Protein–energy

malnutrition

Protein–energy malnutrition (PEM) is a

form of malnutrition that is defined as a
range of pathological conditions arising
from coincident lack of dietary protein
and/or energy (calories) in varying
proportions. The condition has mild,
moderate, and severe degrees.
 Protein–energy malnutrition
Other names Protein–calorie
malnutrition, PEM,
PCM

Specialty Endocrinology 

Disability-adjusted life year for protein–energy

malnutrition per 100,000 inhabitants in 2004.
   no data
   less than 10
   10–100
   100–200
200 300
    200–300
   300–400
   400–500

   500–600
   600–700
   700–800
   800–1000
   1000–1350
   more than 1350

Types include:[1]

Kwashiorkor (protein malnutrition

predominant)
Marasmus (deficiency in calorie intake)
 Marasmic kwashiorkor (marked protein
deficiency and marked calorie
insufficiency signs present, sometimes
referred to as the most severe form of
malnutrition)

PEM is fairly common worldwide in both

children and adults and accounts for 6
million deaths annually.[2] In the
industrialized world, PEM is predominantly
seen in hospitals, is associated with
disease, or is often found in the elderly.[2]

Note that PEM may be secondary to other

conditions such as chronic renal disease[3]
or cancer cachexia[4] in which protein
energy wasting may occur.

Protein–energy malnutrition affects

children the most because they have less
protein intake. The few rare cases found in
the developed world are almost entirely
found in small children as a result of fad
diets, or ignorance of the nutritional needs
of children, particularly in cases of milk
allergy.[5]

Prenatal protein malnutrition

Protein malnutrition is detrimental at any
point in life, but protein malnutrition
prenatally has been shown to have
significant lifelong effects. During
pregnancy, one should aim for a diet that
consists of at least 20% protein for the
health of the fetus. Diets that consist of
less than 6% protein in utero have been
linked with many deficits, including
decreased brain weight, increased obesity,
and impaired communication within the
brain in some animals. Even diets of mild
protein malnutrition (7.2%) have been
shown to have lasting and significant
effects in rats. The following are some
studies in which prenatal protein
deficiency has been shown to have
unfavorable consequences.

Decreased brain size: Protein deficiency

has been shown to affect the size and
composition of brains in rhesus
monkeys. Monkeys whose mother had
eaten a diet with an adequate amount of
protein were shown to have no deficit in
brain size or composition, even when
their body weight amounted to less than
one-half of that of the controls, whereas
monkeys whose mothers had eaten low-
protein diets were shown to have
smaller brains regardless of the diet
given after birth.[6]
Impaired neocortical long-term
potentiation: Mild protein deficiency (in
which 7.2% of the diet consists of
protein) in rats has been shown to
impair entorhinal cortex plasticity
(visuospatial memory), noradrenergic
function in the neocortex, and
neocortical long-term potentiation.[7]
Altered fat distribution: Protein
undernutrition can have varying effects
depending on the period of fetal life
during which the malnutrition occurred.
Although there were not significant
differences in the food intake, there
were increased amounts of perirenal fat
in rats that were protein-deprived during
early (gestation days 0–7) and mid
(gestation days 8–14) pregnancy, and
throughout pregnancy, whereas rats that
were protein-deprived only late in
gestation (gestation days 15–22) were
shown to have increased gonadal fat.[8]
Increased obesity: Mice exposed to a
low-protein diet prenatally weighed 40%
less than the control group at birth
(intrauterine growth retardation). When
fed a high-fat diet after birth, the
prenatally undernourished mice were
shown to have increased body weight
and adiposity (body fat), while those
who were adequately nourished
prenatally did not show an increase in
body weight or adiposity when fed the
same high-fat diet after birth.[9]
Decreased birth weight, and gestation
duration: Supplementation of protein
and energy can lead to increased
duration of gestation and higher birth
weight. When fed a supplement
containing protein, energy, and
micronutrients, pregnant women
showed more successful results during
birth, including high birth weights, longer
gestations, and fewer pre-term births,
than women who had consumed a
supplement with micronutrients and low
energy but no protein (although this
finding may be due to the increase of
energy in the supplements, not the
increase of protein).[10]
Increased stress sensitivity: Male
offspring of pregnant rats fed low-
protein diets have been shown to exhibit
blood pressure that is hyperresponsive
to stress and salt.[11]
Decreased sperm quality: A low-protein
diet during gestation in rats has been
shown to affect the sperm quality of the
male offspring in adulthood. The protein
deficiency appeared to reduce sertoli
cell number, sperm motility, and sperm
count.[12]
Altered cardiac energy metabolism:
Prenatal nutrition, specifically protein
nutrition, may affect the regulation of
 cardiac energy metabolism through
changes in specific genes.[13]
Increased passive stiffness: Intrauterine
undernutrition was shown to increase
passive stiffness in skeletal muscles in
rats.[14]

From these studies it is possible to

conclude that prenatal protein nutrition is
vital to the development of the fetus,
especially the brain, the susceptibility to
diseases in adulthood, and even gene
expression. When pregnant females of
various species were given low-protein
diets, the offspring were shown to have
many deficits. These findings highlight the
great significance of adequate protein in
the prenatal diet.

