RESEARCH Open Access
Co ela es o whole-blood polyunsa u a ed
a y acids among young child en wi h
mode a e acu e malnu i ion
C. W. Yaméogo
1,2,3*
, B. Cichon
2
, C. Fabiansen
2
, M. J. H. Ry e
2
, D. Fau hol -Jepsen
2,4
, K. D. S a k
5
, A. B iend
2,6
,
S. Shephe d
7
, A. S. T ao é
1
, V. B. Ch is ensen
2,8
, K. F. Michaelsen
2
, H. F iis
2
and L. Lau i zen
2
Abs ac
Backg ound: Se e e acu e malnu i ion (SAM) has been associa ed wi h low polyunsa u a ed a y acid (PUFA)
s a us. Howe e , in es iga ions ega ding PUFA s a us and co ela es in child en wi h mode a e acu e malnu i ion
(MAM) om low-income coun ies a e sca ce. The aim o his s udy was o desc ibe whole-blood PUFA le els in
child en wi h mode a e acu e malnu i ion (MAM) and o iden i y co ela es o PUFAs.
Me hods: We conduc ed a c oss-sec ional s udy using baseline da a om a p ospec i e nu i ional in e en ion ial
among 1609 child en wi h MAM aged 6–23 mon hs in Bu kina Faso,Wes A ica. Whole-blood PUFAs we e measu ed by
gas ch oma og aphy and exp essed as pe cen o o al whole-blood a y acids (FA%). Po en ial co ela es o PUFAs
including in ec ion, in lamma ion, hemoglobin, an h opome y (di e ence be ween child en diagnosed as ha ing MAM
based on low mid-uppe -a m-ci cum e ence (MUAC) only, low MUAC and weigh - o -heigh z-sco e (WHZ), o low WHZ
only) and die we e assessed by linea eg ession adjus ed o age and sex.
Resul s: Child en wi h MAM had low concen a ions o whole-blood PUFAs, pa icula ly n-3 PUFAs. Mo eo e , child en
diagnosed wi h MAM based only on low MUAC had 0.32 (95% con idence in e al (CI), 0.14; 0.50) and 0.40 (95% CI, 0.16;
0.63) FA% lowe a achidonic acid (AA) han hose ec ui ed based on bo h low WHZ as well as low MUAC and hose
ec ui ed wi h low WHZ only, espec i ely. In ec ion and in lamma ion we e associa ed wi h low le els o all long-chain
(LC)-PUFAs, while hemoglobin was posi i ely associa ed wi h whole-blood LC-PUFAs.
Conclusion: While PUFA de iciency was no a gene al p oblem, o e all whole-blood PUFA concen a ions, especially o
n-3 PUFAs, we e low. In ec ion, in lamma ion, hemoglobin, an h opome y and die we e co ela es o PUFAs
concen a ions in child en wi h MAM.
T ial egis a ion: The ial is egis e ed a h p://www.is c n.com (ISRCTN42569496).
Keywo ds: Essen ial a y acids, Unde nou ished child en, Die , Mo bidi y
In oduc ion
App oxima ely, 33 million child en wo ldwide su e om
mode a e was ing [1]. The cu en case de ini ion o mod-
e a e acu e malnu i ion (MAM) includes child en wi h
mode a e was ing, de ined as a weigh - o -heigh z-sco e
(WHZ) be ween -2 and -3, based on he 2006 WHO
g ow h s anda d [2], and/o child en wi h a mid-uppe -
a m ci cum e ence (MUAC) be ween 115 and 125 mm [3].
Child en wi h MAM a e a immedia e isk o mo bidi y
and mo ali y om in ec ious diseases [4, 5], and may
p esen wi h lipid me abolism dis u bances likely o impai
blood le els o polyunsa u a ed a y acids (PUFAs) [6].
Tissue concen a ions o PUFAs a e e lec ed in he a y
acid composi ion o plasma and e y h ocy es and he
amoun o a ious PUFAs in hese pools has been shown
o be low in child en wi h se e e malnu i ion [7, 8]. Lim-
i ed da a exis on ea ly li e in ake and blood le els o
* Co espondence: [email p o ec ed]
1
Cen e de Reche che en Sciences Biologiques, Alimen ai es e
Nu i ionnelles, Uni e si é Ouaga I P o Joseph KI-ZERBO, Ouagadougou,
Bu kina Faso
2
Depa men o Nu i ion, Exe cise and Spo s, Uni e si y o Copenhagen,
F ede iksbe g C, Denma k
Full lis o au ho in o ma ion is a ailable a he end o he a icle
© The Au ho (s). 2017 Open Access This a icle is dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (h p://c ea i ecommons.o g/licenses/by/4.0/), which pe mi s un es ic ed use, dis ibu ion, and
ep oduc ion in any medium, p o ided you gi e app op ia e c edi o he o iginal au ho (s) and he sou ce, p o ide a link o
he C ea i e Commons license, and indica e i changes we e made. The C ea i e Commons Public Domain Dedica ion wai e
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Yaméogo e al. Nu i ion Jou nal (2017) 16:44
DOI 10.1186/s12937-017-0264-3
PUFAs in low-income coun ies among malnou ished
child en [9]. The a y acid composi ion in plasma o ed
blood cells om child en wi h mode a e malnu i ion has
only been in es iga ed in wo s udies wi h small samples
sizes [7, 10]. Howe e , in hese s udies included child en
wi h mode a e s un ing and/o unde weigh a he han
was ing and used di e en g ow h e e ences a he han
he cu en WHO g ow h s anda ds om 2006 [2]. No
s udy was ound ha in es iga ed a y acids in child en
wi h MAM based on he abo e de ini ion and compa ed
he a y acid composi ion in whole-blood be ween chil-
d en diagnosed wi h MAM based on low MUAC only,
low MUAC and WHZ, o low WHZ only.
PUFAs play an impo an ole in ea ly li e because hey
a e needed o ensu e op imal g ow h and de elopmen o
all o gan sys ems [11]. Mo e speci ically, linoleic acid
(LA), α-linolenic acid (ALA), docosahexaenoic acid
(DHA) and a achidonic acid (AA) a e in ol ed in nume -
ous me abolic p ocesses in addi ion o ac ing as a sou ce
o ene gy [12]. LA, inco po a ed in skin ce amides, is o
g ea impo ance o skin ba ie in eg i y [13]. DHA is
abundan in he cells o he cen al ne ous sys em and is
impo an o b ain de elopmen [14]. Fu he mo e, DHA
and AA a e inco po a ed in o cell memb ane phospho-
lipids and a e p ecu so s o lipid media o signalling mole-
cules [15, 16], which play impo an oles, among o he s,
in he immune sys em [17]. Conside ing hese impo an
unc ions, mo e a en ion should be paid o PUFA s a us
in child en wi h MAM and i should be in es iga ed how
blood PUFA composi ion co ela es wi h ac o s such as
die , in ec ions (e.g. dia hea, mala ia), in lamma ion and
anemia and whe he he e is an associa ion be ween
PUFAs and an h opome y.
