new field in science

2. “If we could give every individual the right
amount of nourishment & exercise, not too
little & not too much,we would have found
the safest way to health.”
- Hippocrates
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3. WHAT IS NUTRIGENOMICS?
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4. Nutrigenomics is the study of effects of food & food constituents in
gene expression.
Still an expanding field of research.
Nutrigenomics is establishing the effects of ingested nutrients and other
food components on gene expression and gene regulation
It will also determine the individual nutritional requirements based on
the genetic makeup of the person.
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5. NUTRIGENOMICS AND OTHER
OMICS SCIENCES
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6. Omics
Technology
Nutrigenomics
Genomics
Transcriptomics
Proteomics
Metabolomics
DNA
mRNA
Proteins
Metabolites
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7. NUTRIGENETICS
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8.  Nutrigenetics identifies how the genetic make up of a particular
individual co-ordinates his or her response to various dietary nutrients.
 It also reveals why and how people respond differently to the same
nutrients.
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9. NUTRIGENOMICS & NUTRIGENETICS:
Two Sides of a Coin
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10. FOOD/NUTRIENTS
NUTRIGENOMICS
NUTRIGENETICS
GENOME
NUTRIGENOMICS
Concerned with the functional effect of
nutrient/ non-nutrient food components
on genome
NUTRIGENETICS
Concerned with how genetic
variation determines an individual’s
disease risk, nutrient requirements,
metabolic response and
responsiveness to a bioactive
dietary components 10

11. SINGLE NUCLEOTIDE POLYMORPHISM
(SNP)
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12. Single-nucleotide polymorphism (SNP,
pronounced snip) is a DNA sequence
variation occurring when a single
nucleotide adenine (A), thymine (T),
cytosine (C), or guanine (G]) in
the genome (or other shared sequence)
differs between members of a species
or paired chromosomes in an individual.
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13. Most of the genes have small sequence differences – Polymorphisms that
vary among individuals.
SNPs are the most common type of variation.
Specific genetic polymorphisms in human populations change their
metabolic response to diet and influence the risk patterns of disease.
Some SNPs change the recipe for the gene so that either a different
quantity of the protein is produced or the structure of the protein molecule
is altered.
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14. The four basic tenets of nutrigenomics are:
Improper diets are risk factors for disease.
Dietary chemicals alter gene expression.
The degree to which diet influences the balance between healthy and
disease states may depend on an individuals genetic makeup.
Some diet-regulated genes are likely to play a role in the onset, incidence,
progression, and/or severity of chronic diseases.
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15. HOW DOES DIET AFFECTS OUR
GENE EXPRESSION ?
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16.  Genes expression – proteins - Enzymes
 Detoxification by enzymes
E.g., Some foods such as cauliflower, broccoli & brussels sprout contain
chemicals that actually tell our gene to direct biosynthesis of these
enzymes
Phenylketonuria - A genetic disorder of metabolism; lack of the enzyme needed to
turn phenylalanine into tyrosine results in an accumulation of phenylalanine in the
body fluids which causes various degrees of mental deficiency. A diet restricting
this amino acid will stop the damage if detected in early infancy
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Brussel sprout
Broccoli

17. NUTRITION-GENE INTERACTION
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18. 1. Direct interactions: Nutrients after interacting with a receptor, behave
as transcription factors that can bind to DNA and induce gene
expression.
2. Epigenetic interactions: Nutrients can alter the structure of DNA so
that gene expression is altered.
3. Genetic variation: Common genetic variations such as single
nucleotide polymorphisms (SNPs) can alter the expression or
functionality of genes.
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19. GENE DIET DISEASE
INTERACTION
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20.  In nutrigenetic diseases, 97% of the genes have known to be associated with
human diseases result in monogenic diseases.
 Modifying the dietary intake can prevent some monogenetic diseases
Examples:
 In phenylketonuria food containing the amino acid phenylalanine, including
high protein food such as fish, chicken, eggs, milk, cheese, dried beans &
nuts must be avoided.
 In case of defective aldehyde dehydrogenase enzyme, alcohol must be
avoided.
 Patients having galactosemia (lack of a liver enzyme to digest galactose)
should avoid diets which contain lactose or galactose, including milk and milk
products. 20

21. NUTRIGENOMICS AND OBESITY
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As obesity causes a chronic process of inflammation, the use of
Nutrigenomics to modulate this manner is highly promising.
Reports demonstrated that some food contain anti-inflammatory
bioactive, such as the Caffeic acid (found in Yerba mate), tyrosol (found
in olive oil), quercetin (present in fruits and greeneries), and lycopene
(present in tomatoes, guavas, and watermelon).
These molecules act inhibiting the expression of COX2 and iNOS genes
through the reducing the translocation of the Kappa-B nuclear factor from
the cytoplasm to the nucleus

23. NUTRIGENOMICS AND CVD
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1. Differential intestinal metabolism &
uptake of nutrients, depending on gut
microbiome composition.
2. Differential absorption & nutrient
binding, depending on individual
genotype.
3. Modulation of gene expression
through specific transcription factor
binding.
4. Specific effects on methylation &
epigenetic modification.
5. Modulation of metabolic signalling
through lipid, metabolites & proteins.
Potential molecular mechanisms for
nutrigenomics interaction in CVD risk

25. NUTRIGENOMICS AND CANCER
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26.  Inherited mutations in genes can increase one’s susceptibility for cancer.
The risk of developing cancer can be markedly increased if there is a gene
diet interaction.
 Studies of twins show that the likelihood of identical twins developing the
same cancer is less than 10%, indicating that the environment plays an
important role in cancer Susceptibility.
 Deficiency of micronutrients, such as folic acid, vitamins B12, B6, C, and E,
selenium, niacin, and zinc can cause changes into the DNA similar to what
is seen after radiation exposure.
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27. There is an increase risk of colorectal cancer with high consumption of
red meat.
Specific dietary irritants, such as salt and preservatives have been
suggested as being carcinogens for gastric cancer.
It was reported that a stronger relationship existed between the risk of
developing hepatocellular carcinoma in Sudanese population and
consumption of peanut butter with aflatoxins with the glutathione S-
transferase M1 null genotype compared to those lacking the genotype.
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28. NUTRIGENOMICS AND T2DM
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29. Diabetes counts for more than 90% of all diseases of world.
Type II Diabetes is multifactorial pathogenesis that involves the
interaction between genetics and environmental factors.
Genomics studies showed that there are 65 SNPs associated with
the risk of developing type II Diabetes
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30. ADVANTAGES OF NUTRIGENOMICS
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31. Increased focus on a healthy diet and lifestyle.
Increased awareness of risk of certain conditions.
Improved health quality of life.
Focus on prevention of diseases.
Decreased morbidity and premature mortality.
Reduced health care costs.
Better understanding of the mechanisms involved in disease
susceptibility .
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32. CONCLUSION AND FUTURE
PERSPECTIVE
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33. (1) Nutrigenomics researchers must know the challenge of understanding
polygenic diet related diseases.
(2) Short-term goals:
To identify the dietary signals.
To elucidate the dietary sensor mechanisms.
To characterize the target genes of these sensors.
(3) Long-term goals:
 Nutrigenomics is to help to understand how we can use nutrition to
prevent many of the same diseases for which pharmacogenomics is
attempting to identify cures.
 SNP database will be effect on disease risk. 33

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35. THANKYOU
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