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The Cognitive Effects of Malnutrition



Malnutrition affects physical growth, cognitive development, and physical work capacity, and it consequently influences human performance and Heath.
Citation: Mohamed EL Hioui. The Cognitive Effects of Malnutrition. Clin
Neuro Neurological Res Int J 2019, 2(2): 180015.
Copyright © 2019 Mohamed EL Hioui.
Clinical Neuroscience & Neurological Research
International Journal
Volume 2; Issue 2
The Cognitive Effects of Malnutrition
Mohamed EL Hioui*
Department of Biology, Ibn Tofail University, Morocco
*Corresponding author: Dr. Mohamed EL Hioui, Unit for Clinic and Cognitive Neuroscience and Health, Laboratory of
Biology and Health, Department of Biology, Faculty of Sciences, Ibn Tofail University, Kenitra, Morocco, Email:
Received Date: November 26, 2019; Published Date: December 06, 2019
Malnutrition is associated with both structural and
functional pathology of the brain. Structurally
malnutrition results in tissue damage, growth retardation,
disorderly differentiation, reduction in synapses and
synaptic neurotransmitters, delayed myelination and
reduced overall development of dendritic arborization of
the developing brain. There are deviations in the temporal
sequences of brain maturation, which in turn disturb the
formation of neuronal circuits. The brain is vulnerable to
the effects of insults during critical periods of brain
development from the second trimester of pregnancy
until 2 years of age. Indeed, malnutrition experienced at
these ages will have lifelong consequences that are not
reversed by adequate nutrition. Long term effects of
prenatal, postnatal and childhood malnutrition have been
reported even after a long period of recovery from the
illness itself. In addition, malnutrition, a consequence of
various factors, is often related to poor quality of food,
insufficient food intake, and severe and repeated
infectious diseases, or, frequently, combinations of the
three. The major outcomes of malnutrition during
childhood may be classified in terms of morbidity,
mortality and psychological and intellectual development
with important consequences in adult life [1-7].
Malnutrition and Brain Function
Chronic malnutrition affects the growth and maturation of
the brain. The stages of development are numerous and
complex: neural cells must proliferate, migrate to the
right place, establish the right connections, form the right
receptors for neurotransmitters and be well covered with
myelin, a protective substance essential to the proper
transfer of nerve messages. This meticulous assembly of
neural cells is vulnerable to environmental stressors,
including of course, malnutrition [8]. Later, between early
childhood and adolescence, an acute episode of famine
can affect cognition and behavior, but these are more
likely to recover once the child is well fed. It must be
remembered, however, that it is not only a matter of
weight and head circumference. You can have a child with
normal measurements who also has neurocognitive
deficits. Evidences from human and animal studies
indicate that neurocognitive development is influenced by
various environmental factors including nutrition. It has
been established that nutrition affects the brain
throughout life. However, the mechanisms through which
nutrition modulates mental health are still not well
understood. It has been suggested that the deficiencies of
both vitamin B12 and omega-3 fatty acids can have
adverse effects on cognition and synaptic plasticity.
Studies indicate a need for supplementation of vitamin
B12 and omega-3 fatty acids to reduce the risk of
cognitive decline, although the results of intervention
trials using these nutrients in isolation are inconclusive
Brain development continues after birth, where migration
and cellular proliferation takes place. It has been
observed that protein deficiency reduces the thickness of
the visual cortex, parietal neocortex, dentate gyrus, CA3
and cerebellum [10-12]. Moreover, Plagemann et al.
Clinical Neuroscience & Neurological Research International Journal
determined that the Ventromedial Hypothalamic Nucleus
of hypothalamus increased its size while the
Paraventricular Hypothalamic Nucleus is reduced after
malnutrition, demonstrating that perturbations during
development may change the brain organization [13]. The
consequence of malnutrition on brain anatomy, through
changes on brain connectivity, might be the cause of
behavioral deficits observed in malnourished people.
Malnutrition and Neuropsychological
Cognitive deficits caused by malnutrition are manifested
by memory difficulties, intellectual slowness or specific
learning disabilities in reading, writing or mathematics.
