Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5264_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Foreword
- •Preface
- •Editors’ Bio
- •1.1 Introduction
- •1.2 Nervous System Development
- •1.2.1 Spinal Cord Development
- •1.3 Touch and Pain
- •1.5 Artificial Brain and Neural Networks
- •1.5.1 Neural Networks
- •1.5.1.1 Biological Neural Networks
- •1.5.2 Artificial Intelligence (AI)
- •1.6 Neurodegenerative Diseases
- •1.7 Drugs for Brain Disorders
- •1.8 Conclusion
- •References
- •2.1 Introduction
- •1.4 Memory and Learning
- •1.4.1 Types of Memory
- •2.2 Herbs Exhibiting Neuroprotective Properties
- •2.2.1 Ginkgo Biloba L.
- •2.2.2 Panax Ginseng
- •2.2.3 Bacopa Monnieri
- •2.2.4 Terminalia Chebula
- •2.2.5 Convolvulus Pluricaulis
- •2.3.1 Polyphenols
- •2.3.1.1 Flavonoids
- •2.3.1.2 Phenolic Acid
- •2.3.1.3 Tannins
- •2.3.2 Vitamins
- •2.3.3 Alkaloids
- •2.4 Conclusion
- •References
- •3.1 Introduction
- •3.2 Etymology of MANA
- •3.2.1 Manovaha Srotas Kritya
- •3.2.3 Centres Located in Manas
- •3.3 Structural Qualities of Manas
- •3.4 Sensual Perception
- •3.4.2 Qualities of Mana
- •3.4.3 English Equivalent of Component & Functions
- •3.4.4 Characters of an Individual Derived in the Fetus From Manas
- •3.7.3 Ahiphena (Papaver Somniferum)
- •3.7.8 Tagara (Valeriana Wallichii)
- •3.7.11 Common Useful Herbs-Mineral Yogas of Psychotropic Drugs
- •3.8 Conclusion
- •References
- •4.1 Introduction
- •4.5.1 Cell Line Studies
- •4.5.2 Animal Model Studies
- •4.5.3 Human Clinical Trials
- •4.7 Further Considerations
- •4.7.1 Food-Drug and Drug-Drug Interactions
- •4.8 Concluding Remarks
- •References
- •5.1 Introduction
- •5.2 Herbal Medicines in Health and Disease
- •5.4 Plants and Herbs With Nootropic Abilities
- •5.5 Plant Bioactive Compounds With Nootropic Activities
- •5.5 Conclusion
- •Terms and Abbreviations
- •References
- •6.1 Introduction
- •6.2 Therapeutic Potential of Indian Traditional Plants
- •6.2.1 Bacopa Monnnieri (L.) Pennell (Family: Plantaginaceae)
- •6.2.1.1 Neuroprotection in Alzheimer’s Disease
- •6.2.1.2 Neuroprotection in Parkinson’s Disease
- •6.2.2 Centella Asiatica (L.) Urban (Family: Apiaceae)
- •6.2.2.1 Neuroprotection in Alzheimer’s Disease
- •6.2.2.2 Neuroprotection in Parkinson’s Disease
- •6.2.3 Curcuma Longa L. (Family: Zingiberaceae)
- •6.2.3.1 Neuroprotection in Alzheimer’s Disease
- •6.2.3.2 Neuroprotection in Parkinson’s Disease
- •6.2.4 Withania Somnifera (L.) Dunal. (Family: Solanaceae)
- •6.2.4.1 Neuroprotection in Alzheimer’s Disease
- •6.2.4.2 Neuroprotection in Parkinson’s Disease
- •6.2.5 Nardostachys Jatamansi (D. Don) DC. (Family: Caprifoliaceae)
- •6.2.5.1 Neuroprotection in Alzheimer’s Disease
- •6.2.5.2 Neuroprotection in Parkinson’s Disease
- •6.3 Conclusion
- •References
- •7.1 Introduction
- •7.2 Hippocampus
- •7.3 Acetylcholine
- •7.4 Dementia
- •7.5 Nootropics
- •7.5.1 Natural Nootropics
- •7.5.2 Allium Sativum (Family: Amaryllidaceae)
- •7.5.3 Asparagus Racemosus (Family: Asparagaceae)
- •7.5.4 Benincasa Hispida (Family: Cucurbitaceae)
- •7.5.5 Clitoria Ternatea (Family: Fabaceae)
- •7.5.6 Cyperus Rotundus (Family: Cyperaceae)
- •7.5.7 Embelia Ribes (Family: Primulaceae)
- •7.5.8 Huperzia Serrata (Family: Lycopodiaceae)
- •7.5.9 Marsilea Minuta (Family: Marsileaceae)
- •7.5.10 Piper Betel (Family: Piperaceae)
- •7.5.11 Polygala Tenuifolia (Family: Polygalaceae)
- •7.5.13 Vitis Vinifera (Family: Vitaceae)
- •7.6 Conclusion
- •References
- •8.1 Introduction
- •8.2 Amyloidoses
- •8.3 Prion Diseases
- •8.4 Tauopathies
- •8.5 Alzheimer’s Disease
- •8.6 Chronic Traumatic Encephalopathy (CTE)
- •8.7 Progressive Supranuclear Palsy (PSP)
- •8.8 Cortico-Basal Degeneration (CBD)
- •8.9 Synucleinopathies
- •8.10 TDP-43 (Proteinopathies)
- •8.11 Approved Therapies
- •8.12 Marine Natural Products
- •8.13 Conclusion
- •References
- •9.1 Introduction
- •9.2 Phytoconstituents of Walnut
- •9.2.1 Amino Acids
- •9.2.2 Dietary Fibre and Phytosterols
- •9.2.3 Minerals and Vitamins
- •9.2.4 Vitamin E
- •9.2.5 Vitamin B6
- •9.2.6 Vitamin B9
- •9.2.7 Minerals
- •9.3 Therapeutic Benefits of Brain Food
- •9.3.1 Cognitive Benefit
