nutritional genomics basics for nutrition...
TRANSCRIPT
NUTRITIONAL GENOMICS: ESSENTIAL BASICS FOR NUTRITION
PROFESSIONALS
Mariëtte Abrahams MBA RD
Course Outline
Basic Genetics
Nutrigenomics & Nutrigenetics
Personalized health era
Diet-Gene interactions in Chronic diseases
What does testing involve?
Limitations, Ethics & regulation of testing
Nutrigenetics in the marketplace – A global view
Opportunities for Dietitians
Resources & Projects
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Learning outcomes
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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
Part 1 – The Foundation
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What is DNA??
DNA is a long chain ofbuilding blocks (A,T,G,C)
A gene is a unit ofinformation
Genes are located onchromosomes
Every human has 46 chromosomes
All 25 000 genes in everycell
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Human Genome project
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
25 000 genes
3 Billion base pairs
99.9% of DNA is identical
0.1% variance has no functional significance
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%
Gene Variations
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)
Change in Single Nucleotidepair
Most have no direct effect onhealth
http://www.youtube.com/watch?v=9rPDa2ACtog
3-5% are functional andinfluence phenotypicdifferences (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
Must know nomenclature
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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
individual
Nutritional Genomics
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(Stover and Caudill, 2008)
Epigenetics
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“ Studies the silencing and activation of
DNA without changing the nucleotide
sequence”
What is Gene Expression?
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“ The conversion of the information encoded in a
gene into mRNA and then to protein”
Gene expression
DNA codes for RNA
Moves from cell
nucleus to cytoplasm
Directs protein
synthesis
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How Diet, Lifestyle & environment
impact gene expression?
Directly affect gene expression by acting as ligands for transcription factor receptors eg PUFA´s on PPAR´s
Nutrients are metabolized by primary or secondarymetabolic pathways thereby altering concentrations ofsubstrates or intermediates eg folic acid
(Fenech M et al., 2011)
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Omics technologies
Transcriptomics(mRNA,micro RNA, non-coding RNA)
Metabolomics(Metabolites eg Cholesterol levels)
Proteomics(protein structures and function)
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NEW NUTRITION
PARADIGM
The age of personalized health
DNA is not yourdestiny
Genotype does notmean phenotype
Tailoring treatmentand recommendationsto include genetics eg“Pharmacogenomics”
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The Disease continuum
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(Kauwell 2008)
How genomic technology fits in with
Nutrition
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Candidate gene approach
Genome-wide linkage screen
(Lovegrove JA, Gitau R 2008)
From the old into the New
Population basedRecommendations based onRDA from observationalstudies
Adjust intake on nutritionalassessment from diet, anthro,family hx,clinical,ageand sex
General healthy eatingrecommendations or prudentguidelines for general population
Our unique DNA affects ourindividual nutrientrequirements
RDA may be based onmetabotypes or ethnic groups
Individual needs for vitamins, minerals and phytochemicals
Move from single gene-nutrient interaction to a systems biology approach
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Old Paradigm New Paradigm
“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 andsusceptibility to develop chronic diseases
Omics Technology
Type of genetic studies
How there is a shift towards a personalized healthapproach
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
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.
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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
Fat mass Obesity associated gene
(FTO) T>A
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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% twocopies (Frayling et al., 2007)
A-allele carriers are 3kg heavier than non-carriers(Vialeswaran 2012)
Moleres et al 2012Pomegranate Nutrition Consulting copyright 2015
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Moleres et al 2012
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Impact of FTO T>A gene variant
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)
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
Gly16Arg G>A, Gln27Glu C>G
GA 40%, AA 12%, CG 50%, GG 15%
Involved in energy expenditure regulation through
stimulating thermogenesis and lipid metabolism in adipose
tissue
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 against obesity (Bachman et al., 2002)
Beta-2 Adrenergic Receptors (ADRB2)
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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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-265 T/C (TC 47%, 10-15% CC)
Second most abundant protein of HDL particles
SNP results in 30% drop in transcription activity.
CC individuals had higher obesity risk and higher intake of total
fat and SAT FAT.
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).
Apolipoprotein II – (APOA2)
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Corella et al.,2009)
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These figures clearly illustrate the benefit of including
genetics and diet in research studies
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“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
Taste preference (TAS2R38)
Reward deficiency syndrome (DA2D)
Snacking and Binging (MC4R,CLOCK)
Appetite (LEP-R)
Obesity and Gut microbiota
Epigenetics (Barres et al 2013; Hatoum et al 2011)
Motivation and Commitment?