P e ious s udies in es iga ing blood PUFA composi ion
in Bu kina Faso, Wes A ica, ha e been unde aken in
popula ions no su e ing om MAM and in he cen al
egion [18–20], an a ea o he coun y whe e g oundnu s
a e widely a ailable and die s a e high in a [21]. Ou
s udy was ocused on whole-blood PUFA composi ion
among 6–23 mon hs-old child en wi h MAM om he
no he n egion in Bu kina Faso, whe e ood insecu i y is
common. The aim o he s udy was 1) o desc ibe whole-
blood PUFA composi ion in child en wi h MAM and 2)
o iden i y co ela es (e.g. hemoglobin, acu e phase p o-
eins, clinical in ec ion, an h opome y and die ) o PUFA
composi ion.
Subjec s and me hods
S udy se ing and pa icipan s
This is a c oss-sec ional s udy using baseline da a om a
p ospec i e nu i ional in e en ion ial among 1609
child en wi h MAM aged 6–23 mon hs. The s udy ook
place in he P o ince du Passo é, Bu kina Faso, a i e
local go e nmen al heal h cen e s (Gomponsom,
La oden, Baga é, Bokin and Samba). The ec ui men
a ea co e ed a o al o 143 illages and a popula ion o
app oxima ely 258,000. Rec ui men ook place om
Sep embe 2013 o Augus 2014.
Child en, aged 6–23 mon hs, esiding in he ec ui -
men a ea we e in i ed o pa icipa e i hey we e diag-
nosed wi h MAM; based on a WHZ be ween -3 and -2
based on he 2006 WHO g ow h s anda d [2] and/o
MUAC be ween 115 mm and 125 mm [3]. Child en
we e excluded i hey we e ea ed o SAM, i hey
we e al eady in a nu i ional p og am o i hey had
been hospi alized wi hin he pas 2 mon hs, had med-
ical complica ions equi ing hospi aliza ion, o a se-
e e disabili y.
Socio-demog aphic, clinical and die da a collec ion
A local nu se ca ied ou a clinical examina ion and col-
lec ed da a on sociodemog aphic cha ac e is ics as well
as 2 week e ospec i e mo bidi y. Fe e was de ined as
an axilla y empe a u e ≥37.5 °C [22]. The nu se also
collec ed da a on b eas eeding and he child ens’die
using s uc u ed ques ionnai es adminis e ed o he
ca e ake s by ained in e iewe s. Wi h ega d o
b eas eeding, ca e ake s we e asked whe he he child
was e e b eas ed, cu en ly b eas ed and i so how
many imes he child was b eas ed in he p e ious 24 h.
Die a y da a was collec ed using a quali a i e 24-h ecall
in e iew. Mo e speci ically, ca e ake s we e asked wha
he child en consumed in he p e ious 24-h, bu no
quan i ies we e eco ded. I a pa icula dish was men-
ioned, ca e ake ’s we e asked o lis he ing edien s. In-
o ma ion eco ded du ing he quali a i e 24-h ecall
in e iew was hen used o comple e he ood g oup lis
sec ion o he ques ionnai e by answe ing “yes”o “no”
o each ood g oup. The lis o 25 ood g oups was
based on in e na ionally a ailable ques ionnai es om
WHO [23], FAO [24] as well as esea ch abou die s in
Ouagadougou ca ied ou by he Ins i u de Reche che
e Dé eloppemen [25] and adap ed o he local con ex
using die a y in o ma ion collec ed du ing he T ea ood
pilo s udy. Fo easons o simplici y, he 25 ood g oups
was hen agg ega ed in o eigh ood g oups, namely i)
ce eals, oo s, and ube s; ii) legumes and nu s; iii) liquid
oils and a s; i ) dai y; ) lesh oods; i) eggs; ii) i amin
A- ich ui s and ege ables o iii) o he ui s and eg-
e ables as sugges ed by WHO [23].
Blood sampling and analyses
Du ing he medical examina ion up o 2.5 mL o none
as ing enous blood we e collec ed by phlebo omy
using needle and sy inge. One d op o blood was used
o ca y ou apid an igen es o Plasmodium alcip-
a um mala ia (SD Bioline, Mala ia an igen P. .), and a
second d op o de e mina ion o hemoglobin le el by
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 2 o 11
Hemocue (HB 301, Ängelholm, Sweden). A hi d d op
was used o sa u a e 1 cm
2
o a ch oma og aphy pape
s ip ea ed wi h 50 μg 2,6-di- e -bu yl-4-me hylphenol
(bu yla ed hyd oxy oluene) and 1000 μg de e oxamine
mesyla e sal (bo h om Sigma-Ald ich, S . Louis, MI,
USA) as desc ibed p e iously [26]. The blood spo s we e
allowed o ai d y and hen he pape s ip we e kep in
cold boxes in he ield and s o ed in zip lock plas ic bags
a 4 °C un il shipmen o Canada. The emaining blood
sample was pu in o a ube wi h clo ac i a o (BD ube
e e ence #368492; Bec on, Dickinson and Company,
F anklin Lakes, USA) and anspo ed in a coldbox a 2–
8 °C o he ial lab, whe e se um was isola ed ollowing
cen i uga ion a 3000 RPM o 5 min (EBA 20 S He -
ich, Tu lingen, Ge many).
Se um was s o ed a -20 °C un il shipmen o a labo a-
o y in Ge many (Vi amin lab, Wills ae , Ge many) o
analysis. Se um C- eac i e p o ein (CRP) and α
1
-acid
glycop o ein (AGP) we e de e mined using a simple
sandwich enzyme-linked immunoso ban assay [27]. The
h esholds used o de ining abno mal alues o CRP
and AGP we e as ollows: CRP >10 mg/L [28] and AGP
>1 g/L [29].
The a y acid composi ion o whole-blood was ana-
lysed as p e iously desc ibed [30, 31]. In b ie , a y
acid me hyl es e s we e p epa ed om d ied blood
spo s by di ec ans-es e i ica ion in 14% bo on i-
luo ide in me hanol (Pie ce Chemicals, Rock o d, IL,
USA) wi h hexane using a con ec ional block hea e
se a 95 °C o 60 min. The o ganic laye con aining
he a y acid me hyl es e s was collec ed o analysis
on a Va ian 3900 gas ch oma og aph wi h a CP-8400
au osample (Va ian Inc., Mississauga, ON, Canada)
and equipped wi h a DB-FFAP 15 m × 0.10 mm i.d. ×
0.10 μm ilm hickness, ni o e eph halic acid modi ied,
polye hylene glycol, capilla y column (J&W Scien i ic
om Agilen Technologies, Mississauga, ON, Canada).
