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Plant-based Foods and their Implications in Brain Health
18.10.2 protein CluSterS aSSoCiated with neurodegenerative ConditionS are
effeCtively addreSSed by nutraCeutiCalS
lesions, while in PD, it is Lewy complexes. Proteins that have undergone aberrant mutations and
and malfunction of the proteolytic cascades. In an attempt to reduce the neurological impairment
oligomeric complexes [54, 55]. Peptides having 40– 42 amino acids that are amyloidogenic
nobiletin), and galangin, can hinder BACE1 enzyme and ameliorate behavioural impairment in
mouse models of AD [56, 57
icariin, EGCG, rutin, curcumin, and luteolin. Myricetin, rosmarinic acid, and curcumin reduced
58, 59]. The presynaptic
-
cially in PD. The occurrence of oxidative exposure, point mutations (E46K/ A53T/ A30P), metal
cation (Cu
2+
and Fe
3+
), autophosphorylation, and association with lipid matrix all contribute to the
acid, and kaempferol [60, 61
thinner, non- toxic, and unstructured clusters [62].
18.10.3 nutraCeutiCalS mediated upregulation of neurotrophiC faCtorS (nftS) and
neurotrophiC reCeptorS
In healthy human subjects, rodents, and biological prototypes, polyphenolic nutraceuticals have been
proven to augment glial cell- lined derived neurotrophic factor (GDNF) and brain- derived neuro-
Ginkgo biloba therapy
has been demonstrated to improve BDNF levels and cardiopulmonary endurance in healthy and
active males [62]. Flavonoids (like phytometabolites naringenin, hesperidin, and EGCG), piperine
(an alkaloid obtained from Piper nigrum), astaxanthin, resveratrol, and curcumin enhanced BDNF
content in rodent paradigms of ageing, depression, AD, brain ischaemia, ageing, PD, and depres-
sion. Catalpol (iridoid glucoside), harpagoside (terpene glycoside), naringenin, and smilagenin
(steroidal sapogenin) all improved GDNF activity in PD mouse models [63]. Tropomyosin receptor
kinase (Trk) activity and neuroplasticity are enhanced by polyphenolic nutraceuticals, indicating
neuroprotective effects. In experimental models of depression, olive polyphenols upregulated TrkA
of antidepressants [64]. In a rat paradigm of depression, nobiletin (derived from citrus fruits) and
deoxygedunin (derived from Azadirachta indica) stimulated hippocampal neuroplasticity. They also
improved BDNF and TrkB activity in mice models of depression [65].
18.11 CONCLUSION
Nature has endowed mankind with phenomenal pharmacological compounds that have a great
commitment to the treatment and management of lifestyle- induced and life- threatening conditions such
as neurodegeneration. Multiple investigations have explicitly documented how bioactive components
help to mitigate neurodegeneration and avert cognitive impairment. Nutraceutical’s therapeutic
355
Nutraceuticals in Brain Health
restorative functionality, which targeted multiple mediators and channels to increase protein expres-
sion, resulting in neuroprotection. Protein assembly and destruction can be suppressed, resulting
in a powerful neurological network. In this period of several catastrophes confronting the public
therapy of neurological conditions. A modern lifestyle has impaired the body’s defence system
against reactive oxygen radicals by inhibiting antioxidants, leading to excessive oxidative damage.
Age- related declines in antioxidant content in the body make people more vulnerable to long-
term medical problems. As an outcome, for many years the attention has been on focusing on a
range of nutraceuticals for their pharmacological effects. Vitamins and other substances with anti-
oxidative activity work by arresting free radicals and promoting the body’s endogenous production
of antioxidants. The present investigation emphasized the effectiveness of nutraceutical treatment to
stop neurological conditions from advancing. They are the greatest choices for addressing lifestyle-
mediated psychological disorders like depression and neurological disorders since utilizing them in
appropriate and approved doses fosters excellent brain functioning and prevents diseases.
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DOI: 10.1201/9781003300502-19
19
Impact of Prenatal Diet on the
Developing Brain of the Fetus
Kunal Bhattacharya*, Biswajit Devanath, Surender Prasad,
Tasrina Rahman, and Nongmaithem Randhoni Chanu
*Corresponding author
19.1 INTRODUCTION
Diet impacts the fetus’s and the woman’s brain health throughout gestation and the future in life.
It is, therefore, very important to study the food routine of pregnant women. The concept that
mothers’ food patterns may affect children’s ability to function psychologically in the future has
major consequences for public health practice and policy development, for our understanding of
human physiology, for the creation of food products, and for the advancement of the economy
(1
to maximize their child’s cognitive and behavioural results. The present evidence has proposed a
relationship between food and brain health in the growing fetus (2). For growth and development,
the offspring and breastfed child entirely rely on the mother’s food and nutrition. In particular, the
play in programming the fetal brain’s development and subsequent mental processes, the fetus is
extremely susceptible to dietary and nutritional changes during pregnancy (3). Numerous questions
remain unanswered despite the extensive study on the positive effects of adequate nutrition during
pregnancy over the past decades, including the most susceptible times of gestation, the effects of
particular foods and nutrients, and the levels of foods and nutrients needed to improve cognitive
is an impact on a child’s growing brain over the long run (4).