Personalised genotype advice improved motivation(Arkadianos et al., 2009)
Personalized advice more understandable andenjoyable to read (Nielsen and El-Sohemy, 2012)
FTO status does not impact motivation to loseweight(Jrn Gen Couns 2013, Meisel et al 2012)
http://health.usnews.com/health-news/news/articles/2013/09/06/obesity-gene-tests-may-not-hamper-weight-loss-efforts
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What will the future be like?
GenomicKnowledge
Dieteticinput
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GENES AND DIABETES
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
Transcription Factor 7 like 2 (TCF7L-2)
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(Grau et al 2010)Pomegranate Nutrition Consulting copyright 2015
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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
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)
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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
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)
Nutrigenetics and CVD
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DNA cascade screening for Familial
Hypercholesterlaemia (Scotland & Wales)
LDL-R, ApoB, PCSK9
NOS-3 (Ferguson et al., 2010)
MTHFR C677T (Klerk et al., 2002)
Nutrigenetics, Epigenetics and Cancer
Cruciferous veg intake
improves detoxification
function
Contains Sulphoraphane(Ferguson and Schlothauer, 2012)
Epigenetics & polyphenols
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What researchers think…..
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“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.
Summary
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Genes play an important role in health homeostasis
Personalization may lead to improved motivation andoutcomes for chronic diseases
Specific SNP´s have been repeatedly shown to impacthealth 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 thefuture can be used as a tool as part of a effectivepersonalized nutrition intervention strategy
New nutrition research needs to integrate genomic data
Part 3 – Nutrigenetic testing
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WHAT DOES TESTING
INVOLVE?
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Nutrigenetic testing in the market
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 diseasesusceptibility usually small
Interaction between diet-genes and gene-genes (epistatis) not identified
Chronic diseases are poly-environmental
Chronic diseases are more prevalent in some ethnicgroups
Limited Biomarkers to measure impact of SNP´s
Limited standardization of testing and interpretation
Only looks at part of the genome
ETHICS OF PERSONALISED
NUTRITION
Ethical issues
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Individual
Privacy
Discrimination
Psycologicalstigma
Behaviourchange
Reilly and DeBusk 2008,
Görman et al., 2012
Stewart-Knox et al.,2013
Bloss et al 2013
Ready for
practice?
REGULATORY
ENVIRONMENT
Regulation of Genetic testing
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UK HGC /EU
MHRA-medical devices
US (FDA –medical devices)
Hesketh 2013
Part 5 – The Market need
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Food4me project 2013
Who are Consumers and what do
they want?
HCP endorsed (Wendel et
al.,2013)
Personalized Approach if high
risk and symptomatic (Fallaize et
al., 2013)
Actionable Data
Data to be kept safe
Men and older individuals
Highly educated
More likely if result is likely to bepositive
Take preventative action
May have a relative or at at riskthemselves
(Collins et al 2013)
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Where are opportunities for Dietitians?
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
Resources & Projects
Food4me project (http://www.food4me.org)
Human Variome project
HAPMAP consortium
Micronutrient project
DIFM (http://integrativerd.org)
Toybox study
Qua-Li-FY
Competency Framework for Dietitians 2014
http://www.gbhealthwatch.com/healthwatch-tools.php
Diogenes
NuGO (http://www.nugo.org)
ISNN (http://www.isnn.info
NHS Genetics Education centre
http://www.geneticseducation.nhs.uk
OMIM database
AND position paper on Nutritional Genomics 2014
POUNDS-lost TRial
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Books
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The real question…….
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Where is the evidence?
vs
Where should I start?
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 ourroles
The world is moving towards prevention andpersonalisation
The Food industry is responding to consumer demandsfor more healthy and personalised foods
The field needs expert nutrition practitioners to lead, educate and get involved
THANK YOU!!!
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Inspired to learn & Apply?
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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
Individual Coaching
Want to get tested?
Contact me
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Website: http://marietteabrahams.com,
Email: [email protected]
Twitter: @marietteabraham
FB: http://facebook.com/pomegranatenutritionconsulting
Phone: ++351 964450622
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
Products and Services
Business Consulting- Contract
Partnership to provide training
Spokesperson services
Provide strategic advice and consumer & HCP insight
Technical support
New Product development
Creativity & innovation (more details onour website)
Business Coaching
For nutrition professionals
Interested? , Want to get tested?