Fas gas ch oma og aphy se ings wi h hyd ogen as he
ca ie gas we e used as p e iously desc ibed [30, 31].
Peaks we e iden i ied by e en ion imes h ough compa i-
son o an ex e nal mixed s anda d sample (GLC-462, Nu
Chek P ep Inc., Elysian, MN, USA). Whole-blood a y
acid concen a ion is gi en as (μg a y acid/100 μL
whole-blood) and a y acid composi ion da a a e
gi en as weigh pe cen o indi idual a y acids ela-
i e o he o al a y acid concen a ion in each sam-
ple (FA%).
Due o lack o cu -o poin s o whole-blood Mead
acid and n-6 docosapen aenoic acid (DPA), he a ios
Mead acid:AA, n-6 DPA:DHA o n-6/n-3 PUFAs we e
used o de ine PUFA de iciency. Based on da a in heal hy
well-nou ished Danish in an s (Lau i zen e al. unpub-
lished da a), we conside ed a Mead acid:AA a io > 0.02
as an indica o o PUFA de iciency and a a io o n-6
DPA:DHA > 0.2 and a n-6/n-3 PUFA a io > 10.5 was
aken o indica e low n-3 PUFA s a us.
An h opome ic measu es
An h opome ic measu emen s we e done by ained s a ,
a e s anda disa ion sessions. Weigh was measu ed in
duplica e o he nea es 100 g wi h an elec onic scale
(Seca model 881 1021659, Seca GmbH & Co. KG,
Hambu g, Ge many) wi h double weighing unc ion.
Leng h was measu ed in duplica e o he nea es 1 mm
wi h a wooden leng h boa d. MUAC was measu ed o he
nea es 1 mm a he midpoin be ween he olec anon and
he ac omion p ocess using a s anda d measu ing ape.
Da a analysis
The da a we e doubled en e ed in o Epida a 3.1 so wa e
(Epida a Associa ion, Odense, Denma k). The s a is ical
analysis and es s we e pe o med in S a a 12 (S a aCo p,
College S a ion, TX, USA). A WHO WHZ able was used
du ing ec ui men a si es, bu o da a analysis WHZ
sco es we e ecalcula ed using he STATA package
“zsco e06”. Va iables we e es ed o no mali y using
Shapi o-Wilk es s and his og ams. Resul s a e shown as
mean ± s anda d de ia ion (±SD) o median (in e qua ile
ange (IQR)). The di e ence be ween g oups was analyzed
by one-way analysis o a iance (ANOVA) and p- alues
om pos -hoc pai wise compa isons ( h ee compa isons
o each ANOVA es ) we e Bon e oni adjus ed. Mul i a i-
able linea eg ession analysis was pe o med o assess co -
ela es o indi idual PUFAs in child en wi h MAM adjus ed
o age and sex. S a is ical signi icance was se a p<0.05.
Resul s
Among he 1609 ec ui ed child en, a o al o 1572
(97.7%) child en had whole-blood a y acids de e -
mined and 37 (2.3%) did no ei he due o ailu e o
d aw blood o p oblems du ing blood analysis a he
lab. Upon ec ui men , 457 (29%), 786 (50%), and 329
(21%) we e diagnosed wi h MAM based on “MUAC
only”,“MUAC and WHZ”,and“WHZ only”, espec -
i ely, as p e iously epo ed [32]. The median (IQR)
age was 11.3 (8.2; 16) mon hs, hal (54.8%) we e gi ls
(Table 1) and 95% we e s ill b eas ed. As epo ed
elsewhe e [33], co-mo bidi y was common. Among
he 1572 child en wi h a y acid da a, 593 (38.1%)
child en had been ill in he 2 weeks be o e admission
based on ma e nal ecall –he eo 318 (20.2%) wi h
e e and 277 (17.6%) wi h dia hea. A ec ui men ,
629 (40.2%) had a posi i e mala ia es , 275 (17.5%)
had e e and 83 (5.3%) had dia hea. The mean
hemoglobin was 10.0 (±1.6) g/dL, while he median
CRP and AGP we e 2.3 (0.8; 9.5) mg/L and 1.2 (0.9;
1.6) g/L, espec i ely, and 364 (23.6%) had ele a ed
CRP and AGP.
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 3 o 11
The majo i y (85.2%) o he child en had consumed
ce eals, oo s and ube s in he p e ious 24 h, while 285
(18.1%), 237 (15.1%), and 454 (28.9%) had consumed li-
quid oils and a s, legumes and nu s o i amin A- ich
ui s and ege ables, espec i ely (Table 4). Mo e han
hal (54.5%) o he child en had also consumed o he s
ui s and ege ables. Almos all child en we e b eas ed
(95%) and only 6 (0.4%), 60 (3.8) and 107 (6.8%) had
ea en eggs, dai y and lesh oods, espec i ely, on he
day be o e he examina ion.
Concen a ions and co ela es o polyunsa u a ed a y acids
The mean weigh pe cen o whole-blood LA and ALA
we e 16.22 (±2.26) and 0.21 (±0.09) FA%, espec i ely,
while ha o hei espec i e LC-PUFAs, AA and DHA,
we e 7.08 (±1.53) and 1.64 (±0.53) FA%, espec i ely
(Table 2). The mean Mead acid:AA a io o 0.01 (±0.00)
and he gene ally low mean weigh pe cen o Mead acid
(0.07 (±0.03) FA%) indica es ha essen ial a y acid de i-
ciency was no equen in he pa icipan s. Based on
ou de ini ion, only 1.21% o he child en wi h MAM
had signs o PUFA de iciency. Howe e , he mean a io
o 0.25 (±0.10) be ween n-6 DPA and DHA and he
mean n-6/n-3 PUFA a io o 11.23 (±2.85) indica es low
n-3 PUFA s a us. The pe cen s o child en who we e
abo e he mean a io o 0.25 (±0.10) be ween n-6 DPA
and DHA o 11.23 (±2.85) be ween n-6 and n-3 PUFA
we e 51.2 and 45.8% espec i ely.
Compa isons using ANOVA showed ha child en e-
c ui ed based on MUAC only had lowe AA han hose
ec ui ed based on bo h MUAC and WHZ (6.88 s. 7.15
FA%, p= 0.007) and WHZ only (6.88 s. 7.19 FA%, p=
0.013), bu highe ALA han hose ec ui ed based on
WHZ (0.22 s. 0.20 FA%, p= 0.042) (Table 3). Fu he -
mo e, child en ec ui ed based on low MUAC only had
lowe EPA han hose ec ui ed wi h WHZ only (0.12 s.