- •9.3.2 Ageing and Metabolic Effects On Brain Health
- •9.5.1 Animal Studies
- •9.5.2 Clinical Trials in Humans
- •9.6 Conclusion
- •References
- •10.1 Introduction
- •10.2 Brief Attention On NDDs
- •10.2.1 Alzheimer’s Disease (AD)
- •10.2.2 Parkinson’s Disease (PD)
- •10.2.2.2 Neuropsychiatric Disorders
- •10.3 Conclusion and Outlook
- •References
- •11.1 Introduction
- •11.2 Polyphenolsstructure and Classification
- •11.3 Neurodegenerative Disorders
- •11.4 Role of Plant Phenol On Neurochemistry
- •11.5.1 Alzheimer’s Disease
- •11.5.2 Parkinson’s Disease
- •11.5.3 Huntington’s Disease
- •11.6 Conclusion
- •References
- •12.1 Introduction
- •12.2 Phytochemicals and Their Classification
- •12.2.1 Alkaloids
- •12.2.2 Phenolics
- •12.2.3 Terpenoids
- •12.2.4 Saponins
- •12.2.5 Phytosterols
- •12.2.6 Cardiac Glycoside
- •12.3 Phytochemical Extraction Techniques
- •12.3.1 Conventional Methods for Extraction
- •12.3.2 Modern Methods for Extraction
- •12.3.2.1 Supercritical Fluid Extraction
- •12.4.2 Phytochemicals as Nrf2 Activators in Autism Spectral Disorder (ASD)
- •12.5 Conclusion
- •Contribution of Authors
- •Conflict of Research Interests
- •References
- •13.1 Introduction
- •13.2 Traditional Preparations and Formulations
- •13.2.1 Chyawanprash
- •13.2.2 Abana
- •13.2.3 Bramhi Ghrita
- •13.2.4 Memorin
- •13.2.5 Brain-O-Brain
- •13.2.6 Shimotsu-To
- •13.5 The Inclination for Natural Products Over Synthetics
- •13.7 Conclusion
- •References
- •14.1 Introduction
- •14.2 List of Edible Alkaloids
- •143 Biosynthesis of Tryptophan
- •14.4 Biosynthesis of Galantamine
- •14.5 General Biosynthesis of Indole Alkaloids (Figure 14.3)
- •14.6 Toxicity of Edible Alkaloids
- •14.7 Effect of β-Carboline On Memory & Behaviour
- •14.8 Effect of Murraya Koenigii On Memory & Behaviour
- •14.9 Effect of Anonaine On Memory & Behaviour
- •14.10 Conclusion
- •References
- •15 Caffeine and Motor Skills
- •15.1 Introduction
- •15.1.1 Pharmacological Profile and Pharmacokinetics
- •15.1.2 Stimulant Properties
- •15.2 Motor Skills in Normal Subjects
- •15.2.1 Human Subjects
- •15.2.2 Mice and Rats
- •15.2.3 Human Development
- •15.2.4 Rodent Development
- •15.3 Drug Interactions
- •15.3.1 Ethanol
- •15.3.2 Other Sedatives and Benzodiazepines
- •15.3.3 Glutamate
- •15.3.4 Pesticides
- •15.4 Hypoxia/ischaemia and Hypoglycaemia
- •15.4.1 Hypoxia/ischaemia
- •15.4.2 Hypoglycaemia
- •15.5 Traumatic Injury
- •15.5.1 Brain Trauma
- •15.5.2 Spinal Trauma
- •15.6 Non-Cerebellar Neurodegenerative Diseases
- •15.6.1 Amyotrophic Lateral Sclerosis
- •15.6.2 Parkinson’s Disease
- •15.6.3 Alzheimer’s Disease
- •15.7 Cerebellar Disorders
- •15.7.1 Episodic Ataxia Types 1 and 2
- •15.7.2 Spinocerebellar Atrophy
- •15.7.3 Ataxia Telangiectasia
- •15.7.4 Joubert Syndrome
- •15.8 Huntington’s Disease
- •15.9 Concluding Remarks
- •Acknowlegments
- •References
- •16 Melatonin and the Brain
- •16.1 Introduction
- •16.2 Dietary Sources of Melatonin
- •16.2.1 Animal Foods
- •16.2.2 Plant Foods
- •16.2.3 Juices and Beverages
- •16.3 Bioavailability of Melatonin in Humans
- •16.4 Melatonin Synthesis and Metabolism
- •16.5 Pharmacokinetic Properties of Melatonin
- •16.6 Melatonin Receptors
- •16.6.1 MT1 Receptor
- •16.6.2 MT2 Receptor
- •16.6.3 MT3 Receptor
- •16.6.4 Retinoic Acid Receptor-Related Orphan Receptor (ROR)
- •16.7 Mechanism of Action of MT
- •16.8 Melatonin in the Central Nervous System
- •16.8.1 Neuroprotective Capacity
- •16.8.2 Anti-Ischaemic and Anti-Oxidative Effects of Melatonin
- •16.8.3 Anti-Oxidative Effects of Melatonin in Alzheimer’s Disease
- •16.9 Anti-Depressant-Like Action of Melatonin
- •16.10 Conclusion
- •References
- •17 Narcotics and Brain Health
- •17.1 Introduction
- •17.2 Biological Elements Make Addiction to Drugs More Likely
- •17.2.1 Environmental Risk Factors
- •17.2.2 Additional Elements Boost the Chances of Drug Addiction
- •17.3 Drugs Harm the Brain Cells Permanently
- •17.3.1 Opioid Overdose and Brain Injury
- •17.3.2 Alcoholic Effects On the Brain
- •17.3.3 Stimulant Effects On the Brain
- •17.4 Narcotics and Brain Health
- •17.5 How Do Narcotics Make You Feel Good?
