromise caring – and therefore
compromise both growth and development.
The link between poverty and disability,
+/- via Malnutrition.
MALNUTRITION
POVERTY
Insufficient food
-Low (maternal)
education
- Overcrowding
-Poor sanitation
-Poor health practices:breastfeeding, diet ,
reproductive health
(FP), care-seeking,
toxins (alcohol)
-Infections / diseases
-Maternal stress
-(‘Poor parenting’)
-Weak health services
-etc
DISABILITY
Other
-Trauma
-Genetic
-Metabolic
-Asphyxia
-etc
Many of the ‘causes’ / risks are common
MALNUTRITION
DISABILITY
MALNUTRITION
POVERTY and associated risks – overcrowding, poor sanitation, low maternal education, poor
health practices (breastfeeding), maternal stress and depression, stress, ill health, poor
parenting skills (orphans), weak health services etc
Poor reproductive health (extremes maternal age, no child spacing)
Infections – TB, HIV, malaria (anaemia, cerebral infection)
Poor health seeking behaviour (immunisations, care of illness)
Breastfeeding inadequate
Feeding practices inadequate
Neonatal ills (jaundice, asphyxia, preterm)
Recurrent diarrhoea
Genetic, consanguinity, chromosomal,
congenital microcephaly
Environmental toxins (lead)
TRAUMA
LINK 2
Disability is a direct cause of MN.
• Children with disability often develop MN
– Babies suck poorly – breastfeeding failure
– Less actively seek food (motor, sensory, cognitive)
– Neglected by ‘carers’
– Rejected by society
– Develop secondary illnesses
which in turn cause MN (TB)
LINK 3
Malnutrition is a cause of disability
MN
POVERTY
DISABILITY
Risks –
milieu of
poverty
other
?How much disability from
MN is directly due to MN
and how much is due to
the co-existing risks?
• MN directly causes disability
– Stunting
– Wasting
– Micronutrient deficiencies
• Iodine
• Vit A
• Folic acid
• Iron
• MN indirectly causes disability
– IUGR
– Maternal
Vitamin A deficiency and DISABILITY
• May cause irreversible blindness.
• Vit A related blindness is a VERY common
cause of blindness in low resource countries.
Iron deficiency and DISABILITY
• Children who are not otherwise malnourished
but who have iron deficiency and iron deficiency
anaemia have impaired cognitive development
and behaviour when compared to non-iron
deficient children.
• They score lower on cognitive, motor and
behavioural tests.
• Association is less consistent or less strong for
iron deficiency without anaemia.
Folic Acid and Disability
• Spina bifida (neural tube defect,
myelomeningocoele) +/- hydrocephalus
• Vit B12
IODINE deficiency and disability
• Iodine is needed for thyroid hormone,
essential for brain development.
• Irreversible severe intellectual
disability (and stunting) in offspring of
deficient mothers.
• Lesser but significant cognitive
impairment in children in iodine
deficient areas.
• Iodine deficiency is endemic in
mountain populations without
iodinised salt.
Congenital
hypothyroidism
SEVERE ACUTE MALNUTRITION and
DISABILITY
• Children hospitalised with SAM (+/-oedema)
consistently have developmental and
behavioural abnormalities.
– Cognitive scores lower
– Motor lower
– Behaviour markedly abnormal
• No specific deficits.
• With rehabilitation behaviour virtually
returns to normal; other
developmental deficits persist.
• Children /adolescents who were
earlier hospitalised for acute MN show
persistent deficits in cognition, school
function including behaviour –
attention - social interaction.
• How much of the deficit is due to
associated stunting and the social
milieu at home?
Stunting and DISABILITY
• Strong evidence for association between early childhood
stunting and significant cognitive impairment (moderate to
large effect).
• Concurrent and longterm association, through to adulthood.
– Young child height correlates to cognition at 40y!
• Poorer development, lower IQ, poorer school performance
even after controlling for confounders (social milieu). No
specific deficit.
• Younger children also have emotional and behavioural,
attentional problems and relationships at school.
• Individual and population level.