Two of the most frequently studied aspects of fetal programming of neurodevelopment are the
mother’s diet and nutrition during pregnancy. Enough energy, protein, essential fatty acids, and a
number of crucial micronutrients are required during fetal growth to provide the required substrates
for producing fetal neurons within the nervous system and as co- factors in physiochemical processes
that control normal brain development (5). Extreme cases of inadequate nutrition during gesta-
tion, such as those that occurred during starvation, have provided light on the consequences on
brain development throughout time. For instance, it was discovered that the cognitive abilities of
neurodevelopmental outcomes from certain nutritional problems or dietary abnormalities may
also include neural tube defects, language delays, decreased cognitive capacities, and mental and
neurodevelopmental diseases (6).
Around the world, people are becoming more and more concerned about children’s cognitive
development and the aggravation of mental health issues. According to estimates, 35% of chil-
dren in Europe have abnormal cognitive development and mental problems like anxiety, mood,
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Impact of Prenatal Diet on the Developing Brain of the Fetus
impact on society. Understanding the causes and effects of mental diseases and applying this infor-
mation to policies and preventive initiatives is more important than ever because they account for
8.1% of the worldwide disease burden. Studies on both humans and experimental animals show
how important food and nutrition are for neurodevelopment (1). The determent and treatment of
psychological health issues may be more affordable if an improved diet is provided, particularly in
connection to nutrients like iron, zinc, and fatty acids. In healthy children, there is emerging proof
that early nutrition and diet might affect later cognitive behaviour and development (2).
Due to its extended period of development and specialization, the brain is extremely susceptible
to misprogramming. The effects of early brain misprogramming will have an impact not only on
the form and function of the brain but also on other physiological functions. For instance, the brain
-
bolic step necessary for development and growth (1). The effects of a shortfall in a particular food
how long it persists (7).
Due to contemporary non- invasive and computational tools and animal models, fetal brain devel-
opment has grown in importance over the past twenty years and is now a crucial area of study in
for the composition and development of individual nerve cells and entire networks within par-
ticular brain areas, as well as for relating the structures to the functions and effect on brain health
to complications at both the particular neuron and network levels in fetuses and later- developing
children (8). Novel phenotypes are expressed as a result of gene expression variation, which has
consequences for understanding evolution and disease risk (9). During embryonic and fetal life,
subtle brain structure and function changes can progressively and considerably be exaggerated over
time. This causes lasting effects on brain anatomy and physiology (10). Lack of nutrition causes the
placental Peg3 gene to be inactive, which alters 56% of the coexpressed genes in the placenta and
hypothalamus. This has an impact on embryonic development during gestation (11).
19.2 BRAIN DEVELOPMENT STAGES AND NUTRITIONAL REQUIREMENTS
DURING PREGNANCY
The intrauterine environment can profoundly impact the fetal brain’s development. To reach its full
genetic potential, the fetus must grow in an optimal intrauterine environment free from the harmful
effects of illnesses and poisonous substances. It also needs to receive adequate oxygen and nutrients
(12). Our roughly 40 weeks within the uterus determine our life extremely outside of it. There is
now strong evidence that many neurological conditions that manifest after birth have their roots in
fetal development. For instance, epidemiological studies have demonstrated that prenatal rather than
perinatal or postnatal factors account for most cerebral palsy cases. It is believed that neurological
issues have their origins in utero because minimal cerebral brain dysfunction, which is frequently
-
nitive impairments in childhood (13). Based on histology and neurochemical research, it has been
hypothesized that prenatal injury creates a susceptibility in the growing brain, leading someone
with risks such as genetic inheritance to have symptoms of schizophrenia in adolescence or early
adulthood. Autism and epilepsy may also be partially caused by neurodevelopmental issues (14).
Over the past few decades, tremendous progress has been made in our knowledge of the intricate
series of mechanisms that result in the formation of the entire nervous system from a specialized
layer of cells just on the dorsal side of the embryo (15). Different parts of the brain develop at
-
the type of neuronal injury, its impact on the person’s postnatal function, and the manifestation of
16).
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Plant-based Foods and their Implications in Brain Health
The three prenatal phases of brain development line up with the three trimesters of pregnancy.
The neural tube grows in the initial trimester of pregnancy. In the second trimester, the brain grows
to its full capacity. For the latter three trimesters of pregnancy, the fetus’s brain contains the same
number of neurons as an adult brain (17).
The essential stages are:
1. Massive growth of immature brain cells.
2. The movement of the cells in the brain toward a target area and the start of their differentiation
into the type of cell best suited to that area.