- •17.5.1 Dopamine’s Role in Drug Use Reinforcement
- •17.8 Addiction: Is It Curable?
- •17.8.1 Is a Drug Relapse a Sign That Therapy Was Ineffective?
- •17.9 Devices and Medications for the Treatment of Drug Abuse
- •17.9.1 Treatment for Withdrawal
- •17.9.2 Remaining in Therapy
- •17.9.3 Avoiding Relapse
- •17.9.4 Treatment With Behavioural Therapy
- •17.11 Conclusion
- •References
- •18 Nutraceuticals in Brain Health
- •18.1 Introduction
- •18.4 Nutraceuticals in Alzheimer’s Disease
- •18.4.1 Apigenin and Luteolin
- •18.4.2 Flavonoids
- •18.4.3 Crocin
- •18.4.4 Carotenoids
- •18.4.5 Anthocyanidins
- •18.5 Nutraceuticals in Parkinson’s Disease
- •18.6 Nutraceuticals in Depression
- •18.7 Nutraceuticals in Multiple Sclerosis
- •18.8 Nutraceuticals in Hungtington’s Disease
- •18.9 Nutraceuticals in Psychotic Disorders
- •18.10.1 Nutraceuticals Enhance Biogenesis and Maintain Mitochondrial Health
- •18.11 Conclusion
- •References
- •19.1 Introduction
- •19.3 The Brainstem
- •19.4 The Development of the Medulla
- •19.5 The Development of the Midbrain
- •19.6 Role of Thyroid Hormone in Fetal Brain Development
- •19.8 Food
- •19.8.1 Dietary Guidelines During Pregnancy
- •19.9 Discussion
- •19.10 Conclusion
- •References

364
Plant-based Foods and their Implications in Brain Health
-
thyroid hormone production does not start until midgestation, the development of the fetus’s brain
depends exclusively on maternal T4 until it is at least 24 to 26 weeks old (29).
Normal thyroid- stimulating hormone (TSH) levels and maternal concentrations of free-
thyroxine under the normal range for the pregnancy stages are the hallmarks of the illness known
as hypothyroxinemia (30). Primary thyroid failure and autoimmune thyroid disease are anticipated
-
ciency have the potential to negatively impact the outcome of pregnancy. Neurodevelopmental
29). During the embryonic
period, there were 23 internationally accepted morphological stages.
19.7 ESSENTIAL FOODS AND NUTRIENTS DURING PREGNANCY
AND THEIR EFFECT ON THE BRAIN HEALTH OF THE FETUS
When it comes to cognitive development, there are delicate and crucial stages of growth when out-
side factors, like food, can have a lasting impact. Early malnutrition affects neurogenesis, which
affects cell numbers for any given location. For instance, neonatal starvation can impact the cerebral
cortex’s size and shape. Variations in neurotransmitter production, uptake and receptor synthesis
mechanisms are among the neurochemical changes (31
of development can cause long- lasting variations in brain assembly and, consequently, cognitive
experienced malnutrition suffered long- lasting negative consequences on their children’s mental
health (32).
For proteins involved in brain energy metabolism, iron accretion, dopamine metabolism, and
antioxidant action in the fetal and neonatal brain, copper, a divalent cation, is required. The growth
33). Different
-
ally dependent on vitamin A. Furthermore, it is essential during periods of rapid growth, such as
during pregnancy and early life years (34). The vitamin A derivative retinoic acid, which has been
the expression of numerous genes and promoting cellular growth, is essential for the regulation of
neurodevelopment (35). Additionally, it has been demonstrated that retinoic acid transmission is
crucial for the formation of striatal functional pathways, which are engaged in dopamine- regulated
cognitive and motor activities. A current study discovered that children’s skills were selectively
the language domains of grammar and lexical retrieval but not conceptual or general cognitive
problems (36).
Due to its contribution, folate is essential for brain development and has a well- documented role
in the reduction of neural tube abnormalities during early gestation. Folates appear to affect memory
as well as disorders like depression and schizophrenia (37). Low maternal folate levels enhance the
of pregnancy. Children of folic acid- supplemented mothers display fewer behavioural problems at

365
Impact of Prenatal Diet on the Developing Brain of the Fetus
18 months, improved cognitive, psychological adjustment, and attention tests at 4 years, and fewer
hyperactivity and peer problems at eight years (38).
