NUTRITIONAL GENOMICS:
ESSENTIAL BASICS FOR NUTRITION
PROFESSIONALS
Mariëtte Abrahams MBA RD
Course Outline
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Basic Genetics
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Nutrigenomics & Nutrigenetics
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Personalized health era
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Diet-Gene interactions in Chronic diseases
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What does testing involve?
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Limitations, Ethics & regulation of testing
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Nutrigenetics in the marketplace – A global view
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Opportunities for Dietitians
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Resources & Projects
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Learning outcomes
 Outline the structure and function of DNA and how it is organised in cells to form the human genome
 Explain what gene expression is and how environmental factors such as diet can influence gene
expression and genome function thereby influencing health and susceptibility to disease
 Explain what the fields of nutrigenomics, nutrigenetics and epigenetics are
 Demonstrate an understanding of the genetic basis of some chronic diseases
 Demonstrate a broad understanding of relevant genetics and genomics principles.
 Explain how genetic testing is conducted in practice
 Understand and be able to explain the limitations of gene testing
 Understand and explain the ethical and legal frameworks surrounding personalised health
 Visualise and create future opportunities where chronic disease prevention is concerned
 Outline relevant resources for accessing further detailed information
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Part 1 – The Foundation
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What is DNA??
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DNA is a long chain of
building blocks (A,T,G,C)
A gene is a unit of
information
Genes are located on
chromosomes
Every human has 46
chromosomes
All 25 000 genes in every
cell
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Human Genome project
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13 year project
Completed April 2003
Mapped entire human
genome sequence
Identified all genes in
human DNA
Cost $3 billion
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The outcome
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25 000 genes
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3 Billion base pairs
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99.9% of DNA is identical
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0.1% variance has no functional significance
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Approx Only 1-5% of DNA code for genes
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Monogenetic vs Polygenetic diseases
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Monogenetic disorders eg PKU
Polymorphisms are common in the
population >1%
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Gene Variations
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Everyone has them!
Changes in genetic information
Single Nucleotide (base change, insert,deletion)
Groups of nucleotides (repeats)
Whole chromosomes (insert, delete,rearranged)
Impact can be positive, negative or non-existent
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Single Nucleotide Polymorphism (SNP)
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Change in Single Nucleotide
pair
Most have no direct effect on
health
http://www.youtube.com/wat
ch?v=9rPDa2ACtog
3-5% are functional and
influence phenotypic
differences (Yamada et al
2008)
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Reading the literature
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Gene name C275T
MTHFR 677C>T
ADRB3 Trp64Arg
Rs 123456
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Must know nomenclature
Description
Allele
A variation of a gene
Wild type, homo/heterozygote
Most common version, two copies, 1 copy of each
Locus/loci
An arbitrary region of the genome that can have
mutations /polymorphisms
Genotype vs Phenotype
Inherited DNA vs measureable characteristics
Polymorphism
Differences in DNA sequence found commonly in
>1% of population
SNP vs Genome
A change in a single nucleotide/ your total sum of
DNA
Rs numbers
All SNP´s are assigned a unique rs number eg rs
9939609
Mutations
Differences in DNA sequence in an individual that are
rare (<1% of population) and may be unique to the
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Nutritional Genomics
(Stover and Caudill, 2008)
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Epigenetics
“ Studies the silencing and activation of
DNA without changing the nucleotide
sequence”
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What is Gene Expression?
“ The conversion of the information encoded in a
gene into mRNA and then to protein”
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Gene expression
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DNA codes for RNA
Moves from cell
nucleus to cytoplasm
Directs protein
synthesis
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How Diet, Lifestyle & environment
impact gene expression?
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Directly affect gene expression by acting as ligands for
transcription factor receptors eg PUFA´s on PPAR´s
Nutrients are metabolized by primary or secondary
metabolic pathways thereby altering concentrations of
substrates or intermediates eg folic acid
(Fenech M et al., 2011)
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Omics technologies
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Transcriptomics
(mRNA,micro RNA, non-coding RNA)
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Metabolomics
(Metabolites eg Cholesterol levels)
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Proteomics
(protein structures and function)
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NEW NUTRITION
PARADIGM
The age of personalized health
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DNA is not your
destiny
Genotype does not
mean phenotype
Tailoring treatment
and recommendations
to include genetics eg
“Pharmacogenomics”
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The Disease continuum
(Kauwell 2008)
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How genomic technology fits in with
Nutrition
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Candidate gene approach
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Genome-wide linkage screen
(Lovegrove JA, Gitau R 2008)
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From the old into the New
Old Paradigm
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Population based
Recommendations based on
RDA from observational
studies
Adjust intake on nutritional
assessment from diet,
anthro,family hx,clinical,age
and sex
General healthy eating
recommendations or prudent
guidelines for general
population
New Paradigm
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Our unique DNA affects our
individual nutrient
requirements
RDA may be based on
metabotypes or ethnic groups
Individual needs for vitamins,
minerals and phytochemicals
Move from single genenutrient interaction to a
systems biology approach
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“One man´s food is
another man´s poison”
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Quick recap!!