3. Comparable cell types gathering into discrete locations.
4. Many connections are formed between neurons, both within and between regions.
5. Competition among these connections causes many to be selectively eliminated, with the roughly
events do not take place in a strict order but rather overlap in time. No new neurons are added
after the age of about 18 months, and the division of different cell types into separate regions is
-
cial step in determining the structure of the mature brain goes on for years (18).
The number of brain cells in the cerebral cortex increases between 15 and 20 weeks after conception
the seventh month, which may be heard via the mother’s abdomen. Although it remains essential
until birth and for some months following, several lines of evidence indicate that good nutrition is
most vital for the development of the brain at this point (19).
There are ten stages in the development of the fetal brain:
1. The creation of the neural preplate and the genesis of the neuroectoderm from the ectoderm.
2. The neural plate is created by the preplate splitting.
3. The neural plate’s sides rise up and fold inward to form an arch and a neural tube.
4. The development of neuroepithelium produces juvenile nerve cells called neuroblasts. Neuroblasts
migrate, sprout leading appendages, and then assemble in certain, genetically predetermined
sites, starting with the area that will eventually become the brainstem and spinal cord.
5. The separation of the neuroepithelium into the subventricular and ventricular zones results in
distinct waves of mobile neuroblasts.
6. The neural tube bends, twists, and ascends as a result of ongoing neuroblast production and
neuron multiplication, resulting in the formation of three cerebral vesicles initially, followed by
another two (medulla, pons, midbrain, diencephalon, telencephalon).
7. The gathering, differentiating, and division of neurons that eventually give rise to the limbic
system, striatum, layers I and VII (VIa and VIb), and the nuclei of the medulla, pons, midbrain,
and hypothalamus.
8. The development of neocortical layers II through VI as a series of neuroblastic waves produces
columns and layers while squeezing between neocortical layers I and VII (VIa and VIb).
9. Dendritic growth, synaptic development, myelination, and neuronal differentiation of active
brainstem axons that have made dendritic synaptic connections.
10. The medulla, the pons, the midbrain, the diencephalon, the forebrain, and the neocortex all
develop functionally after that (20).
19.3 THE BRAINSTEM
reached their target locations and formed their synaptic connections, and the medulla and pons have
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Impact of Prenatal Diet on the Developing Brain of the Fetus
nearly completed their cycle of myelination. Because the brainstem continues to develop well after
21).
19.4 THE DEVELOPMENT OF THE MEDULLA
The medulla, pons, and midbrain make up the brainstem, which matures in a caudal- to- rostral arc
result, the medulla’s nuclei typically arise and myelinate before the pons’, which in turn emerge and
myelinate before the midbrain. As previously mentioned, the fetus and newborn exhibit this pattern
of functional development in behavioural terms (21).
The principal medulla structures are created by the seventh to eighth week of gestation, three
system along with the glossopharyngeal, hypoglossal, spinal accessory, and vagus cranial nuclei
(22). As previously mentioned, these nuclei and activation pathways promote arousal, generalized
body movements, head movement, shoulder elevation, heart rate, and respiration.
Around the eighth week of pregnancy, the pons starts to appear following the medulla as the
brainstem develops in a caudal to the rostral manner (23). The pons takes longer than the medulla to
mature and myelinate, and it does not reach advanced stages of development until about the seventh
month of pregnancy. Therefore, many of the pons- related functions arise later in fetal development,
around the seventh month of pregnancy. Similar to the medulla, some functions emerge earlier than
others and in an erroneous or incomplete manner (24).
19.5 THE DEVELOPMENT OF THE MIDBRAIN
Superior visual colliculus development starts during the eighth week of pregnancy, following the
caudal- to- rostral pattern of brainstem maturation that is also typical of the midbrain. The inferior-
auditory colliculus starts its cycle of maturation around the sixth week of gestation (20). The
superior colliculus establishes itself several weeks after the lower colliculus; therefore, the develop-
ment cycle is highly drawn out. However, the inferior colliculus does not fully develop until the 17th
week. Furthermore, myelination and midbrain development do not reach their peak until soon after
birth. The superior colliculus responds to and orients to visual inputs, whereas the inferior colliculus
involve turning the head and initiating eye movements when they are activated (25). As a result, the
fetus’s midbrain matures, making it more sensitive to sound. If adequately stimulated or intensely
But when a baby is overstimulated, the brainstem normally reacts by dozing off and causing rapid
(lateral) eye movements (REM). It is hypothesized that the late- term fetus will display REM and
comparable arousal- induced sleep behaviours (26).
19.6 ROLE OF THYROID HORMONE IN FETAL BRAIN DEVELOPMENT
To achieve optimal neurodevelopment, appropriate fetal concentrations of thyroid hormone must
before the start of fetal thyroid function, especially by six weeks of pregnancy and in quantities that
27). T3 levels, however, are essentially
in much higher concentrations in the human fetal brain as early as nine weeks of pregnancy than
iodothyronine deiodinase produces this iodothyronine locally from T4 (28). In addition, studies
demonstrate that by eight weeks of pregnancy, nuclear thyroid hormone receptors are produced in