All membranes, including those in the grey and white matter, need choline to make them, and
-
ability causes deprived brain growth and continuing cognitive and behavioural issues due to the
developing central nervous system’s sensitivity to choline availability (39). Infants born to pregnant
mothers who consume diets low in choline are more likely to have neural tube abnormalities and
orofacial clefts. Studies on adults have found that people who consume diets higher in choline have
whether choline nutrition during gestation improves the developing brain in newborns, especially
memory (40).
-
nancy is linked to reduced intellectual capacity and will produce irreversible abnormalities
in brain development. Inadequate iodine levels during the initial stage of pregnancy are also
negatively correlated with the mental development of children at the age of eight (41). Zinc
concentrations and is crucial for appropriate cognitive development both before and after birth.
It performs both functional and structural roles (42
negative impact on how the brain develops. An iron shortage in newborns may result in abnor-
malities in the metabolism of dopamine and the myelination of neurons that may last for years.
-
chemical signature (43).
Docosahexaenoic acid (DHA), an n- 3 fatty acid, and arachidonic acid (AA), an n- 6 fatty acid, are
the two primary long- chain polyunsaturated fatty acids (LC- PUFAs). DHA starts to accumulate in
second half of gestation, timed to correspond with the development spike in the grey matter (44).
After delivery, babies receive fatty acids via breast milk, and during pregnancy, the mother’s LC-
PUFA contributes to the fetus is mediated by maternal- fetal placental transfer. Enhanced maternal
plasma levels of DHA lead to increased DHA transfer to the fetus as a result of higher maternal DHA
intake. Reduced DHA has been linked to issues with babies’ cognitive and behavioural development
(45). Improved prenatal AA and DHA status has been linked to better neurodevelopmental outcomes
up to at least 18 months of age, and studies looking at the effects of prenatal LC- PUFA status or pre-
natal LC- PUFA supplementation have also shown that subsequent psychomotor development and
46).
Additionally, most of the research on zinc, vitamin A, iron and iodine supplements suggests
that taking all four together may have a bigger impact on some outcomes than just one compo-
nent alone. Because of the widespread effects of hypothyroidism on the structure and function of
neurons, iodine shortage can impact cognitive function and development (47). Evidence suggests
that low iron status negatively affects psychological performance due to the brain’s iron- containing
enzymes’ lower activity and the body’s diminished ability to synthesize haemoglobin (48). A zinc
-
sion. Decreased weight of the brain, disrupted formation of the hippocampus, impaired systems
of neurotransmitters, and alterations in phosphorylation of protein are just a few of the negative
consequences of protein limitation on the brain (49).
19.8 FOOD
The brain has two distinct features. First, it is 60% lipid, and second, it consumes much energy.
During its most active phase of fetal growth, it consumes up to 70% of the mother’s energy and
60% of the energy delivered postnatally. The fetus does not use fat as a source of energy, but it does

366
Plant-based Foods and their Implications in Brain Health
store fat, which can be a supply of LCPUFAs postnatally while also acting as a vital energy buffer
to guarantee the growing brain’s demands are met (50).
Every year, approximately 1.4 million kids are born with or acquire severe neurodevelopment
abnormalities that have long- term repercussions (51
cretinism was discovered. Inadequate nutrition has been linked to neurodevelopment abnormalities,
which can be reversed with proper nutritional intervention (52).
The mother bears sole responsibility for the development of the brain. Before birth, around 70%
of an individual’s total number of brain cells split (53). The initial few weeks of embryonic develop-
ment are the most active for brain cell division (54). A woman is pregnant almost before she realizes
it. Because the placenta has not yet developed, the embryo’s nutrition is dependent on its mother’s
health, nutrition, and metabolism (55).
19.8.1 dietary guidelineS during pregnanCy
The Food Guide Pyramid is the foundation for dietary and nutritional recommendations for women
during pregnancy. Due to the requirement for more protein, it is advised to consume more meat,
how the retina and neuronal system of newborn babies develop. Additionally, it is advised for preg-
nant mothers to consume more milk products because they are an excellent source of phosphorus,
the fetus’s teeth and bone structure (66).
Safe food handling is a crucial component of sound dietary practices to avoid food- related
disorders during gestation, including toxoplasmosis and listeriosis. Pregnant women are advised
to steer clear of cool, ready- to- eat foods that have not been freshly cooked, raw, or improperly
cooked fresh meat to lower their risk of listeriosis and toxoplasmosis. Before eating fresh fruit and
vegetables, they should also peel them and wash them thoroughly to get rid of any contaminated
FIGURE 19.1 Structure of important chemical constituent required for fetal brain development.

367
Impact of Prenatal Diet on the Developing Brain of the Fetus
soil (67). It is advised against pregnant women to consume liver due to high levels of vitamin A,
which is related to teratogenic and miscarriage consequences. A healthy lifestyle at the time of
gestation should also include reasonable exercise, abstaining from alcohol, avoiding both direct
and indirect exposure to tobacco smoke, and avoiding other dangerous substances (68). Preterm
birth, gestational diabetes, hypertension, and preeclampsia are all lower risks for pregnant women
who exercise. The American College of Obstetricians and Gynaecologists advises pregnant ladies
each day (69).
