Review Article

Nutrigenetics—Personalized Nutrition in the Genetic Age

Emma L. Beckett1*, Patrice R. Jones2, Martin Veysey3 and Mark Lucock2
1School of Medicine & Public Health, University of Newcastle, Australia;
2School of Environmental & Life Sciences, University of Newcastle, Australia; 3Hull York Medical School, UK

Abstract

Diet is an important modifiable determinant of disease, and it is becoming clear that diet and genetic risk factors
are interactive in determining risk for diseases such as cardiovascular disease, diabetes and cancers. Advances in
technology have improved our understanding of gene-nutrient interactions, and lead to the development of nutri-
genetics, personalized nutrition based on genetics. While evidence is strong for some associations, others remain
unclear. As such, the implementation of nutrigenetics remains controversial. While some argue it is not ready for
clinical use, it has also been argued that nutrigenetics is unfairly held to a higher standard than traditional nutri-
tion research. Despite the future promise of nutrigenetic testing for improving health outcomes, several barriers
in science, technology, acceptance and ethics exist to its implementation. Gene-nutrient associations have been
identified in a number of lifestyle-associated diseases, and better understanding of these relationships may lead
to improved health outcomes. However, the success of nutrigenetics is not only dependent on the strength of the
science, but in consumer acceptance and uptake. This narrative review provides an overview of the current land-
scape for nutrigenetics in relation to key disease states, and addresses the potential barriers to implementation.

Introduction the individual.6

Current public health initiatives and nutritional guidelines, both
Diet is an important lifestyle exposure and is the largest modifiable on a global and national scale, are generic recommendations. These
determinant of risk for non-communicable disease, including car- recommendations are based on population estimates of required in-
diovascular disease, diabetes and some cancers. Importantly, diet takes and the prevention of deficiency.7 However, it is well known
is an ongoing, essential and unavoidable exposure for all people that there is considerable variance in how individuals respond to
throughout life. Worldwide, non-communicable diseases account the same nutritional stimuli, and this alters the outcomes in terms
of benefits and risks. The broader concept of personalized nutrition
for 43% of the burden of disease currently, and the World Health
is not new, and population guidelines recognize some of this vari-
Organization predicts they will represent 60% of the disease bur-
ance in limited cases, with some recommendations tailored to age,
den and 73% of all deaths by 2020.1 The number of people with
sex, or conditions such as pregnancy.8 Ranges of recommended in-
diabetes worldwide rose to 422 million in 2014,2 cardiovascular
take values also account for a portion of this biological variance, as
disease is the leading cause of death,3 and incidence of cancers re-
do specific recommendations related to the diagnosis of particular
lated to dietary risk factors, such as colorectal and esophageal can-
conditions, such as allergies or chronic diseases such as diabetes,9
cers, are also rising.4 Today, most of the world’s population lives
cardiovascular disease and cancers.10,11
in a country where overweight and obesity kills more people than
However, population guidelines, even with stratification, may
underweight.5 Diet is, therefore, considered as a primary preven-
not meet the needs of all individuals equally in terms of optimizing
tion strategy to reduce the risk for chronic diseases. However, as
health outcomes and reduction of disease risk.12,13 With improv-
highlighted by the “Rose prevention paradox”, a lifestyle measure
ing technology and advances in our understanding of genetics, the
that reduces risk in an entire population may offer little benefit to
concept of personalized nutrition via nutrigenetics has emerged,
where dietary recommendations can take into account the variance
between individuals by tailoring to each person’s unique genet-
Keywords: Nutrigenetics; Personalized nutrition; Genetics; Nutrition.
Abbreviations: FTO, fat mass and obesity associated gene; GWAS, genome-wide
ics.13–15 While personalized nutrition based on genetics has sig-
association studies; TCF7L2, transcription factor 7-like 2 gene. nificant future promise, there are many challenges in translating
Received: August 01, 2017; Revised: October 23, 2017; Accepted: November 07, scientific advances into successful strategies for managing dietary
2017 intake and diet-related health outcomes on a large scale. These is-
*Correspondence to: Emma Beckett, School of Medicine and Public Health, Uni-
sues include the translation of reductionist research outcomes into
versity of Newcastle, Chittaway Rd, Ourimbah, NSW 2258, Australia. Tel: (02) 4348 practice, public perception and the likelihood of uptake, issues of
4158, E-mail: [email protected]
How to cite this article: Beckett EL, Jones PR, Veysey M, Lucock M. Nutrigenet-
privacy and ethics, commercialization, and the level of evidence
ics—Personalized Nutrition in the Genetic Age. Exploratory Research and Hypoth- required before the transition from traditional approaches is ben-
esis in Medicine 2017;2(4):109–116. doi: 10.14218/ERHM.2017.00027. eficial. It is important to consider if these challenges can be met