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How it all started
Basic Genetics
What Nutritional Genomics is
How diet and lifestyle impact our Genotype and
susceptibility to develop chronic diseases
Omics Technology
Type of genetic studies
How there is a shift towards a personalized health
approach
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Part 2 – The Genes
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GENES AND OBESITY
Genetic contribution to BMI
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40-90% difference within individuals in a
population due to genetics (Atwood et al 2002)
32 loci explains <1.5% of variation in BMI
It is certainly not the holy grail, but only part of the
story
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Four levels of genetic contribution to
Obesity
1.
Genetic obesity - mutation in a single gene despite environment
(1 - 5%)
2.
Strong predisposition - overweight in non-obesogenic
environment and obese in obesogenic environment
3.
Slight predisposition - normal weight in non-obesogenic
environment and overweight in obesogenic environment
4.
Genetically resistant - normal weight in obesogenic
environment.
(Loos and Bouchard 2003)
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Fat mass Obesity associated gene
(FTO) T>A
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GWAS identified FTO SNPs as have the most important
effects on obesity susceptibility and BMI
FTO may play role in eating behaviour, satiety and
dietary intake.
 Rs9939609 T>A associated with higher body
weight, fat mass and higher risk of obesity.
 Minor allele carriers have higher intake of total
energy and fat
 Association was replicated in several populations
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FTO T>A genotype
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Prevalence 46%-74% Europeans have 1 copy
18% have two copies (A allele)
51% West Africans
28-44% of Asian descent (Kalpelainen TO et al
16% Chinese
Increases risk of obesity by 30% one copy, 70% two
copies (Frayling et al., 2007)
A-allele carriers are 3kg heavier than non-carriers
(Vialeswaran 2012)
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Moleres
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et al 2012
Moleres et al 2012
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Impact of FTO T>A gene variant
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In A allele carriers high-fat diets increase obesity
susceptibility.
A allele increased obesity risk when consuming high
SAT FAT.
A allele carriers reported to consume more fat and
total energy, experience less satiety. Especially
children.
Low physical activity accentuates the susceptibility
to obesity by A allele.
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Peroxisome Proliferator activated
receptor gamma (PPAR-y)
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Nuclear Transcription factor
Plays a role in Adipocyte growth and differentiation
Role in Lipid and glucose metabolism
Reduced transciption related to increased regain of weight
Decreased insulin sensitivity (Masud et al., 2005)
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Impact of PPAR-y gene variant
Pro12Ala C>G
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CC most common version
Memisoglu et al., 2003 – Nurses health study
CC individuals particularly sensitive total amount of
fat in the diet with higher BMI
No difference in Ala carriers
MUFA intake inversely associated with BMI in Ala
carriers
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Beta-2 Adrenergic Receptors (ADRB2)
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Gly16Arg G>A, Gln27Glu C>G
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GA 40%, AA 12%, CG 50%, GG 15%
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Involved in energy expenditure regulation through
stimulating thermogenesis and lipid metabolism in adipose
tissue
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Knockout mouse studies have conclusively shown that the
adrenergic receptors are necessary for diet-induced
thermogenesis, and play a critical role in the body’s
defense againstPomegranate
obesityNutrition
(Bachman
et al.,2015
2002)
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ADRB2 SNPs associated with obesity, especially
central obesity
Gln27Glu (C>G)
 Glu27 (G) carriers more resistant to losing weight, lose weight
slower, associated with all measures of obesity
 Martinez et al. (2003) found a significant interaction between high
consumption of CHO and obesity in Glu27 carriers
Gly16Arg (G>A)
 Long term studies showed that weight gain from childhood to
adulthood and weight gain during adulthood are higher in Gly16
allele (Ellsworth et al 2002)
 Also Gly16 more resistant to weight loss and more likely to regain
body weight after 6 months (Masuo et al., 2005)
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dietary intake of CHO >49% E
produced an increased obesity risk in
women carrying the Glu27 allele
dietary intake of CHO >49% E associated
with higher insulin levels in women carrying
the Glu27 allele
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Apolipoprotein II – (APOA2)
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-265 T/C (TC 47%, 10-15% CC)
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Second most abundant protein of HDL particles
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SNP results in 30% drop in transcription activity.