Alcohol use is discouraged for women who may become pregnant due to the link between it and
fetal alcohol syndrome (FAS). At any point during pregnancy, a harmless amount of alcohol con-
and raises the risk of placental defects, spontaneous abortion, early labour, and neonatal mortality.
According to research, pregnant women who smoke are more likely to consume inadequate amounts
of antioxidants and other nutrients than those who do not. A recent study found that pregnant women
who smoke may negatively impact the offspring’s adult cognition (70).
bad eating habits. Writing advice down can affect knowledge about better eating, but it does not
seem to change attitudes or behaviour in the real world. If nutrition counselling for pregnant mothers
accounts for both the regular demands of the family and the additional needs that pregnancy imposes,
may have on their child’s neuronal development (71).
FIGURE 19.2 Nutrients required for fetal brain development.

368
Plant-based Foods and their Implications in Brain Health
TABLE 19.1
Different nutrients and their sources
1. Omega 3 fatty acids containing foods (56)
Plant source Seeds and nuts Chia seed, walnuts
Oils Flax seed oil, soya bean oil,
canola oil
Mineral source Tuna, salmon, herring
Yogurts, soy beverages
2. Iron- containing foods (57)
Animal source Eggs and meat Chicken, pork, dried beef, Liverwurst, veal, lamp, turkey, ham, beef, liver,
eggs (any style)
Mineral source Seafood scallops, clams, tuna, mackerel, oysters, shrimp, haddock, sardines
Plant source Different vegetables Kale, beet greens, broccoli, chard, spinach, sweet potatoes, collard greens,
peas, string beans, and dandelion greens
Fruit Figs, dates, raisins, dates, watermelon, prunes, prune juice, and
strawberries. Dried peaches and apricots
Cereals and bread sliced bread (enriched), wheat- free bread, improved pasta, items made
Other foods and beans Beans (garbanzo, kidney, or white, canned), tofu, and tomato- based items
(e.g., paste), roasted peas, roasted beans, Lentils, quick breakfast,
Molasses, maple syrup, and corn syrup
3. Iodine- containing foods (58)
Plant source Potatoes Potatoes are another excellent source of iodine; however, only organic
potatoes should be consumed because conventionally cultivated
potatoes have a tendency to absorb a lot of pesticide
Fruits A select few fruits, like pineapple, cranberries, and strawberries, are good
and abundant sources of iodine
Beans Both green beans and navy beans are known for their high iodine content.
Some green beans contained 3/ mcg of iodine, which is equivalent to
2% of the daily need
Bananas Although bananas are not fruits, they are high in potassium and iodine.
A single banana has 3/ mcg of iodine, which provides 2% of the daily
iodine requirement
Animal source Milk Although bananas are not fruits, they are high in potassium and iodine.
A single banana has 3/ mcg of iodine, which provides 2% of the daily
iodine requirement
Eggs Hard- boiled eggs are popular due to their high iodine content. Eggs are
high in Zinc, Vitamin D, Vitamin A and calcium, in addition to iodine
Using enriched iodized salt instead of conventional salt when cooking
is an easy method to integrate iodine into your daily diet. Regular salt
is a crystal of sodium and chloride, whereas iodized salt is a mineral
enhanced with iodine
Cheese Many people do not include cheese and other dairy products, such as
pasteurized goods, in their regular diets despite the fact that they are a
good source of calcium, protein, and iodine
Yogurt Yogurt, particularly organic yogurt, is high in iodine. It contains a lot of
iodine in addition to protein and calcium
Mineral source Seafood Minerals and nutrients can be found in abundance in seafood. Iodine is one
of the minerals that is most frequently present in different kinds of seafood
4. Vitamin A containing food (59)
Animal- sourced
foods
Liver of beef 6,421 mcg (713% DV) per slice: 9,442 mcg (1,049% DV) in 100 grams
Liver of lamb 2,122 mcg (236% DV) per ounce: 7,491 mcg (832% DV) in 100 games

369
Impact of Prenatal Diet on the Developing Brain of the Fetus
Feta cheese 35 mcg (4% DV) per ounce: 125 mcg (14% DV) in 100 grams
Caviar 43 mcg (5% DV) per tablespoon: 271 mcg (30% DV) per 100 grams
Cream cheese 45 mcg (5% DV) per tablespoon: 308 mcg (34% DV) per 100 grams
Blue cheese 56 mcg (6 percent DV) per ounce: 198 mcg (22% DV) in 100 grams
Trout
Hard- boiled egg 74 mcg (8% DV) per 1 big egg: 149 mcg (17% DV) in 100 grams
Roquefort cheese 83 mcg (9% DV) per ounce: 294 mcg (33% DV) in 100 grams
Camembert 92 mcg (10% DV) per wedge: 241 mcg (27% DV) in 100 grams
Cheddar 92 mcg (10% DV) per slice: 330 milligrams (37% DV) in 100 grams
Limburger cheese 96 mcg (11% DV) per slice: 340 mcg (38% DV) in 100 grams
Butter 97 mcg (11% DV) per tablespoon: 684 mcg (76% DV) in 100 grams