0.14 FA%, p= 0.040). Fu he mo e, mul iple eg ession
Table 1 Backg ound da a, an h opome ic, clinical and
biochemical cha ac e is ics among 1572 child en wi h mode a e
acu e malnu i ion
Age (mon hs), median (IQR) 11.3 (8.2; 16.0)
6-11, n (%) 854 (54.3)
12-17, n (%) 447 (28.5)
18-23, n (%) 271 (17.2)
Sex
Boys, n (%) 682 (45.2)
Gi ls, n (%) 710 (54.8)
B eas eeding s a us
S ill b eas ed, n (%) 1488 (94.8)
No b eas ed, n (%) 82 (5.2)
An h opome ics indica o s, mean (±SD)
WHZ −2.2 (±0.5)
HAZ −1.7 (±1.1)
MUAC (mm) 122.6 (±4)
Biochemical
Hemoglobin (g/dL), mean (±SD) 10.0 (±1.6)
AGP (g/L), median (IQR) 1.2 (0.9; 1.6)
CRP (mg/L), median (IQR) 2.3 (0.8; 9.5)
Mo bidi y
Ill he las wo weeks
No, n (%) 967 (61.9)
Yes, n (%) 596 (38.1)
Dia hea a ec ui men
No, n (%) 1489 (94.7)
Yes, n (%) 83 (5.3)
Fe e a ec ui men
No, n (%) 1295 (82.5)
Yes, n (%) 275 (17.5)
Mala ia a ec ui men
No, n (%) 936 (59.8)
Yes, n (%) 629 (40.2)
Da a a e o al numbe s (%), mean (±SD) o median (in e qua ile ange (IQR):
25
h
;75
h
pe cen ile) as indica ed. Numbe s in ca ego ies may no sum up
1572 due o missing da a, e.g. da a on b eas eeding we e a ailable om
1570, on AGP o CRP om 1541, on ill he las wo weeks om 1563, on e e
om 1570 and on mala ia om 1565
Table 2 Whole blood a y acids composi ion in 1572 child en
wi h mode a e acu e malnu i ion
Mean (±SD)
Sa u a ed a y acid 45.29 (±2.99)
Monounsa u a ed a y acid 22.57 (±3.39)
Polyunsa u a ed a y acid (PUFA) 28.52 (±2.78)
n-6 PUFA 25.99 (±2.65)
Linoleic acid (LA) 18:2n-6 16.22 (±2.26)
Dihomo-y-linolenic acid 20:3n-6 0.85 (±0.21)
A achidonic acid (AA) 20:4n-6 7.08 (±1.53)
Ad enic Acid 22:4n-6 0.95 (±0.26)
n-6 Docosapen aenoic acid (DPA) 22:5n-6 0.38 (±0.12)
n-3 PUFA 2.48 (±0.65)
α-Linolenic acid (ALA) 18:3n-3 0.21 (±0.09)
Eicosapen aenoic acid (EPA)
a
20:5n-3 0.13 (0.10; 0.18)
n-3 Docosapen aenoic acid 22:5n-3 0.43 (±0.12)
Docosahexaenoic acid (DHA) 22:6n-3 1.64 (±0.53)
Mead acid 20:3n-9 0.07 (±0.03)
Mead acid:AA 20:3n-9/20:4n-6 0.01 (±0.00)
n-6 DPA:DHA 22:5n-6/22:6n-3 0.25 (±0.10)
n-6 PUFA:n-3 PUFA 11.13 (±2.85)
Da a a e gi en as mean (± s anda d de ia ion, SD) in weigh pe cen ela i e
o o al a y (FA%), i no o he wise indica ed. Mean o al a y acid concen a ion
was 417 (±183) μg/100 μL whole blood in s udy child en.
a
Median (in e qua ile
ange: 25
h
;75
h
pe cen ile)
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 4 o 11
analyses, adjus ed o age and sex, e ealed ha he chil-
d en who we e ec ui ed based on MUAC only had 0.32
(95% con idence in e al (CI), 0.14; 0.50) FA% lowe AA
han hose ec ui ed based on bo h MUAC and WHZ
and 0.40 (95% CI, 0.16; 0.63) FA% lowe AA han hose
ec ui ed based on WHZ only. Rec ui men based on
MUAC only was also associa ed wi h 0.09 (95% CI, 0.01;
0.17) FA% lowe DHA han hose ec ui ed based on
WHZ only, whe eas ec ui men based on bo h MUAC
and WHZ was associa ed wi h a highe a io o n-6 DPA
ela i e o DHA (0.01 [95% CI, 0.00; 0.02]) and highe
Mead acid (0.004 [95% CI, 0.000; 0.007] FA%) compa ed
o hose ec ui ed wi h WHZ only. Being ec ui ed based
on MUAC only compa ed o WHZ only was posi i ely
associa ed wi h Mead acid:AA a io (β= 0.001, 95% CI,
0.000; 0.002). Al hough median age di e ed be ween
child en ec ui ed based on MUAC only, bo h MUAC
and WHZ, o WHZ only, he di e ence in AA, DHA
and Mead acid:AA ac oss ec ui men c i e ia was no
con ounded by age, sex and b eas eeding.
Die was ound o be a co ela e o whole-blood PUFA
s a us adjus ed o age and sex (Table 4). Rela i e o chil-
d en who we e no b eas ed, b eas ed child en had
1.17 (95% CI, 0.64; 1.70), 0.75 (95% CI, 0.39; 1.11), and
0.13 (95% CI, 0.01; 0.25) FA% highe LA, AA, and DHA,
espec i ely. Child en who had consumed oods om
he legumes and nu s g oup o he oils and a s g oup in
he p e ious 24 h had 0.38 (95% CI, 0.16; 0.59) and 0.32
(95% CI, 0.12; 0.52) FA% lowe AA, espec i ely, com-
pa ed o hose who did no consume hese oods. This
was also he case o child en wi h a die a y in ake om
he i amin A- ich ui s and ege ables g oup. Child en
wi h a die a y in ake om he oils and a s g oup o he
lesh ood g oup had 0.08 (95% CI, 0.09; 0.15) and 0.23
(95% CI, 0.12; 0.33) FA% highe DHA, espec i ely com-
pa ed o hose who had no ea en hese oods. Die a y
in ake om he lesh oods g oup was ound o be asso-
cia ed wi h a highe p opo ion o DHA ela i e o ha
o AA and ha was also he case o die a y in ake o
oils, which we e mainly ege able oils. Die a y in ake
om bo h o hese ood g oups was also ound o p o-
ide a la ge di e ence in he p opo ion o n-3 PUFAs
han in n-6 PUFAs.