The child may have behavioral problems such as attention
deficit hyperactivity disorder, emotional regulation or
socialization difficulties [14]. In extreme cases, there will
be mental retardation. It is estimated that the "survivors"
of malnutrition have on average a deficit of 5-15 points in
standard intelligence tests compared to well-nourished
children living in the same environment [15]. The degree
of cognitive impairment is proportional to the severity of
In a study of children in the Kenitra city of Morocco who
suffered from moderate to severe malnutrition in their
first year, attention deficit disorder with or without
hyperactivity, lower intelligence quotients, more
disorders were observed of learning, which ultimately led
to more failures in national school exams [14] . These
effects persisted over time, at least until adolescence. In a
study about children in the Cleveland, demonstrates that
children with signs of poor nutrition as measured by
growth also have associated high rates of developmental
delays. In addition, these children have early signs of
cognitive deficits. Longitudinally, these children were able
to show motor and cognitive gains toward the normal
range with improvements in their nutritional status.
While maximizing nutrition after periods of under-
nutrition is crucial to support cognitive recovery,
ensuring adequate and consistent nutrition for vulnerable
children with developing minds to prevent cognitive
injury is paramount [16]. The neuropsychological
interpretation of the cognitive processes more severely
affected in malnourished children suggests a diffuse
cortical involvement. This is with reference to deficits
pertaining to functions mediated by dorsolateral
prefrontal cortex (poor performance on tests of attention,
fluency and working memory), right parietal (poor
performance on tests of visuospatial functions) and
bilateral temporal cortex (poor performance on tests of
comprehension, verbal learning, and memory for verbal
and visual material). The prefrontal cortex may be
particularly vulnerable to malnutrition [17].
This review of the literature shows that malnutrition
remains important to local and regional worldwide.
Malnutrition results in cognitive impairments as well as
slowing in the rate of the development of cognitive
processes. The biochemical and physiological mechanisms
underlying often malnutrition connecting a neuron-
impaired cognitive function are clear.
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Clinical Neuroscience & Neurological Research International Journal
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Full-text available
The prevalence of psychiatric disorders which are characterized by cognitive decline is increasing at an alarming rate and account for a significant proportion of the global disease burden. Evidences from human and animal studies indicate that neurocognitive development is influenced by various environmental factors including nutrition. It has been established that nutrition affects the brain throughout life. However, the mechanisms through which nutrition modulates mental health are still not well understood. It has been suggested that the deficiencies of both vitamin B 12 and omega-3 fatty acids can have adverse effects on cognition and synaptic plasticity. Studies indicate a need for supplementation of vitamin B 12 and omega-3 fatty acids to reduce the risk of cognitive decline, although the results of intervention trials using these nutrients in isolation are inconclusive. In the present article, we provide an overview of vitamin B 12 and omega-3 fatty acids, the possible mechanisms and the evidences through which vitamin B 12 and omega-3 fatty acids modulate mental health and cognition. Understanding the role of vitamin B 12 and omega-3 fatty acids on brain functioning may provide important clues to prevent early cognitive deficits and later neurobehavioral disorders.
Full-text available
Malnutrition is one of the major factors affecting brain development. In particular, protein malnutrition can result in abnormal development with behavioral consequences. Protein malnutrition reduces brain size, dendritic arborization and cell maturation. In addition, perinatal low protein diet produces changes on neurotransmitters and oxidative status of the brain. As a consequence, failure in normal development produces social and behavioral disabilities that persist during the adult life. The duration and point of onset of dietary restriction is important to comprehend the detrimental effects of low protein diet on brain function. Although during last decades a lot of effort has been done to understand the long lasting effects of perinatal malnutrition, several questions are still unsolved. The present review is focused on neuroanatomical, neurochemical and functional changes observed in rodent models of perinatal malnutrition as well as the future directions of the field.
Full-text available
Maternal malnutrition affects every aspect of fetal development. The present study asked the question whether a low-protein diet of the mother could result in motor deficits in the offspring. Further, to examine whether cerebellar pathology was correlated with motor deficits, several parameters of the postnatal development of the cerebellum were assayed. This is especially important because the development of the cerebellum is unique in that the time scale of development is protracted compared with that of the cortex or hippocampus. The most important result of the study is that animals born to protein-deficient mothers showed significant delays in motor development as assessed by rotarod and gait analysis. These animals also showed reduced cell proliferation and reduced thickness in the external granular layer. There was a reduction in the number of calbindin-positive Purkinje cells (PC) and granular cells in the internal granular layer. However, glial fibrillary acidic protein-positive population including Bergmann glia remained unaffected. We therefore conclude that the development of the granular cell layer and the PC is specifically prone to the effects of protein malnutrition potentially due to their protracted developmental period from approximately embryonic day 11 to 13 until about the third postnatal week.
