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The empirical development of a
therapeutic formula for the
treatment of malnutrition from
F100 to therapeutic pastes (RUF).
Importance of delivering the full
spectrum of micronutrients to
acutely malnourished children
Michael Golden.
MSF satellite meeting, Hanoi, 2008
History of feeding the severely
malnourished
• 1945: Concentration camps. Used protein
hydrolysates – 80% mortality – results
supressed by Churchill
• 1956: MRC units Jamaica and Uganda. Milk,
Sugar, Oil mixes – basically the same recipe
only Uganda 100kcal/100ml, Jamaica
135kcal/100ml
• 1960 added large amounts of Potassium on
per kilo child basis (Alleyne, Garrow et al)
• 1962 added magnesium (Montgomery et al)
• Biafra: K-mix-2 was used, based upon casein, sugar
and oil: no mineral or vitamin mix
• 1976: development of separate formula (low
protein/Na) for initial treatment (Picou-Golden mix =
PG-mix)
• 1978: Zinc and copper requirements calculated and
added (Golden + Golden)
• 1982: Other trace element requirements assessed
and added to diet. eg Selenium, vitamin E (Golden +
Ramdath)
• 1983: importance of balance of Anions and Cations
recognised to prevent acidosis from mineral salts
chosen (particularly Magnesium salt)
• 1985 recognition of the importance of the type of oil used –
EFA deficiency recognized and comparison of diets with
coconut and arachis oil on biochemical recovery (Ramdath)
• 1986: change from concept of giving nutrients per kilo child
to formulation of diet – nutrients per 1000kcal of diet.
Allowed for single diet for all instead of treatment tailored
for individuals
• 1987: development of original F100 diet formulation.
Formally tested in Jamaica (Morris + Golden)
• 1991: refinement and roll out of F100 and F75 (Started as
PG-mix then known as F-TS standing for Formula for toxic
shock) at MSF meeting (Golden and Briend).
• 1993: Inauguration of ACF Scientific committee
• 1993: commercial production of F100 organised by Grellety
and made by Nutriset
• 1994 First use of F100 in Rwanda after genocide. Results
revolutionary! Extensive use of F100 and F75 by most
NGOs (Grellety)
• 1995: refusal of patients in North Uganda to come for
treatment (Lord’s Resistance Army kidnapping children) –
need for ready-to-use food recognised by Grellety
• 1996: ACF scientific committee discussed options and
developed the idea of a paste based on premixes seen in
Liberia (Golden, Grellety, Briend)
• 1997: successful use of local fortified foods for treatment
of SAM by ICDDRB (Kituri and Halva)
• 1997: Briend observed acceptance of “Nutella”and
decided to flavour product with peanuts. Resigned
from ACF committee and worked with Nutriset to
develop products
• 1997: “Plumpy-nut” tested in Tchad (Prudhon) with
good results
• 1998 demonstration by Briend that bacteria do not
grow in Plumpy nut and extensive testing in many
setting initiated by Briend/Nutriset.
• 1999: adoption of F100 and F75 by WHO as standard
treatment for SAM
• 2000 Further extension of treatment to outpatients
by Collins and Concern
• 2004 Spearheaded by Valid International - use of
outpatient management by many NGOs particularly
Concern + SCF. Data presented to show dramatic
increase in coverage and low mortality
• 2006 extension of treatment to moderately
malnourished by MSF
• 2007: lipid based spreads used to prevent
malnutrition at population level in Niger (MSF)
Rational for formulation
• Based on development of type 1, type 2 classification of
nutrients (published 1988)
• Recognition of different requirements for catch-up growth (all
forms of weight loss – SAM, MAM, convalescence) from that
for normal children
• Verified by experimental results (balance studies, growth
studies, biochemical studies) in recovering severely
malnourished children in metabolic ward (1956-1990).
• Over 40 nutrients are essential to health
• If any one is deficient then the person will not
be healthy and resist disease
• Many are ignored by doctors and nutritionists
and their deficiency is not recognised or
corrected
• They are divided into two groups in terms of
the response to a deficiency
• Type 1
• Functional
nutrients
• Type 2
• Growth
nutrients
• has a body store
• reduces in concentration
with deficiency
• Specific signs of
deficiency
• Growth failure not a
feature
• variable in breast milk
• has no body store
• stable tissue
concentration
• no specific signs of
deficiency
• Growth failure the
dominant feature
• stable in breast milk
• Type 1
• Type 2
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iron
iodine
copper
calcium
selenium
thiamin
riboflavin
pyridoxine
niacin
folate
cobalamin
vitamin A, D, E, K
nitrogen
essential amino acids
potassium
magnesium
phosphorus
sulphur
zinc
sodium
chloride
Type II nutrients
Deficiency of any one leads to the same
response
• tissue repair and growth ceases
• Rapid turnover of tissues vulnerable
(enterocyte + some white cell series)
• No convalescence from illness
• negative balance for all type II nutrients
• anorexia (if diet is unbalanced in type II)
• growth rate is the dominant determinant of
requirement
Muscle biopsy (vastus lateralis) from a
malnourished and normal child.
Treatment was with an old diet not balanced in type
II nutrients
Malnourished
<70%WfH
Recovered 100% WfH
Old HEM diet
Normal child
100% WfH
growth rate determines requirement of type II
nutrients: The example of zinc
Weight gain at 15g/kg/d
Half lean tissue: half fat tissue
Lean tissue contains 0.1 mg/g
• Then growth takes 15 x ½ x 0.1= 0.75mg/kg/d
• a 6 kg child will need to retain 4.5mg/ d
• availability from a good diet is 30% (but less than
15% from a cereal/pulse diet)
• dietary intake will need to be 15mg/d
RDA for this child is only 5mg/d
Local diets
• Briend has shown by linear programming that it is
not possible to get the same nutrient concentrations
from local diets without fortification with some
minerals and vitamins.
• The best diets contain a large variety of local foods
mixed together
• However, addition of mineral and vitamin mix to
mixtures of local foods can indeed result in a diet
that emulates F100 and derivative diets
• There remains the problems of anti-nutrients and
the necessity to test new diets against the gold
standard (F100/RUTF).
Effect of adding CSB, UNIMIX or family plate to growth
of recovering SAM children
Change from CSB to SP450 (roasted
oats/dehulled soya + CMV) on wet feeding
program outcomes
Comparison of growth with CSB and SP450 (Cyanika, Rwanda)
Conclusions
• Malnutrition is mainly due to deficiency in
type II nutrients in the diet in an available
form
• They can be supplied by special products or
appropriately fortified and formulated local
diets
• There is now a major research agenda to
further define requirements and develop diets
and foods that are cheap enough to be widely
used for prevention of malnutrition