IUGR and disability
• Some studies found cognitive deficits in infancy for
IUGR babies vs normally nourished newborns.
• Review of IUGR studies,
controlling for confounding (preterms, other
neonatal problems eg asphyxia, causes of IUGR,
home environment, quality of NBC) concluded
that, provided no secondary asphyxia, there is
little effect of IUGR on developmental outcome.
Maternal malnutrition and DISABILITY
• No direct link between maternal malnutrition and
disability however
– Maternal malnutrition is a cause of IUGR which may
lead to stunting.
– Maternal malnutrition increases the risk of maternal
death (delivery complications)
• ‘Motherless children don’t do well’ (malnutrition and
disability). Orphan studies.
LINK 4
Interventions for MN + disability.
MN
DISABILITY
POVERTY
MILIEU
OF POVERTY
At risk kids
OTHER
1.
Interventions for root causes will reduce MN and disability of all causes.
2.
Interventions which prevent MN will prevent disability due to MN.
3.
Interventions which treat MN reduce reversible disability due to MN.
4.
Interventions for disability may also improve growth.
5.
Combined interventions are most effective.
Nutrition interventions
•
PREVENTIVE
– Supplementation
• Micronutrient
• Macronutrient (food / milk)
– Health education
•
•
•
•
Breastfeeding
Complementary
Sanitation / hygiene
Disease prevention
– HIV, IPT, zinc, BCG
• STIMULATION
– Root cause strategies
• Poverty alleviation
• Food security
• Family planning
• ‘CURATIVE’
– Treatment of acute severe
MN (in/outpatient)
– Supplementation for catch up
growth for IUGR and stunting
– Micronutrients
• Vit A, iron, folic acid
• Iodine, zinc
– Health education
– STIMULATION
Prevention strategies for
Micronutrient deficiency/disability.
Micronutrient deficiencies cause severe and often
irreversible disability. Effective prevention
strategies exist for at risk populations.
• Vit A
– Regular supplements to children.
• Iron supplementation (fortification)
– Prevents iron deficiency and anaemia.
– Improves developmental outcomes.
– Is recommended for young children except in malaria
endemic areas.
– Deworming
• Folic acid supplementation pre-conception in all contexts
prevents folate deficiency and related disability.
• Iodine
– Antenatal supplements (oil or inject) begun before T2
reduces stillbirths, prevents congenital hypothyroidism and
improves childhood cognitive outcomes even for
subclinical deficiency.
– Childhood supplementation (oil) may improve cognition but
results mixed. Supplementation at school recommended
for girls.
– Universal salt iodinisation is a very effective strategy.
Treatment for micronutrient
deficiencies/disability.
• Except for iron for school aged children with IDA,
these strategies are less effective.
– Iron
• May not fully reverse the developmental disability in infants
/preschool children with IDA.
• In school age deficits are reversible.
– Iodine – lesser grades of disability may be improved if
treatment started early.
– Vitamin A – only early eye changes are reversible.
– Folic acid disability is not reversible.
Preventing IUGR and childhood MN
• IUGR can be reduced with
– Antenatal supplementation interventions
• Childhood MN can be prevented
– Antenatal interventions
– Interventions in infancy / very early childhood
– These interventions, in turn, reduce maternal
malnutrition
• Via prevention of childhood stunting
Preventive interventions.
• Food to pregnant / lactating women / infants
•
•
•
•
Food is more effective than individual micronutrients.
Improves birthweight.
Improves infant growth and prevents stunting
Improves developmental outcomes in infancy and the
benefit may be sustained
• Stimulation interventions pregnancy / postnatally
• Improve developmental outcomes
• May improve growth
• Food + stimulation
• May improve growth better than food alone
• Has a greater effect on cognition than either
intervention alone.
These interventions have most effect if interventions
begin in pregnancy or at birth and continue
through 2-3 years. More effective in populations
at risk of malnutrition including maternal MN and
IUGR.
Treatment interventions
The developmental disability of MN is partly
reversible.
• FOOD
– Reverses weight loss of wasting
– Stunting is more difficult to reverse; may improve if
food supplementation before 3 years.