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CC individuals had higher obesity risk and higher intake of total
fat and SAT FAT.
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Three populations have shown a mean increase in BMI in CC
genotypes with high SAT FAT intake but not low SAT FAT intake
(Corella, 2011).
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Corella et al.,2009)
These figures clearly illustrate the benefit of including
genetics and diet in research studies
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(Corella et al.,2009)
“Subjects on Diets Appropriate for their
Genotype Achieved Statistically significant
Average Weight Loss of 6.2% of Body Weight
at one year Compared to Individuals not on a
Diet Matched to Genotype (2.4%)”-
Stanford Univ
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Other areas in weight management
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The Human Obesity gene map
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Taste preference (TAS2R38)
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Reward deficiency syndrome (DA2D)
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Snacking and Binging (MC4R,CLOCK)
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Appetite (LEP-R)
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Obesity and Gut microbiota
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Epigenetics (Barres et al 2013; Hatoum et al 2011)
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Motivation and Commitment?
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Personalised genotype advice improved motivation
(Arkadianos et al., 2009)
Personalized advice more understandable and
enjoyable to read (Nielsen and El-Sohemy, 2012)
FTO status does not impact motivation to lose
weight(Jrn Gen Couns 2013, Meisel et al 2012)
http://health.usnews.com/health-news/news/articles/2013/09/06/obesity-gene-tests-may-nothamper-weight-loss-efforts
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What will the future be like?
Genomic
Knowledge
Dietetic
input
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GENES AND DIABETES
Transcription Factor 7 like 2 (TCF7L-2)
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Identified in 2006
TCF7L2 gene associated with type 2 diabetes,
MetS and obesity.
Associated with increased T2D risk possibly
due to defective beta-cell functioning and
impaired insulin secretion
Operates via impaired glucagon-like peptide
1(GLP-1) secretion
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(Grau et al 2010)
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Mean weight loss was -6.81 kg. All subjects no
difference between HF and LF.
CC & CT subjects no difference between HF and LF.
TT genotype weight loss was 2.57kg smaller with HF
than LF diet.
TT do better on a LF diet.
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TCF7L2 C>T
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During lifestyle intervention, T allele carriers
displayed lower reduction in BMI and total body
fat.
T allele requires more long term intervention to
manage weight and prevent IR and diabetes.
Need to manage QUALITY of CHO. GL & GI.
Implement all diet & lifestyle changes that will
prevent development of IR.
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EPIC-interAct study (May 2014)
The absolute high risk associated with obesity at any
level of genetic risk highlights the importance of
universal rather than targetted approach to lifestyle
http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1001647
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Nutrigenetics and Alzheimer´s disease
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ApoE4 increases risk of CVD by 40% (Lovegrove &
Gitau 2008)
25% in UK population
40% population will develop late onset AD
Diet & lifestyle intervention
REVEAL study - Impact of disclosure of APOE4
status
Genotype status did impact motivation to change
(Chao et al., 2008)
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Nutrigenetics and CVD
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DNA cascade screening for Familial
Hypercholesterlaemia (Scotland & Wales)
LDL-R, ApoB, PCSK9
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NOS-3 (Ferguson et al., 2010)
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MTHFR C677T (Klerk et al., 2002)
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Nutrigenetics, Epigenetics and Cancer
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Cruciferous veg intake
improves detoxification
function
Contains Sulphoraphane
(Ferguson and Schlothauer, 2012)
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Epigenetics & polyphenols
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What researchers think…..
“Dietitians and doctors can act as a reality check to
Nutrigenomics, they know what goes on in the heads
of their patients and clients a lot better than scientists
and can therefore bridge science and practical
application”
Laura Bouwman PhD Wageningen university.
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Summary
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Genes play an important role in health homeostasis
Personalization may lead to improved motivation and
outcomes for chronic diseases
Specific SNP´s have been repeatedly shown to impact
health in different populations
We don´t have all the answers in terms of gene-gene,
gene-nutrient interactions, but we certainly have a
starting point
Although it is early days for a nutrigenomics, in the
future can be used as a tool as part of a effective
personalized nutrition intervention strategy
New nutrition research needs to integrate genomic data
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Part 3 – Nutrigenetic testing
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WHAT DOES TESTING
INVOLVE?