Full-text available
Malnutrition is associated with both structural and functional pathology of the brain. A wide range of cognitive deficits has been reported in malnourished children. Effect of chronic protein energy malnutrition (PEM) causing stunting and wasting in children could also affect the ongoing development of higher cognitive processes during childhood (>5 years of age). The present study examined the effect of stunted growth on the rate of development of cognitive processes using neuropsychological measures. Twenty children identified as malnourished and twenty as adequately nourished in the age groups of 5-7 years and 8-10 years were examined. NIMHANS neuropsychological battery for children sensitive to the effects of brain dysfunction and age related improvement was employed. The battery consisted of tests of motor speed, attention, visuospatial ability, executive functions, comprehension and learning and memory Development of cognitive processes appeared to be governed by both age and nutritional status. Malnourished children performed poor on tests of attention, working memory, learning and memory and visuospatial ability except on the test of motor speed and coordination. Age related improvement was not observed on tests of design fluency, working memory, visual construction, learning and memory in malnourished children. However, age related improvement was observed on tests of attention, visual perception, and verbal comprehension in malnourished children even though the performance was deficient as compared to the performance level of adequately nourished children. Chronic protein energy malnutrition (stunting) affects the ongoing development of higher cognitive processes during childhood years rather than merely showing a generalized cognitive impairment. Stunting could result in slowing in the age related improvement in certain and not all higher order cognitive processes and may also result in long lasting cognitive impairments.
Full-text available
Internationally adopted children often arrive from institutional settings where they have experienced medical, nutritional and psychosocial deprivation. This study uses a validated research assessment tool to prospectively assess the impact of baseline (immediately post adoption) nutritional status on fifty-eight children as measured by weight-for-age, height-for-age, weight-for-height and head circumference-for-age z scores, as a determinant of cognitive (MDI) and psychomotor development (PDI) scores longitudinally. A statistical model was developed to allow for different ages at time of initial assessment as well as variable intervals between follow up visits. The study results show that both acute and chronic measures of malnutrition significantly affect baseline developmental status as well as the rate of improvement in both MDI and PDI scores. This study contributes to the body of literature with its prospective nature, unique statistical model for longitudinal evaluation, and use of a validated assessment tool to assess outcomes.
Some effects of undernutrition were noted in the brains of 21-day-old rat pups undernourished from birth by being reared by nursing dams fed on a low protein diet. As compared to the normally fed control pups, the body weight, brain weight, and thickness of the parietal neocortex and paravermal cerebellar cortex were significantly lower in the undernourished pups (p < 0.001), while the thickness of the cortices of the dentate gyrus and hippocampus CA3 only reached significance at the 5% level. Again, as compared to the control pups, the number of spines per unit length on the distal dendritic segments of the pyramidal cells of lamina III of the parietal neocortex and of the hippocampus CA3 reached significance at the 5% level whereas that of the granule cells of dentate gyrus and Purkinje cells of the paravermis did not reach significance at the 5% level. The myelination of the pyramidal tract and spinal trigeminal tract in the lower medulla was less advanced in the undernourished pups.To date, the demonstration of precise functional correlates for the observed changes of morphological and physiological parameters in animals subjected to undernutrition has been elusive. An approach that may lead to unraveling this problem is suggested in a discussion of relating sources of input to the specific dendritic segments where the spine counts were made.
The current and long-term effects of famine and malnutrition on cognitive and behavioral development are reviewed. The brain is vulnerable to the effects of insults during critical periods of brain development from the second trimester of pregnancy until 2 years of age. Malnutrition experienced at these ages will have lifelong consequences that are not reversed by adequate nutrition. Long-term effects of prenatal, postnatal and childhood malnutrition have been reported even after a long period of recovery from the illness itself. We summarize results of our longitudinal study in Barbados in which we followed individuals, now 28–34 years of age, who experienced moderate to severe malnutrition during their first year of life and a healthy comparison group from the same classrooms. Our studies showed that malnutrition had a negative impact on cognitive and behavioral functioning throughout childhood and adolescence, even after controlling for socioeconomic conditions and other factors in the home environment. The most striking finding in our series of studies was a fourfold increase from 15% to 60% in the frequency of attention deficit disorder following infantile malnutrition. Attention deficits persisted at least through adolescence and was closely associated with poor performance on a national high school examination at 11 years of age. We conclude that, under conditions of famine, it is important to include early and comprehensive interventions to reverse not only medical conditions resulting from malnutrition, but also cognitive and behavioral deficits arising from famine. In the absence of appropriate interventions, compromised behavioral function may continue long beyond the episode, may impact on the quality of life over the long-term of survivors, and increase costs to society.