Epidemiology

Deaths from protein-energy malnutrition per million

persons in 2012
   0-0
   1-3
   4-6
   7-13
   14-22
23 38
    23-38
   39-65
   66-182

   183-313
   314-923

Although protein energy malnutrition is

more common in low-income countries,
children from higher-income countries are
also affected, including children from large
urban areas in low socioeconomic
neighborhoods. This may also occur in
children with chronic diseases, and
children who are institutionalized or
hospitalized for a different diagnosis. Risk
factors include a primary diagnosis of
intellectual disability, cystic fibrosis,
malignancy, cardiovascular disease, end
stage renal disease, oncologic disease,
genetic disease, neurological disease,
multiple diagnoses, or prolonged
hospitalization. In these conditions, the
challenging nutritional management may
get overlooked and underestimated,
resulting in an impairment of the chances
for recovery and the worsening of the
situation.[15]
PEM is fairly common worldwide in both
children and adults and accounts for 6
million deaths annually.[2] In the
industrialized world, PEM is predominantly
seen in hospitals, is associated with
disease, or is often found in the elderly.[2]

Co-morbidity
A large percentage of children that suffer
from PEM also have other co-morbid
conditions. The most common co-
morbidities are diarrhea (72.2% of a
sample of 66 subjects) and malaria
(43.3%). However, a variety of other
conditions have been observed with PEM,
including sepsis, severe anaemia,
bronchopneumonia, HIV, tuberculosis,
scabies, chronic suppurative otitis media,
rickets, and keratomalacia. These co-
morbidities tax already malnourished
children and may prolong hospital stays
initially for PEM and may increase the
likelihood of death.[16]