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Nutrigenetic testing in the market
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Weight Loss
Wellness
Sports Performance
Disease risk
Lactose Intolerance
Coeliac disease
Urine metabolites
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Nutrigenetics a global view
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Part 4 – Limitations, Ethics and
Regulation
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LIMITATIONS OF GENE-SNP
TESTING
Limitation of DNA testing
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Chronic diseases are polygenic
Contribution of single SNP to overall disease
susceptibility usually small
Interaction between diet-genes and gene-genes
(epistatis) not identified
Chronic diseases are poly-environmental
Chronic diseases are more prevalent in some ethnic
groups
Limited Biomarkers to measure impact of SNP´s
Limited standardization of testing and interpretation
Only looks at part of the genome
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ETHICS OF PERSONALISED
NUTRITION
Ethical issues
Privacy
Ready for
practice?
Behaviour
change
Individual
Discrimination
Psycological
stigma
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Reilly and DeBusk 2008,
Görman et al., 2012
Stewart-Knox et al.,2013
Bloss et al 2013
REGULATORY
ENVIRONMENT
Regulation of Genetic testing
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UK HGC /EU
MHRA-medical devices
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US (FDA –medical devices)
Hesketh 2013
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Part 5 – The Market need
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Food4me project 2013
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Who are Consumers and what do
they want?
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Men and older individuals
Highly educated
More likely if result is likely to be
positive
Take preventative action
May have a relative or at at risk
themselves
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HCP endorsed (Wendel et
al.,2013)
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Personalized Approach if high
risk and symptomatic (Fallaize et
al., 2013)
(Collins et al 2013)
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Actionable Data
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Data to be kept safe
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Where are opportunities for Dietitians?
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Lead research
Genomic educators in Dietetic curriculum
Evolve public health guidelines
Lead and contribute to commercial teams
Educate public
Integrate into clinical practice
Development of functional foods
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Colleen Draper,
R.deBusk
Market trends & Highlights 2014/15
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23and me banned from selling personal genome test in
2013
23andme launched in the UK 2014
AND position paper on Nutritional Genomics published
First NGx sessions at both Canadian and ADA
conferences
Biggest investment yet in digital health
Fitgenes, RevUP launch integrated platform
100 000 genome project gets more funding
Competency on NGx standard for UK RD´s published
BBC documentary on Personalised Nutrition aired
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Resources & Projects
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Food4me project (http://www.food4me.org)
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Human Variome project
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Diogenes
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NuGO (http://www.nugo.org)
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ISNN (http://www.isnn.info
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NHS Genetics Education centre
HAPMAP consortium
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Micronutrient project
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DIFM (http://integrativerd.org)
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Toybox study
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Qua-Li-FY
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Competency Framework for Dietitians 2014
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http://www.gbhealthwatch.com/healthwatch-tools.php
http://www.geneticseducation.nhs.uk
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OMIM database
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AND position paper on Nutritional Genomics 2014
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POUNDS-lost TRial
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Books
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The real question…….
Where is the evidence?
vs
Where should I start?
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Key messages
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1 SNP does not equal chronic disease
Start Learning your special interest topics
Digital and Genomic technologies are changing our
roles
The world is moving towards prevention and
personalisation
The Food industry is responding to consumer demands
for more healthy and personalised foods
The field needs expert nutrition practitioners to lead,
educate and get involved
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THANK YOU!!!
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Inspired to learn & Apply?

Basic Nutritional Genomics webinar- April 16th 2015 &
June 2015- Book within next 72hrs for £145 discount

5-week online course- starts May 2015

Practical Nutrigenomics eBook – 2nd Edition
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Individual Coaching
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Want to get tested?
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Contact me
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Website: http://marietteabrahams.com,
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Email: [email protected]
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Twitter: @marietteabraham
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FB:
http://facebook.com/pomegranatenutritionconsulting
Phone: ++351 964450622
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What is next?
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Send final quizz and feedback questionnaire via
email to [email protected]
Certificate of completion sent on return of both
Pick a topic and find literature!
Ask questions in LinkedIn group
You will receive our weekly newsletter
Share the knowledge and bring a friend- earn £10
Give us a “Tweet” about the course
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Products and Services
Business Consulting- Contract
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Partnership to provide training
Spokesperson services
Provide strategic advice and consumer &
HCP insight
Technical support
New Product development
Creativity & innovation (more details on
our website)
Business Coaching

For nutrition professionals
Interested? , Want to get tested?
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References
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MOLERES, A., OCHOA, M. C., RENDO-URTEAGA, T., MARTÍNEZ-GONZÁLEZ, M.
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