Mo bidi y and biochemical ma ke s o in ec ion we e
also co ela es o whole-blood PUFA con en a e ad-
jus men o age and sex (Table 5). Child en who had
Table 3 Whole blood a y acids composi ion by ec ui men c i e ia in 1572 child en wi h mode a e acu e malnu i ion
MUAC
(n= 457)
MUAC and WHZ
(n= 786)
WHZ
(n= 329)
Median age (IQR)
9.6 (7.3; 13.6)
Median age (IQR)
11.6 (8.4; 16.4)
Median age (IQR)
13.3 (9.9; 17.8)
Mean FA (±SD) Mean FA (±SD) Mean FA (±SD)
Sa u a ed a y acid 45.35 (±3.38) 45.29 (±2.82) 45.24 (±2.82)
Monounsa u a ed a y acid 22.77 (±3.53) 22.57 (±3.34) 22.29 (±3.31)
Polyunsa u a ed a y acid (PUFA) 28.40 (±2.69) 28.54 (±2.78) 28.68 (±2.92)
n-6 PUFA 25.91 (±2.53) 25.99 (±2.67) 26.11 (±2.77)
Linoleic acid (LA) 18:2n-6 16.37 (±2.16) 16.15 (±2.31) 16.22 (±2.29)
Dihomo-y-linolenic acid 20:3n-6 0.87 (±0.21) 0.85 (±0.21) 0.85 (±0.21)
A achidonic acid (AA) 20:4n-6 6.88 (±1.53)
1,2
7.15 (±1.53) 7.19 (±1.54)
Ad enic Acid 22:4n-6 0.92 (±0.26)
2
0.96 (±0.27) 0.97 (±0.27)
n-6 Docosapen aenoic acid (DPA) 22:5n-6 0.37 (±0.13) 0.39 (±0.13) 0.38 (±0.13)
n-3 PUFA 2.42 (±0.64) 2.50 (±0.68) 2.51 (±0.62)
α-Linolenic acid (ALA) 18:3n-3 0.22 (±0.09)
2
0.22 (±0.09) 0.20 (±0.09)
Eicosapen aenoic acid (EPA)
a
20:5n-3 0.12 (0.09; 0.18)
2
0.13 (0.10; 0.18) 0.14 (0.10; 0.20)
n-3 Docosapen aenoic acid 22:5n-3 0.43 (±0.12) 0..45 (±0.13) 0.44 (±0.12)
Docosahexaenoic acid (DHA) 22:6n-3 1.60 (±0.52) 1.65 (±0.54) 1.67 (±0.53)
Mead acid 20:3n-9 0.07 (±0.03) 0.07 (±0.03) 0.07 (±0.02)
Mead acid:AA 20:3n-9/20:4n-6 0.01 (±0.01) 0.01 (±0.00) 0.01 (±0.01)
n-6 DPA:DHA 22:5n-6/22:6n-3 0.25 (±0.10) 0.25 (±0.10) 0.24 (±0.09)
n-6 PUFA:n-3 PUFA 11.40 (2.91) 11.10 (2.86) 11.00 (2.77)
Da a a e gi en as mean (±s anda d de ia ion, SD) weigh pe cen o o al whole blood a y acids, i no o he wise indica ed. p- alue o di e ence be ween
admission g oups a e based on ANOVA es wi h Bon e oni adjus men . Abb e ia ions:WHZ weigh- o -heigh z-sco e, MUAC mid-uppe a m ci cum e ence
1
p<0.05 be ween MUAC and, MUAC and WHZ, and
2
p<0.05 be ween MUAC and WHZ
a
Median (in e qua ile ange: 25
h
;75
h
pe cen ile) and ANOVA es on log alue
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 5 o 11

Table 4 Co ela ions be ween indi idual whole blood polyunsa u a ed a y acid and die a y in ake o a ious ood componen es based on a 24-hou ecall in 1572 child en wi h
mode a e acu e malnu i ion
n (%) n-6 polyunsa u a ed a y acids n-3 polyunsa u a ed a y acids Ra ios
LA
18:2n-6
AA
20:4n-6
n-6 DPA
22:5n-6
ALA
18:3n-3
DHA
22:6n-3
Mead acid
20:3n-9
Mead acid/AA
20:3n-9/20:4n-6
n-6 DPA/DHA
22:5n-6/22:6n-3
G ains, oo s, and ube s g oup
No 231 (14.8) Re Re Re Re Re Re Re Re
Yes 1335 (85.2) −0.05 (-0.38 ; 0.27) 0.01 (-0.21 ; 0.22) 0.006 (-0.01 ; 0.02) −0.01 (-0.02; 0.01) 0.03 (-0.04 ; 0.10) 0.001 (-0.003; 0.004) 0.000 (-0.001; 0.001) −0.00 (-0.01; 0.01)
Legumes and nu s g oup
No 1335 (84.9) Re Re Re Re Re Re Re Re
Yes 237 (15.1) 0.07 (-0.24 ; 0.38) −0.38 (-0.59 ; -0.16) * −0.03 (-0.04 ; -0.01) ** 0.02 (0.00; 0.03)* −0.05 (-0.13 ; 0.01) −0.000 (-0.004; 0.003) 0.001 (0.000; 0.001)* −0.01 (-0.02; 0.01)
Oils and a s g oup
No 1286 (81.9) Re Re Re Re Re Re Re Re
Yes 285 (18.1) −0.01 (-0.31 ; -0.28) −0.32 (-0.52 ; -0.12)** −0.04 (-0.05 ; -0.02)** −0.02 (-0.01; 0.01) 0.08 (0.09 ; 0.15)* 0.001 (-0.002; 0.004) 0.001 (0.000; 0.002)** −0.03 (-0.04; -0.01)**
Dai y g oup
No 1512 (96.2) Re Re Re Re Re Re Re Re
Yes 60 (3.8) −0.41 (-0.99 ; 0.17) 0.002 (-0.39 ; 0.39) 0.02 (-0.01 ; 0.05) 0.01 (-0.02; 0.03) 0.01 (-0.12 ; 0.15) 0.008 (0.002; 0.010)* 0.001 (-0.000; 0.020) 0.01 (-0.01; 0.04)
Flesh oods g oup
No 1464 (93.2) Re Re Re Re Re Re Re Re
Yes 107 (6.8) −0.24 (-0.69 ; 0.20) −0.18 (-0.49 ; 0.11) −0.03 (-0.06 ; -0.01)* −0.01 (-0.03; 0.00) 0.23 (0.12 ; 0.33)** −0.003 (-0.008; 0.002) −0.000 (-0.001; 0.006) −0.04 (-0.05; -0.02)*
Eggs g oup
No 1561 (99.6) Re Re Re Re Re Re Re Re
Yes 6 (0.4) −1.11 (-2.93; 0.70) −0.96 (-2.19; 0.26) −0.02 (-0.12; 0.08) 0.04 (-0.03; 0.12) −0.04 (-0.47; 0.37) −0.004 (-0.020; 0.010) 0.001 (-0.003; 0.005) −0.01 (-0.08; 0.07)
Vi amin A- ich ui s and ege ables g oup
No 1116 (71.1) Re Re Re Re Re Re Re Re