The effect of protein deprivation on rapid Golgi impregnated pyramidal neurons in layers II/III and V of the rat visual cortex was studied at 30, 90, and 220 days of age using morphometric methods. In order to mimic human under-nutrition female rats were adapted to either an 8% or control 25% casein diet 5 weeks prior to conception and maintained on these diets during gestation and lactation. The pups were then weaned and maintained on their respective diets. The undernourished rats showed a significant decrease in brain weight only at 90 days, indicating that the protein deprivation had a mild effect on brain development. Correspondingly, the number of significant histological differences between the two diet groups were least at 30 and 220 days of age. The effect of the diet was greater on layer V than on layer II/III pyramids. At 30 days of age the effect of the diet was different on the pyramids of these two cell layers, at 90 days there was a mixture of similar and dissimilar effects, and at 220 days the pyramids of these two cell layers showed only minor differences between the two diet groups. Analysis of age-related changes indicated that the effect of the diet was different on layer II/III pyramids compared to layer V pyramidal cells. These different effects apparently accounted for the progression from a dissimilar effect of the diet at 30 days on the pyramids of the two cell layers to only minor differences between them at 220 days. Further analysis of these age-related changes shows that two prominent effects of protein deprivation are for age-related changes to occur in undernourished rats but not in controls and for age-related changes to be out-of-phase with each other in the two diet groups. From these findings, and a review of similar studies in the literature, we propose that these mechanisms are a prominent effect of undernutrition in the post-weaning period and help account for the unexpected increases in morphometric measurements noted in undernourished rats in this and other studies.
It is generally recognized that low birth weight can be caused by many factors. Because many questions remain, however, about which factors exert independent causal effects, as well as magnitude of these effects, a critical assessment and meta-analysis of the English and French language medical literature published from 1970 to 1984 were carried out. The assessment was restricted to singleton pregnacies of women who lived at sea level and who had no chronic illnesses. Extremely rare factors were also excluded, as were complications of pregnancy. In this way, 43 potential determinants were identified. A set of a priori methodological standards were established for each potential determinant. Studies that satisfactorily met (SM) or partially met (PM) these standards were used to assess the existence and magnitude of an independent causal effect on birth weight, gestational age, prematurity, and intrauterine growth retardation (IUGR). A total of 921 relevant publications were identified, of whihc 895 were successfully located and reviewed. Factors with well-established direct causal impacts on intrauterine growth include infant sex, racial/ethnic origin, maternal height, pre-pregnancy weight, paternal weight and height, maternal birth weight, parity, history or prior low-birth-weight infants, gestational weight gain and caloric intake, general morbidity and episodic illness, malaria, cigarette smoking, alcohol consumption, and tobacco chewing. In developing countries, the major determinants of IUGR are Black or Indian racial origin, poor gestational nutrition, low pre-pregnancy weight, short maternal stature, and malaria. In developed countries, the most important single factor, by far, is cigarette smoking, followed by poor gestational nutrition and low pre-pregnancy weight. For gestational duration, only pre-pregnancy weight, prior history of premature or spontaneous abortion, in utero exposure to diethylstilbestrol, and cigarette smoking have well-established causal effects, and the majority of prematurity occurring in both developing and developed country settings remains unexplained. Modifiable factors with large effects on intrauterine growth or gestational duration should be targeted for public health intervention in the two settings, with an emphasis on IUGR in developing countries and prematurity in developed countries. Future research should focus on factors of potential quantitative importance for which data are either unavailable or inconclusive. In developing countries, the most important of these for intrauterine growth are caloric expenditure (maternal work), antenatal care, and certain vitamins and trace elements. For prematurity, especially in developed countries, factors deserving further study include genital tract infection, antenatal care, maternal employment and physical activity, and stress and anxiety.