Tel : +351964450622
Skype: pnutritionconsulting
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E-Book available on
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Question time
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References
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ARKADIANOS, I., VALDES, A. M., MARINOS, E., FLOROU, A., GILL, R. D. & GRIMALDI, K. A. 2007. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J, 6, 29.
ATWOOD, L. D., HEARD-COSTA, N. L., CUPPLES, L. A., JAQUISH, C. E., WILSON, P. W. & D'AGOSTINO, R. B. 2002. Genomewide linkage analysis of body mass index across 28 years of the Framingham Heart Study. Am J Hum Genet, 71, 1044-50.
BACHMAN, E. S., DHILLON, H., ZHANG, C. Y., CINTI, S., BIANCO, A. C., KOBILKA, B. K. & LOWELL, B. B. 2002. betaAR signaling required for diet-induced thermogenesis and obesity resistance. Science, 297, 843-5.
CHAO, S., ROBERTS, J. S., MARTEAU, T. M., SILLIMAN, R., CUPPLES, L. A. & GREEN, R. C. 2008. Health behavior changes after genetic risk assessment for Alzheimer disease: The REVEAL Study. Alzheimer Dis Assoc Disord, 22, 94-7.
CORELLA, D., ARNETT, D. K., TSAI, M. Y., KABAGAMBE, E. K., PEACOCK, J. M., HIXSON, J. E., STRAKA, R. J., PROVINCE, M., LAI, C. Q., PARNELL, L. D., BORECKI, I. & ORDOVAS, J. M. 2007. The -256T>C polymorphism in the apolipoprotein A-II gene promoter is associated with body mass index and food intake in the genetics of lipid lowering drugs and diet network study. Clin Chem, 53, 1144-52.
CORELLA, D., TAI, E. S., SORLÍ, J. V., CHEW, S. K., COLTELL, O., SOTOS-PRIETO, M., GARCÍA-RIOS, A., ESTRUCH, R. & ORDOVAS, J. M. 2011. Association between the APOA2 promoter polymorphism and body weight in Mediterranean and Asian populations: replication of a gene-saturated fat interaction. Int J Obes (Lond), 35, 666-75.
CORNELIS, M. C., QI, L., KRAFT, P. & HU, F. B. 2009. TCF7L2, dietary carbohydrate, and risk of type 2 diabetes in US women. Am J Clin Nutr, 89, 1256-62.
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ELLSWORTH, D. L., COADY, S. A., CHEN, W., SRINIVASAN, S. R., ELKASABANY, A., GUSTAT, J., BOERWINKLE, E. & BERENSON, G. S. 2002. Influence of the beta2-adrenergic receptor Arg16Gly polymorphism on longitudinal changes in obesity from childhood through young adulthood in a biracial cohort: the Bogalusa Heart Study. Int J Obes Relat Metab Disord, 26, 928-37.
FALLAIZE, R., MACREADY, A. L., BUTLER, L. T., ELLIS, J. A. & LOVEGROVE, J. A. 2013. An insight into the public acceptance of nutrigenomic-based personalised nutrition. Nutr Res Rev, 26, 39-48.
FENECH, M., EL-SOHEMY, A., CAHILL, L., FERGUSON, L. R., FRENCH, T. A., TAI, E. S., MILNER, J., KOH, W. P., XIE, L., ZUCKER, M., BUCKLEY, M., COSGROVE, L., LOCKETT, T., FUNG, K. Y. & HEAD, R. 2011. Nutrigenetics and nutrigenomics: viewpoints on the current status and applications in nutrition research and practice. J NutrigenetNutrigenomics, 4, 69-89.
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FERGUSON, J. F., PHILLIPS, C. M., MCMONAGLE, J., PÉREZ-MARTÍNEZ, P.,
SHAW, D. I., LOVEGROVE, J. A., HELAL, O., DEFOORT, C., GJELSTAD, I. M.,
DREVON, C. A., BLAAK, E. E., SARIS, W. H., LESZCZYŃSKA-GOŁABEK, I., KIEC-
WILK, B., RISÉRUS, U., KARLSTRÖM, B., LOPEZ-MIRANDA, J. & ROCHE, H. M.
2010. NOS3 gene polymorphisms are associated with risk markers of
cardiovascular disease, and interact with omega-3 polyunsaturated fatty acids.
Atherosclerosis, 211, 539-44.
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