Yes 454 (28.9) 0.15 (-0.1; 0.40) −0.24 (-0.41; -0.07)* −0.02 (-0.03; -0.00)** 0.01 (-0.00; 0.02) 0.01 (-0.05; 0.07) −0.000 (-0.003; 0.002) 0.000 (-0.000; 0.001) −0.01 (-0.02; 0.00)
O he s ui s and ege ables g oup
No 715 (45.5) Re Re Re Re Re Re Re Re
Yes 857 (54.5) −0.06 (-0.29; 0.17) 0.10 (-0.05; 0.26) 0.12 (-0.00; 0.02) −0.01 (-0.02; -0.00)* 0.03 (-0.02; 0.09) 0.001 (-0.001; 0.004) 0.000 (-0.000; 0.001) −0.00 (-0.01; 0.01)
B eas eeding
No 82 (5.2) Re Re Re Re Re Re Re
Yes 1488 (94.8) 1.17 (0.64; 1.70)** 0.75 (0.39; 1.11)** 0.00 (-0.02; 0.03) −0.01 (-0.03; 0.01) 0.13 (0.01; 0.25)* −0.020 (-0.030;-0.020)** −0.005 (-0.006;-0.004)** −0.04 (-0.06; -0.01)**
Da a a e gi en as eg ession coe icien s (95% con idence in e al) in weigh pe cen o o al whole blood a y acid concen a ion a e adjus men o age and sex. Abb e ia ions:LA Linoleic acid, AA A achidonic acid,
n-6DPA n-6 Docosapen aenoic acid, ALA α-Linolenic acid, DHA Docosahexaenoic acid, e e e ence g oup. Numbe s in ca ego ies may no sum up o 1572 due o missing da a. Da a on in ake o g ains, oo s, and
ube s g oup we e a ailable o 1566 child en, on in ake o lesh oods om 1571, eggs om 1567, on i amin A- ich ui s and ege ables and b eas eeding om 1570. *p<0.05; **p<0.01
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 6 o 11
Table 5 Biochemical and mo bidi y co ela es o indi idual polyunsa u a ed a y acid in 1572 child en wi h mode a e acu e malnu i ion
n (%) n-6 polyunsa u a ed a y acids n-3 polyunsa u a ed a y acids Ra ios
LA
18:2n-6
AA
20:4n-6
n-6 DPA
22:5n-6
ALA
18:3n-3
DHA
22:6n-3
Mead acid
20:3n-9
Mead acid/AA
20:3n-9/20:4n-6
n-6 DPA/DHA
22:5n-6/22:6n-3
Hemoglobin
g/dl 1572 (100) −0.22 (-0.29; -0.15)** 0.39 (0.35; 0.44)** 0.02 (0.01 ; 0.02)** −0.02 (-0.02; -0.01)** 0.11 (0.10; 0.13)** 0.000 (-0.001; 0.001) −0.001 (-0.001;
-0.001)**
−0.004 (-0.008;-
0.001)**
≥11 472 (30.0) Re Re Re Re Re Re Re Re
<11 1100 (70.0) 0.73 (0.49; 0.98)** −0.77 (-0.93; -0.61)** −0.03 (-0.05; -0.02)** 0.03 (0.02; 0.04)** −0.27 (-0.33; -0.21)** −0.001 (-0.004; 0.002) 0.001 (0.007;
0.002)**
0.02 (0.01; 0.03)**
CRP
<10mg/L 1166 (75.7) Re Re Re Re Re Re Re Re
≥10mg/L 375 (24.3) −0.04 (-0.30 ; 0.23) −0.91 (-1.10; -0.74)** −0.05 (-0.06 ; -0.03)** 0.04 (0.02; 0.05)** −0.23 (-0.30; -0.17)** −0.005 (-0.008; -0.002)** 0.001 (0.000;
0.001)**
0.01 (-0.00; 0.16)
AGP
<1g/L 516 (33.5) Re Re Re Re Re Re Re Re
≥1g/L 1025 (66.5) 0.01 (-0.22; 0.25) −0.60 (-0.76; -0.43)** −0.02 (-0.04 ; -0.12)** 0.02 (0.01; 0.03)** −0.10 (-0.15; -0.04)* 0.001 (-0.001; 0.004) 0.001 (0.001;
0.002)**
0.00 (-0.01; 0.10)
Dia hea
No 1489 (94.7) Re Re Re Re Re Re Re Re
Yes 83 (5.3) −0.64 (-1.14; -0.14)* 0.20 (-0.13; 0.55) 0.02 (-0.01; 0.05) −0.02 (-0.04; 0.00) 0.16 (0.05; 0.28)** −0.004 (-0.010; 0.001) −0.001 (-0.002;
0.000)
−0.02 (-0.04; 0.00)
Fe e
No 1295 (82.5) Re Re Re Re Re Re Re Re
Yes 275 (17.5) −0.52 (-0.82; -0.23)** −0.29 (-0.49; -0.09)** −0.01 (-0.02; 0.005) 0.01 (-0.00; 0.02) −0.10 (-0.17; -0.03)** −0.005 (-0.009; -0.002)** −0.000 (-0.001;
0.000)
0.01 (-0.00; 0.02)
Mala ia
No 936 (59.8) Re Re Re Re Re Re Re Re
Yes 629 (40.2) 0.20 (-0.02; 0.43) −1.06 (-1.20; -0.91)** −0.02 (-0.04; -0.01)** 0.05 (0.04; 0.05)* −0.30 (-0.35; -0.25)** 0.002 (-0.001; 0.004) 0.002 (0.001;
0.003)**
0.02 (0.01; 0.03)**
Da a a e gi en as eg ession coe icien s (95% con idence in e al) in weigh pe cen o o al whole blood a y acids concen a ion a e adjus men o age and sex. Abb e ia ions:LA Linoleic acid, AA A achidonic acid,
n-6DPA n-6 Docosapen aenoic acid, ALA α-Linolenic acid, DHA Docosahexaenoic acid, e e e ence g oup. Numbe s in ca ego ies may no sum up o 1572 due o missing da a, e.g. da a on CRP and AGP we e a ailable
o 1541 child en, on e e om 1570, on mala ia om 1565. *p<0.05; **p<0.01
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 7 o 11
e e a ec ui men had lowe LA, AA and DHA by
0.52 (95% CI, 0.23; 0.82), 0.29 (95% CI, 0.09; 0.49) and
0.10 (95% CI, 0.03; 0.17) FA%, espec i ely. Simila ly,
e e in he 2 weeks p io o ec ui men was associa ed
wi h low AA and DHA, bu no LA. Dia hea a ec ui -
men was nega i ely associa ed wi h LA, bu posi i ely
associa ed wi h DHA, which was also seen wi h dia hea
based on ma e nal ecall (p< 0.05, da a no shown).