Goat cheese 115 mcg (13% DV) per slice: 400 mcg (45% DV) in 100 grams
Goose liver pate 130 mcg (14% DV) per tablespoon: 1,001 mcg (111% DV) in 100 grams
214 mcg (24% DV) per ounce: 757 mcg (84% DV) in 100 grams
Salmon
King mackerel
Cod liver oil 1,350 mcg (150% DV) per teaspoon: 30,000 mcg (3,333% DV) in 100 grams
Liver sausage 1,495 mcg (166% DV) per slice: 8,384 mcg (923% DV) in 100 grams
Vegetables
source food
containing
provitamin A
Sweet potato (cooked) 1,836 mcg (204% DV) per cup: 1,043 mcg (116% DV) in 100 grams
Romaine lettuce (raw) 122 mcg (14% DV) per big leaf: 436 mcg (48% DV) in 100 grams
Spinach (raw) 141 mcg (16% of DV) per cup: 469 mcg (52% DV) in 100 grams
Swiss chard (raw) 147 mcg (16% DV) per leaf: 306 mcg (34% DV) in 100 grams
Sweet red pepper (raw) 257 mcg (29% DV) per big pepper: 157 mcg (17% DV) in 100 grams
Carrot (cooked) 392 mcg (44% DV) per medium carrot: 852 mcg (95% DV) in 100 grams
Turnip greens (cooked) 549 mcg (61% DV) per cup: 381 mcg (42% DV) in 100 grams
Collards (cooked) 722 mcg (80% DV) per cup: 380 mcg (42% DV) in 100 grams
Kale (cooked) 885 mcg (98% DV) per cup: 681 mcg (76% DV) in 100 grams
Winter squash (cooked) 1,144 mcg (127% DV) per cup: 558 mcg (62% DV) in 100 grams
Fruits source
containing
Provitamin-
A: Provitamin
A is found
in higher
concentrations
in vegetables
than in fruits.
However,
only a few
fruits provide
adequate
amounts.
Cantaloupe. 169 mcg (19%) per large wedge: 172 mcg (19% DV) in 100 grams.
Mango 181 mcg (20% DV) per medium mango: 54 mcg (6% DV) in 100 grams
Passion fruit 12 mcg (1% DV) per medium fruit: 64 mcg (7% DV) in 100 grams
Guava 17 mcg (2% DV) per medium guava: 31 mcg (3% DV) in 100 grams31 mcg
Nectarine 24 mcg (3% DV) per medium nectarine: 17 mcg (2% DV) in 100
grams17 mcg
Tangerine 30 mcg (3% DV) per medium tangerine: 34 mcg (4% DV) in 100 grams
Apricot 34 mcg (4% DV) per medium apricot: 96 mcg (11% DV) in 100 grams
Papaya 74 mcg (8% DV) per small papaya: 47 mcg (5% DV) in 100 grams
Watermelon 80 mcg (9% DV) per wedge: 28 mcg (3% DV) in 100 grams
Pink or red grapefruit 143 mcg (16% DV) per medium grapefruit: 58 mcg (6% DV) in 100
grams
5. Vitamin- B
12
containing food (60– 65)
Plant source Vegetables Asparagus, Tessa jute, water shield, Japanese butterbur, broccoli, mung
bean sprouts, and mushrooms
leaves of tea 0.1 – 1.2 g of vitamin B12 per 100 g of dry weight
Animal source Non- vegetables
Soybean- based
fermented
Vitamin B12 is present in large amounts in Tempe
Fermented korean
vegetables
B12 is present in trace amounts in Kiamichi
TABLE 19.1 (Continued)
Different nutrients and their sources

370
Plant-based Foods and their Implications in Brain Health
19.9 DISCUSSION
Being one of the most prevalent health problems in today’s society, mental health illnesses are not
only comorbid but also impact how the brains of future generations develop. There is growing evi-
dence that diet- induced parental programming of a child’s metabolism, brain function, emotional
-
genetic alterations that might affect how genes are expressed in offspring and the growth of the
microbiota- gut- brain axis, which has a real impact on brain health, neurological development, and
behaviour.
It is widely acknowledged that the mother’s nutritional health during gestation pregnancy can
abilities. For iron, n- 3 fatty acids, and folic acid, the evidence of a relationship between prenatal
nutrition and neurological growth appears to be more reliable. Additionally, it is widely accepted
that micronutrients positively impact health, particularly when pregnant women eat well to maxi-
mize their baby’s cognitive development. Recent research has shown that supplementing with a
Good nutrition of the mother is a major component inducing the health of both child and mother
throughout pregnancy, a crucial time. Maintaining a healthy diet will give you the right kinds and
amounts of nutrients to ensure both mother and unborn child as healthy as possible sure both you
and your unborn child are as healthy as possible, both physically and mentally. Pregnant women
can choose appropriate food to meet their increased nutritional and energy needs while meeting the
growing fetus’s demands.
19.10 CONCLUSION
The authors concluded that numerous groups would need to work together in sizable national and
-
tively impact children’s mental health. The information gleaned from this study will strengthen the
Regarding how mental health affects behaviour, education, work potential, and brain diseases in
every age group, the discovery and adoption of nutritional recommendations are the ultimate of
broad social value for the general community. Therefore, genetic variation caused by nutrition
during fetal brain development and its positive and negative effects on future mental health should
be considered in future research when assessing the effects of nutrition and making nutritional
recommendations.