– Concurrent benefits on motor and cognitive
development. May be sustained, especially if begun <
2 yrs, but evidence limited.
– Effect on development is not as strong as with
preventive interventions.
• STIMULATION
– Benefits development
• FOOD + STIMULATION
– May improve growth better than food alone.
– Significantly improves cognitive development in
wasting and stunting.
• Do not reach level of normally nourished
• Effect on development is sustained
– Best results on growth and cognition if begin < 2yrs.
SUPPLEMENTATION + STIMULATION for stunting
Stunted children have long term deficits in cognition. Deficit
improved by stimulation +supplementation, but not to normal.
Walker SP, Chang SM, Gratham-McGregor SM. Effects of early childhood psychosocial stimulation and
nutritional supplementation on cognition and education in growth-stunted Jamaican children: prospective
cohort study. Lancet 2005; 366: 1804-07.
‘Developmental intervention’ for children
with MN is more effective if begun < 2yrs.
L3 ….
Developmental interventions
• Benefits
– Lots of evidence of effectiveness in improving
developmental outcomes, school readiness and
educational outcomes.
– Effective in developing world settings
– May improve nutritional status
• Interventions are most effective if
–
–
–
–
–
Target populations / groups most likely to benefit (MN)
Input is intensive - targets both children and carers
Begun antenatally and continued for at least 3 years
Good quality
Delivered together with nutritional intervention!
The mutual reinforcement of nutritional and
developmental interventions.
• Developmental interventions hope to
– Improve the way mothers CARE for their children
• includes caring for feeding, hygiene, health seeking
• become more responsive to children’s needs
• Nutrition interventions make children stronger
– child can benefit more from his environment
– can elicit more care
Key messages.
• MN and disability are both highly prevalent and co-exist
in poor populations.
• Both may be the result of the risks that co-exist in
poverty and each may cause or aggravate the other.
• Early growth impacts cognitive development
• Effects of MN and malnutrition induced disability
(educational failure) are perpetuated through
generations, for biological and environmental reasons.
• The economic consequences of this are very significant
and government, including non-health sectors, need to
be aware of this.
• Interventions for each affect the other. The most
effective interventions for both MN and disability are
those which include both a nutritional and
developmental component.
• Preventive interventions are more effective than
treatment because some malnutrition induced
disability is irreversible.
• Interventions are most effective if begun during
pregnancy or the first two years (most intensive
periods of both growth and development) and if they
target at-risk populations.
Considerations for programming
• Examine existing MNCH systems and services from a life cycle
approach
– Review what is being done that affects MN and / or disability
– Are there any key intervention gaps?
• Consider if your health system can improve efficiency or can
feasibly increase interventions
– Combine interventions that target similar ages and are to be
delivered by same HW
– Select priorities based on local epidemiology (Iodine, bed nets)
– Beware high cost and complex interventions
– Phase in changes and target risk groups
• Multi-sectoral collaboration (education, root causes)
EG. Preventing malnutrition + disability
PRECONCEPTIONAL PRENATAL
NEONATAL
EARLY YEARS
POVERTY REDUCTION / WATSAN/EDUCATION/ACCESS to HEALTH SERVICES
Salt iodinisation; ?iron or folate fortification
Health Education
-Reproductive
Supplement at risk
mothers
Supplement at
risk mothers
Supplementing
Family Planning
(adolescent
pregnancy)
‘Stimulation’
Parent education
Newborn
screening
Iron, zinc, vitA, deworm
Iron/folate
Iodine, Fefol
At risk FU (LBW)
‘Stimulation’ ECD
ANC, counsel, bed nets
SBA, EMONC
Parent education at risk
NBC/PNC
Growth/development
monitoring and
counseling
Breastfeeding
IMCI/referral/danger
sign awareness /
vaccination
Most important messages of all.
•Preventing malnutrition
(in its various forms) is a
priority for reducing the
burden of disability in low
resource contexts.
A WELL BALANCED DIET AND A
STIMULATING ENVIRONMENT ARE
GOOD FOR CHILDREN!