Child en wi h ele a ed CRP had 0.91 (95% CI, 0.74;
1.10) and 0.23 (95% CI, 0.17; 0.30) FA% lowe AA and
DHA, espec i ely, bu 0.04 (95% CI, 0.02; 0.05) FA%
highe ALA. Ele a ed AGP was also associa ed wi h
lowe AA and DHA (0.60 [95% CI, 0.43; 0.76] and 0.10
[95% CI, 0.04; 0.15] FA%, espec i ely) bu highe ALA
(0.02 [95% CI, 0.01; 0.03] FA%). A posi i e mala ia es
was associa ed wi h lowe AA and DHA (1.06 [95% CI,
0.91; 1.20] and 0.30 [95% CI, 0.25; 0.35] FA%, espec i ely)
and highe ALA (0.05 [95% CI, 0.04; 0.05] FA%). O e all,
ele a ed se um CRP and AGP, and a posi i e mala ia es
we e associa ed wi h a highe Mead acid:AA a io. A posi-
i e mala ia es was also associa ed wi h a highe n-6
DPA/DHA a io. Fo each 1 g/dl inc ease in hemoglobin,
LA and ALA dec eased by -0.22 (95% CI, -0.29; -0.15) and
-0.02 (95% CI, -0.02; -0.01) FA%, espec i ely. Howe e ,
o each 1 g/dl inc ease in hemoglobin, AA and DHA in-
c eased by 0.39 (95% CI, 0.35; 0.44) and 0.11 (95% CI,
0.10; 0.13) FA%, espec i ely.
Discussion
While we ound ha PUFA de iciency was no a gene al
p oblem in child en wi h MAM, o e all PUFA concen-
a ions, especially o n-3 PUFAs, we e low. The e could
be a numbe o explana ions o his. Fi s ly, he low
le els o whole-blood n-3 PUFAs ound in child en wi h
MAM could be linked o hei die [34]. The child en
we e om a popula ion wi h a mainly plan -based die
ich in LA, including peanu oils and peanu based-
p oduc s, co ons seed oils and ce eals. In an s and
young child en in such a popula ion will ha e an n-3
PUFA in ake a below he ecommended in ake [35].
P e ious s udies om he cen al egion in Bu kina Faso
ha e demons a ed a high p opo ion o n-6 PUFAs ela-
i e o n-3 PUFAs in b eas milk o heal hy mo he s
nu sing 5-mon hs-old in an s and his was nega i ely as-
socia ed wi h g ow h [18]. The low ela i e le els o n-3
PUFAs in child en wi h MAM was compensa ed o by
a high p opo ion in SFA, which is in line wi h da a om
mode a ely was ed Pakis ani child en [6]. This high p o-
po ion o SFA in ou s udy could be due o mo e
b eas eeding in Bu kina Faso as shown in p e ious s ud-
ies [18, 36]. Secondly, he low whole-blood n-3 PUFAs
could be due o me abolic dis u bances occu ing wi h
malnu i ion [6]. Mic onu ien de iciencies such as zinc
and i on combined wi h p o ein de iciency may impai
del a-6 desa u ase ac i i y [5, 37] and dec ease he con-
e sion o ALA o DHA.
As expec ed, b eas eeding, lesh oods, ege able oils
and a s we e ound o be co ela es o PUFAs in chil-
d en wi h MAM. B eas milk is ecognised as a good
sou ce o LC-PUFAs [38], al hough his is in luenced by
ma e nal die [39]. Child en who we e b eas ed on he
day be o e blood sampling had highe LA, AA, and
DHA compa ed o hose who we e no b eas ed. Chil-
d en who consumed lesh oods (mea and ish) in he
p e ious 24 h also had highe whole-blood n-3 PUFAs
and DHA han hose who did no consume hese ypes
o oods. This is in line wi h mea and speci ically ish
being he dominan sou ces o n-3 LC-PUFAs [34]. A
high in ake o n-3 LC-PUFAs has been shown o in-
c ease EPA and DHA in plasma and issue phospho-
lipids [40], which is o en compensa ed by a educ ion in
LA, AA and n-6 DPA.
Wi h ega d o an h opome y, child en ec ui ed by
MUAC only seem o ha e lowe whole-blood n-6 PUFAs
and n-3 PUFAs compa ed o hose ec ui ed by WHZ
only. Speci ically, ec ui men by MUAC only was asso-
cia ed wi h low AA and DHA and his could be ela ed
o a low muscle mass. Low MUAC only has been shown
o be ela ed o low a m muscle mass [41], which is gen-
e ally associa ed wi h hype co isolemia occu ing wi h
malnu i ion [42]. Hype co isolemia inc eases es ing
ene gy expendi u e ueled by inc eased oxida ion o a
[43], and his may dec ease whole-blood LC-PUFA s a-
us in child en wi h low MUAC. Ano he explana ion
could be ha in ake o LC-PUFAs and p o ein quali y
could be ela ed, as seen in a Canadian popula ion [44],
and hus a ec muscle and whole-blood LC-PUFAs in
pa allel. The issue mos a ec ed by malnu i ion in
he i s mon hs o li e is muscle mass [45]. I could
also be specula ed ha low MUAC is mo e ela ed o
long- e m in lamma ion, which may be he cause o
low PUFA s a us.
Ma ke s o in ec ion and in lamma ion we e nega-
i ely associa ed wi h whole-blood PUFAs. This ind-
ing could be explained by an in ec ion-induced
sup ession o appe i e and could be a di ec e ec o
die a y in ake, bu may also be ela ed o impai ed
abso p ion, poo nu ien u iliza ion and/o inc eased
nu ien ca abolism caused by he in lamma o y s a e
[46, 47]. We specula e ha he nega i e associa ion o
LA bu posi i e associa ion o DHA wi h dia hea
could be due o low abso p ion o a du ing dia hea
esul ing in low plasma iacylglyce ols and hus, ela-
i ely highe le els o DHA om he blood cells.
Fe e du ing in ec ion leads o an inc ease in ene gy
equi emen [48] and possibly an inc eased use o
PUFAs as uel. In ec ion-induced in lamma ion has
been sugges ed o inc ease LC-PUFA ca abolism,
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 8 o 11
mainly o AA and DHA o he p oduc ion o p o-
and an i-in lamma o y media o s [49] and is likely
con ibu ing o he educed AA and DHA seen in he
MAM child en, speci ically hose wi h low MUAC. Fi-
nally, hemoglobin was ound o posi i ely co ela e
wi h whole-blood LC-PUFAs, mos ly AA and DHA,
which could possibly be due o hei inco po a ion in
phospholipids o e y h ocy e memb anes [14]. The
nega i e associa ion be ween hemoglobin and whole-
blood LA could be caused by a p e e en ial ino po a-
ion o LC-PUFAs in e y h ocy e memb anes a he
expense o LA. The associa ion wi h anemia and
hemoglobin may he e o e in pa e lec changes in
blood composi ion (e y h ocy e numbe ) and may
he e o e no be an ideal indica o o whole blood
PUFA s a us.