REFERENCES
(1) Anjos, T., Altmäe, S., Emmett, P., Tiemeier, H., Closa- Monasterolo, R., Luque, V., … & Campoy, C.
(2013). European Journal of Nutrition, 52(8), 1825– 1842.
(2) Nyaradi, A., Li, J., Hickling, S., Foster, J., & Oddy, W. H. (2013). Frontiers in Human
Neuroscience, 7, 97.
(3) Lindsay, K. L., Buss, C., Wadhwa, P. D., & Entringer, S. (2019). Biological Psychiatry, 85(2),
135– 149.
(4) Arija, V., & Canals, J. (2021). Nutrients, 13(5), 1644.
(5) Lindsay, K. L., Buss, C., Wadhwa, P. D., & Entringer, S. (2019). Biological Psychiatry, 85(2),
135– 149.
(6) Georgieff, M. K., Ramel, S. E., & Cusick, S. E. (2018). Acta Paediatrica, 107(8), 1310– 1321.
(7) Benton, D. (2010). Molecular Nutrition & Food Research, 54(4), 457– 470.
(8) Linderkamp, O., Janus, L., Linder, R., & Skoruppa, D. B. (2009). International Journal of Prenatal
and Perinatal Psychology and Medicine, 21(1/ 2), 4– 16.

371
Impact of Prenatal Diet on the Developing Brain of the Fetus
(9) Hanson, M., Godfrey, K. M., Lillycrop, K. A., Burdge, G. C., & Gluckman, P. D. (2011). Progress in
Biophysics and Molecular Biology, 106(1), 272– 280.
(10) Lindsay, K. L., Buss, C., Wadhwa, P. D., & Entringer, S. (2019). Biological Psychiatry, 85(2),
135– 149.
(11) Broad, K. D., & Keverne, E. B. (2011). Proceedings of the National Academy of Sciences, 108(37),
15237– 15241.
(12) Heijtz, R. D. (2016, December). Seminars in fetal and neonatal medicine. (Vol. 21, No. 6, pp. 410–
417). WB Saunders, USA.
(13) Rees, S., & Harding, R. (2004). Neuroscience Letters, 361(1– 3), 111– 114.
(14) Cohen, E., Baerts, W., & van Bel, F. (2015). Neonatology, 108(4), 269– 276.
(15) Stiles, J., & Jernigan, T. L. (2010). Neuropsychology Review, 20(4), 327– 348.
(16) Rice, D., & Barone Jr, S. (2000). Environmental Health Perspectives, 108(suppl 3), 511– 533.
(17) Dobbing, J. (1990). Brain, behaviour, and iron in the infant diet (pp. 1– 17). Springer, London.
(18) Linderkamp, O., Janus, L., Linder, R., & Skoruppa, D. B. (2009). International Journal of Prenatal
and Perinatal Psychology and Medicine, 21(1/ 2), 4– 16.
(19) De Escobar, G. M., Obregón, M. J., & Del Rey, F. E. (2004). European Journal of Endocrinology,
151(Suppl_ 3), U25– U37.
(20) Joseph, R. (2000). Developmental Review, 20(1), 81– 98.
(21) Herschkowitz, N. (2000). Brain and Development, 22(7), 411– 416.
(22) Izac, M. S. M. (2006). American Journal of Electroneurodiagnostic Technology, 46(1), 18– 38.
(23) Prayer, D., Kasprian, G., Krampl, E., Ulm, B., Witzani, L., Prayer, L., & Brugger, P. C. (2006).
European Journal of Radiology, 57(2), 199– 216.
(24) Grady, F. S., Boes, A. D., & Geerling, J. C. (2022). Frontiers in Neuroscience, 16 , 1–16. Article no.: 930514.
(25) Sprague, J. M., & Meikle Jr, T. H. (1965). Experimental Neurology, 11(1), 115– 146.
(26) MAAKS, D. L. G. (2019). Burns’ Pediatric Primary Care E- Book, 7th ed., 63–72.
(27) Miranda, A., & Sousa, N. (2018). Brain and Behavior, 8(2), e00920.
(28) Braun, J. M. (2017). Nature Reviews Endocrinology, 13(3), 161– 173.
(29) de Escobar, G. M., Obregón, M. J., & del Rey, F. E. (2004). Best Practice & Research Clinical
Endocrinology & Metabolism, 18(2), 225– 248.
(30) Skeaff, S. A. (2011). Nutrients, 3(2), 265– 273.
(31) Prado, E. L., & Dewey, K. G. (2014). Nutrition Reviews, 72(4), 267– 284.
(32) Herlenius, E., & Lagercrantz, H. (2004). Experimental Neurology, 190, 8– 21.
(33) Georgieff, M. K., Ramel, S. E., & Cusick, S. E. (2018). Acta Paediatrica, 107(8), 1310– 1321.
(34) Thompson, R. A. (2001). The future of children (pp. 21– 33) Princeton University, Princeton, New
Jersey, USA.
(35) Malik, M. A., Blusztajn, J. K., & Greenwood, C. E. (2000). Journal of Nutritional Biochemistry,
11(1), 2– 13.
(36) Berk, L. E. (2022). Infants and Children: Prenatal Through Middle Childhood. SAGE Publications,
New York, USA.
(37) Jain, K. K. (2019). Medlink- The information resource for clinical neurology. MedLink Neurology,
San Diego, USA.