The general explanation of increased

infectious comorbidity in malnourished
people is that (1) the immune system is
what prevents such diseases from being
more widespread in healthy, well-
nourished people and (2) malnutrition
stresses and diminishes immune function.
In other words, malnutrition tends to cause
(mild or moderate) immunodeficiency,
eroding the barriers that normally keep
infectious diseases at bay. For example,
this reversal is well established regarding
the variable natural history of tuberculosis
in the pre–TB drug era. Epidemiologically,
there are also associations between
malnutrition and other health risks via the
common underlying factor of poverty. For
example, condoms can reduce spread of
HIV, but impoverished people often may
not have money to buy condoms or a
nearby place to buy them. Also, once a
poor person has any particular infection,
they may not have access to optimal
treatment of it, which allows it to get
worse, present more chances of
transmission, and so on. Even when a
developing country nominally/officially has
national health insurance with universal
health care, the poorest quarter of its
population may face a de facto reality of
poor health care access.
References
1. Franco, V.; Hotta, JK; Jorge, SM; Dos
Santos, JE (1999). "Plasma fatty
acids in children with grade III
protein–energy malnutrition in its
different clinical forms: Marasmus,
marasmic kwashiorkor, and
kwashiorkor". Journal of Tropical
Pediatrics. 45 (2): 71–5.
doi:10.1093/tropej/45.2.71 .
PMID 10341499 .
2. "Dietary Reference Intake: The
Essential Guide to Nutrient
Requirements" published by the
Institute of Medicine and available
online at
https://www.nap.edu/read/11537/ch
apter/14?term=protein-
energy+malnutrition#151
3. Muscaritoli, Maurizio; Molfino,
Alessio; Bollea, Maria Rosa; Fanelli,
Filippo Rossi (2009). "Malnutrition
and wasting in renal disease". Current
Opinion in Clinical Nutrition and
Metabolic Care. 12 (4): 378–83.
doi:10.1097/MCO.0b013e32832c7a
e1 . PMID 19474712 .
4. Bosaeus, Ingvar (2008). "Nutritional
support in multimodal therapy for
cancer cachexia". Supportive Care in
Cancer. 16 (5): 447–51.
doi:10.1007/s00520-007-0388-7 .
PMID 18196284 .
5. Liu, T; Howard, RM; Mancini, AJ;
Weston, WL; Paller, AS; Drolet, BA;
Esterly, NB; Levy, ML; et al. (2001).
"Kwashiorkor in the United States:
Fad diets, perceived and true milk
allergy, and nutritional ignorance".
Archives of Dermatology. 137 (5):
630–6. PMID 11346341 .
6. Portman OW, Neuringer M, Alexander
M (November 1987). "Effects of
maternal and long-term postnatal
protein malnutrition on brain size and
composition in rhesus monkeys" .
The Journal of Nutrition. 117 (11):
1844–51.
doi:10.1093/jn/117.11.1844 .
PMID 3681475 .
7. Hernández A, Burgos H, Mondaca M,
Barra R, Núñez H, Pérez H, Soto-
Moyano R, Sierralta W, Fernández V,
Olivares R, Valladares L (2008).
"Effect of prenatal protein
malnutrition on long-term
potentiation and BDNF protein
expression in the rat entorhinal cortex
after neocortical and hippocampal
tetanization" . Neural Plasticity. 2008:
1–9. doi:10.1155/2008/646919 .
PMC 2442167 . PMID 18604298 .
8. Bellinger L, Sculley DV, Langley-Evans
SC (May 2006). "Exposure to
undernutrition in fetal life determines
fat distribution, locomotor activity
and food intake in ageing rats" .
International Journal of Obesity. 30
(5): 729–38.
doi:10.1038/sj.ijo.0803205 .
PMC 1865484 . PMID 16404403 .
9. Sutton GM, Centanni AV, Butler AA
(April 2010). "Protein malnutrition
during pregnancy in C57BL/6J mice
results in offspring with altered
circadian physiology before obesity" .
Endocrinology. 151 (4): 1570–80.
doi:10.1210/en.2009-1133 .
PMC 2850243 . PMID 20160133 .
10. Rasmussen KM, Habicht JP
(February 2010). "Maternal
supplementation differentially affects
the mother and newborn" . The
Journal of Nutrition. 140 (2): 402–6.
doi:10.3945/jn.109.114488 .
PMID 20032480 .
11. Augustyniak RA, Singh K, Zeldes D,
Singh M, Rossi NF (May 2010).
"Maternal protein restriction leads to
hyperresponsiveness to stress and
salt-sensitive hypertension in male
offspring" . American Journal of
Physiology. Regulatory, Integrative
and Comparative Physiology. 298 (5):
R1375–82.
doi:10.1152/ajpregu.00848.2009 .
PMC 2867525 . PMID 20200128 .
12. Toledo FC, Perobelli JE, Pedrosa FP,
Anselmo-Franci JA, Kempinas WD
(2011). "In utero protein restriction
causes growth delay and alters
sperm parameters in adult male
rats" . Reproductive Biology and
Endocrinology. 9: 94.
doi:10.1186/1477-7827-9-94 .
PMC 3141647 . PMID 21702915 .
13. Slater-Jefferies JL, Lillycrop KA,
Townsend PA, Torrens C, Hoile SP,
Hanson MA, Burdge GC (August
2011). "Feeding a protein-restricted
diet during pregnancy induces altered
epigenetic regulation of peroxisomal
proliferator-activated receptor-α in the
heart of the offspring" . Journal of
Developmental Origins of Health and
Disease. 2 (4): 250–255.
doi:10.1017/S2040174410000425 .
PMC 3191520 . PMID 22003431 .
14. Toscano AE, Ferraz KM, Castro RM,
Canon F (2010). "Passive stiffness of
rat skeletal muscle undernourished
during fetal development" . Clinics
(São Paulo, Brazil). 65 (12): 1363–9.
doi:10.1590/s1807-
59322010001200022 .
PMC 3020350 . PMID 21340228 .
15. "Marasmus and Kwashiorkor" .
Medscape Reference. May 2009.
16. Ubesie, Agozie C.; Ibeziako, Ngozi S.;
Ndiokwelu, Chika I.; Uzoka, Chinyeaka
M.; Nwafor, Chinelo A. (2012-01-01).
"Under-five Protein Energy
Malnutrition Admitted at the
University of In Nigeria Teaching
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retrospective review" . Nutrition
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2891-11-43 . ISSN 1475-2891 .
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Further reading
 Bistrian, Bruce R.; McCowen, Karen C.; Chan,
Samuel (1999). "Protein–energy malnutrition
in dialysis patients". American Journal of
Kidney Diseases. 33 (1): 172–5.
doi:10.1016/S0272-6386(99)70278-7 .
PMID 9915286 .
Protein–Energy Undernutrition at Merck
Manual of Diagnosis and Therapy
Professional Edition

External links
Classification ICD-10: E40 -E44 • D

ICD-9-CM: 260 -
263 •

MeSH: D011502

External resources eMedicine: derm/797

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