The cu en s udy is he i s o in es iga e whole-
blood PUFA composi ion and co ela es among a la ge
sample o child en wi h MAM. Also, his is he i s
s udy o show a ela ionship be ween low MUAC and
PUFAs. The di e si y o co ela es such as in ec ion, in-
lamma ion, die , and an h opome y highligh he com-
plexi y o ac o s which may a ec whole-blood PUFA
composi ion in child en wi h MAM, and hese ac o s
should be aken in o accoun in s udies in es iga ing
PUFAs among malnou ished child en. Howe e , he
s udy had some limi a ions, in pa icula he lack o a
con ol g oup om he same s udy se ing, which makes
i di icul o di e en ia e be ween po en ial e ec s o
die and he o e all low nu i ional s a us. Di e ences in
die could con ound di e ences in nu i ional s a us
e en i we had been able o collec da a om a well-
nou ished g oup o child en in Bu kina Faso. The die
in o ma ion was based on a single quali a i e 24-h ecall
which may ha e educed accu acy and hus, educed he
associa ion be ween die and PUFAs. The obse ed asso-
cia ions we e howe e meaning ul. Fu he mo e, PUFA
s a us was only based on a single non- as ing whole-
blood sample and may no p o ide a measu e o
long- e ms a usasis hecase o exampleinadipose
issue samples [50], bu whole-blood EPA and DHA
co ela es wi h and p edic s e y h ocy e EPA and
DHA [51]. I may howe e , ma ch he sho - e m col-
lec ion o die a y in o ma ion and also mo bidi y,
which was based only on ecall da a om he p e i-
ous 2 weeks and da a om clinical examina ions on
he day o ec ui men .
In conclusion, al hough PUFA de iciency based on he
de ini ion used he e was no common, child en wi h
MAM in Bu kina Faso ha e low whole-blood n-3 PUFA
concen a ions. Low n-3 PUFA le els a e likely o be, o
some ex en , explained by a low in ake o animal based
oods, ege able oils and a sou ces o n-3 PUFA, o by
o he co ela ing ac o s such anemia, in ec ion and
in lamma ion. Child en wi h low MUAC seem o ha e
lowe whole-blood PUFAs compa ed o child en wi h
MAM based on WHZ. This obse a ion needs o be con-
i med in u u e in es iga ions among child en wi h
MAM.
Abb e ia ions
AA: A achidonic acid; AGP: α
1
-acid glycop o ein; ALA: α-linolenic acid;
ANOVA: Analysis o a iance; CI: Con idence in e al; CRP: C- eac i e p o ein;
DHA: Docosahexaenoic acid; DPA: Docosapen aenoic acid; EPA: Eicosapen aenoic
acid; FA%: Fa y acid pe cen ; IQR: In e qua ile ange; LA: Linoleic acid;
LC-PUFA: Long-chain polyunsa u a ed a y acid; MAM: Mode a e acu e
malnu i ion; MUAC: Mid-uppe -a m-ci cum e ence; MUFA: Monounsa u a ed
a y acid; PUFA: Polyunsa u a ed a y acid; SAM: Se e e acu e malnu i ion;
SD:S anda dde ia ion;SFA:Sa u a ed a yacid;WHO:Wo ldheal h
o ganiza ion; WHZ: Weigh - o -heigh z-sco e
Acknowledgemen s
We a e g a e ul o he s udy pa icipan s and hei amilies, and he s a o
he Alliance o In e na ional Medical Ac ion (ALIMA) o hei aluable
con ibu ion o his s udy. We hank he Minis y o Heal h in Bu kina Faso,
he heal h and illage au ho i ies in P o ince du Passo é, and he s a a he
heal h cen e s and o hei suppo o his s udy.
Funding
The s udy was unded by he Danish In e na ional De elopmen Assis ance
(DANIDA, 09-097 LIFE), Médecins Sans F on iè es (MSF Denma k & MSF
No way), Wo ld Food P og am (WFP), which was pa o a dona ion o WFP
om a gene ous suppo o he Ame ican people h ough he suppo o
he U.S. Agency o In e na ional De elopmen 's O ice o Food o Peace
(USAID). Alliance o In e na ional Medical Ac ion (ALIMA) and he Eu opean
Union’s humani a ian aid unds, in pa ne ship wi h Ac ion Con e la Faim
(ACF), A id Nilsson ounda ion.
The unding agencies had no ole in he design o s udy, da a collec ion and
analysis, o p esen a ion o he esul s.
A ailabili y o da a and ma e ials
All da a gene a ed o analysed du ing his s udy a e included in his
published a icle.
Au ho s’con ibu ions
The au ho s’con ibu ions o he manusc ip we e as ollows: MJHR, AB, SS,
VBC, KFM, and HF concei ed and designed he s udy; CWY, BC, CF, MJHR
and KDS conduc ed he esea ch; CWY, DFJ, HF and LL analyzed he da a
and CWY w o e he i s d a o he manusc ip and had p ima y esponsibili y
o he inal con en . CWY, BC, CF, MJHR, DFJ, KDS, AB, SS, AST, VBC, KFM, HF
and LL made e isions o he manusc ip and ead and app o ed he inal
submi ed e sion o he manusc ip .
E hics app o al and consen o pa icipa e
The s udy p o ocol was app o ed by he E hics Commi ee o Heal h Resea ch
in Bu kina Faso (2012-8-059) and consul a i e app o al was ob ained om he
Danish Na ional Commi ee on Biomedical Resea ch E hics (1208204). Consen
was ob ained e bally and in w i ing (signa u e o inge p in s) om ca e ake s o
he child en be o e inclusion. The in o ma ion and consen o m was ansla ed
in o he local language and back ansla ed o ensu e accu acy. The s udy was
ca ied ou in acco dance wi h he decla a ion o Helsinki and in e na ional
e hical guidelines o biomedical esea ch in ol ing human subjec s, published
by he Council o In e na ional O ganiza ions o Medical Sciences. Medical
ea men was p o ided acco ding o an adap ed e sion o he In eg a ed
Managemen o Childhood Illness guidelines and na ional p o ocol. This s udy
was a pa o T ea ood ial which was egis e ed a h p://www.is c n.com
(ISRCTN42569496).
Consen o publica ion
“No applicable”.
Compe ing in e es s
The au ho s decla e ha hey ha e no compe ing in e es s.
Yaméogo e al. Nu i ion Jou nal (2017) 16:44 Page 9 o 11