(38) Naninck, E. F., Stijger, P. C., & Brouwer- Brolsma, E. M. (2019). Advances in Nutrition, 10(3),
502– 519.
(39) Derbyshire, E., & Obeid, R. (2020). Nutrients, 12(6), 1731.
(40) Holford, P. (2010). Optimum nutrition for the mind. Hachette, UK.
(41) Glinoer, D. (2004). Best Practice & Research Clinical Endocrinology & Metabolism, 18(2), 133– 152.
(42) Osredkar, J., & Sustar, N. (2011). Journal of Clinical Toxicology, 3(2161), 0495.
(43) Lozoff, B., & Georgieff, M. K. (2006, September). Seminars in Pediatric Neurology (Vol. 13, No. 3,
pp. 158– 165). WB Saunders, Elsevier USA.
(44) Strickland, A. D. (2014). Medical Hypotheses, 82(5), 522– 528.
(45) Acta Biochimica Polonica, 62(3), 499–507.
(46) Escolano- Margarit, M. V., Ramos, R., Beyer, J., Csábi, G., Parrilla- Roure, M., Cruz, F., & Campoy,
C. (2011). The Journal of Nutrition, 141(6), 1216– 1223.
(47)
Child Undernutrition Study Group. (2008). The Lancet, 371(9608), 243– 260.

372
Plant-based Foods and their Implications in Brain Health
(48) Hercberg, S., & Galan, P. (1989). Acta Paediatrica, 78, 63– 70.
(49) Cortés- Albornoz, M. C., García- Guáqueta, D. P., Velez- van- Meerbeke, A., & Talero- Gutiérrez, C.
(2021). Nutrients, 13(10), 3530.
(50) Broadhurst, C. L., Wang, Y., Crawford, M. A., Cunnane, S. C., Parkington, J. E., & Schmidt, W. F.
(2002). Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology,
131(4), 653– 673.
(51) Synnes, A., & Hicks, M. (2018). Clinics in Perinatology, 45(3), 393– 408.
(52) Kretchmer, N., Beard, J. L., & Carlson, S. (1996). The American Journal of Clinical Nutrition, 63(6),
997S– 1001S.
(53) Crawford, M. A., Costeloe, K., Ghebremeskel, K., Phylactos, A., Skirvin, L., & Stacey, F. (1997).
The American Journal of Clinical Nutrition, 66(4), 1032S– 1041S.
(54) Bello, B., Reichert, H., & Hirth, F. (2006). The brain tumor gene negatively regulates neural pro-
genitor cell proliferation in the larval central brain of Drosophila. Development, 133, 2639–2648.
(55) Williamson, C. S. (2006). Nutrition Bulletin, 31(1), 28– 59.
(56) Ganesan B., Brothersen C., & McMahon D. J. (2014 Jan 1). Critical Reviews in Food Science and
Nutrition. 54(1), 98– 114.
(57) Monsen E. R., Hallberg L., Layrisse M., Hegsted D. M., Cook J. D., Mertz W., & Finch C. A. The
American Journal of Clinical Nutrition, 31(1), 134– 141.
(58) Haldimann M., Alt A., Blanc A., & Blondeau K. (2005 Sep 1). Journal of food Composition and
Analysis, 18(6), 461– 471.
(59) Arnarson, A. (2024). Healthline. https://www.healthline.com/nutrition/foods-high-in-vitamin-a
(60) Nout, M. J. R., & Rombouts, F. M. (1990). Journal of Applied Bacteriology, 69
(61) Okada, N., Hadioetomo, P. S., Nikkuni, S., Katoh, K., & Ohta, T. (1983). Report of National Food
Research Institute (Japan), 43
(62) Kwak, C. S., Hwang, J. Y., Watanabe, F., & Park, S. C. (2008). Korean Journal of Nutrition, 41,
(63) Miyamoto, E., Kittaka- Katsura, H., Adachi, S., & Watanabe, F. (2005). Vitamins 79, 329– 332.
(64) Watanabe, F., Schwarz, J., Takenaka, S., Miyamoto, E., Ohishi, N., Nelle, E., Hochstrasser, R., &
Yabuta, Y. (2012). Journal of Nutritional Science and Vitaminology, 58
(65) Watanabe, F., Takenaka, S., Katsura, H., Masumder, S. A., Abe, K., Tamura, Y., & Nakano, Y. (1999).
Journal of Agricultural and Food Chemistry, 47
(66) Jackson, A. A., & Robinson, S. M. (2001). Public Health Nutrition, 4(2b), 625– 630.
(67) Ortega, R. M. (2001). Public Health Nutrition, 4(6a), 1343– 1346.
(68) Malek, L., Umberger, W., Makrides, M., & Zhou, S. J. (2016). Public Health Nutrition, 19(7),
1155– 1163.
(69) Caut, C., Leach, M., & Steel, A. (2020). Maternal & Child Nutrition, 16(2), e12916.
(70) Forbes, L. E., Graham, J. E., Berglund, C., & Bell, R. C. (2018). Nutrients, 10(8), 1032.
(71) Kadawathagedara, M., Ahluwalia, N., Dufourg, M. N., Forhan, A., Charles, M. A., Lioret, S., & de
Lauzon-Guillain, B. (2021). Maternal & Child Nutrition, 17(3), e13140.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