Exploratory Research and Hypothesis in Medicine 2017 vol. 2 | 109–116

Copyright: © 2017 Authors. This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 4.0 International License
(CC BY-NC 4.0), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Explor Res Hypothesis Med Beckett E.L. et al: Nutrigenetics in personalized nutrition

and whether personalized nutrition can produce improved health An early application of nutrigenetics has been the diagnosis of
outcomes and socioeconomic benefits relative to conventional ge- conditions caused by single polymorphisms, such as genetic lac-
neric dietary advice. tose intolerance and phenylketonuria.25 In many cases, genetic
testing is not required for monogenic conditions, as the phenotype
is sufficient basis for deciding on the appropriate dietary interven-
Gene-nutrient interactions tion. However, for complex polygenic traits, such as cardiovas-
cular disease or diabetes, it is much more challenging to find evi-
Dietary factors can interact with the genome in a number of ways. dence for the involvement of genes in disease development. These
Firstly, genetic variance can influence nutritional status by modu- conditions have genetic risk factors, dietary risk factors, and these
lating nutrient intake, uptake and metabolism. This is referred to as risks are modified by the interaction between the two and other
nutrigenetics.16 Furthermore, nutrients can regulate gene expres- lifestyle factors.26,27 As such, it is difficult to elucidate the involve-
sion in a number of ways. Some nutrients can directly regulate ment and modifiable component of the interactive factors, and a
gene expression via the interaction of stimulated receptors with medical model of nutrigenetics, held to a clinical genetics level of
response elements in the genome, acting as nuclear transcription evidence, may not be appropriate.
factors. This direct interaction is referred to as nutrigenomics.16
Nutrients can also modify gene expression indirectly, via modula-
tion of gene regulatory factors such as epigenetic marks, including Cardiovascular disease
the involvement of DNA methylation and miRNA.17 Importantly,
nutrigenetics can impact upon the nutrigenomic and epigenetic Cardiovascular disease has both genetic and dietary risk factors,
responses and the sum of these events can modify disease risk.18 and risk is likely modified by the interactions between the two.28
With improving technology, and completion of ground-breaking The predictive value of single polymorphisms may be small rela-
research, such as the human genome project, we are learning more tive to known risk factors, such as family history of cardiovascular
about gene-nutrient interactions. This has led to a dramatic increase disease.29 Multiple minor genetic differences could be modulated
in research in this area. However, there are significant challenges to by multiple dietary factors, resulting in multiple minor changes
the translation of genetic data into personalized dietary advice, and in gene expression. Depending on the interactions, these variables
it is questionable as to whether our level of understanding is suf- could result in negligible changes in final phenotype and therefore
ficient for personalized nutrigenetics to progress. The majority of disease risk; however, they could also accumulate to significantly
the published data on gene-nutrient interactions stem from observa- alter phenotype and outcomes. We do not yet have enough evi-
tional studies and as such cannot definitively demonstrate cause and dence to elucidate the mechanisms and outcomes of these complex
effect, and results can often be conflicting. Purpose-specific dietary interactions, and it is likely that additional interactions remain
intervention studies conducted by genotype are needed to achieve undiscovered.30 In the future, advances in this understanding may
this. However, these are complex and expensive, and there are dif- be supported by increased research investment in whole genome
ficulties in considering multiple polymorphisms. Numerous genetic sequencing and bioinformatics initiatives, as well as improving
variants that influence nutrient metabolism have been identified, technology and reducing associated testing costs.
but it can be difficult to conclusively link single variants to the risk Homocysteine is accepted as an independent risk factor for car-
for multifactorial diseases, due to interactive and additive effects of diovascular disease,31 with homocysteine levels being inversely as-
multiple variants in defining nutrient metabolism and health out- sociated with folate levels. It has been established that the MTH-
comes. There is a need for quantitative assessment and mathemati- FR-677T allele results in the enzyme methylenetetrahydrofolate
cal modelling of multiple genetic effects. reductase having reduced activity (~35% of the MTHFR-677C
Ultimately, the most important question is whether nutrigenet- variant).32 Low folate status, therefore, impacts homocysteine levels
ics can deliver results superior to population recommendations. It more severely in individuals with the MTHFR-677TT genotype, and
has been argued that the evidence for nutrigenetics is still too im- the standard recommendations for folate intake have been shown to
mature to be used in practice.19,20 However, it has also been argued be insufficient to maintain homocysteine levels below the risk level
that nutrigenetics is often held to a higher standard of evidence in this population. It is accepted that increasing folate intake (from
than generic nutritional advice,21,22 resulting in high-quality evi- 200 µg/day to 400–600 µg/day) reduces the risk for hyperhomo-
dence for several gene-diet interactions potentially being ignored. cysteinemia in most MTHFR-677TT individuals. There is no reli-
Given the complexity of gene-nutrient interactions, and the known able evidence that these levels cause harm, and they remain below
variance in nutrition-related health outcomes, regardless of genet- the upper intake limits found in generic advice.33 As such, this is
ics, we need to consider if we have set this standard too high. Nu- an example of where personalized recommendations may result in
trition is complex and outcomes difficult to assess, with or without improved outcomes. However, this could also support the increase
a genetic component. It is, therefore, necessary to consider person- in population-wide intakes, as homocysteine levels are reduced in
alized nutrition in the same context as generic nutrition recommen- populations exposed to folic acid fortification programs.34–37
dations and not in the same context as clinical genetics.23 The response of plasma low-density lipoprotein and triacylg-
Nutrigenetic research often takes a reductionist approach to lycerols (triglycerides) to supplementation with fish oil are clear
gene-nutrient interactions, examining the interactions between examples of individual variability in response to an intervention
single polymorphisms and individual disease biomarkers, and resulting from the influence of both genetic and environmental fac-
how they are modified by single nutrients or food components.23,24 tors. In a study of fish oil supplementation in 55 males, the mean
Each individual possesses potentially hundreds of gene variants change in plasma triacylglycerol was a 35% reduction. However,
that may have nutrigenetic consequences, and each consumes their the variance of individual changes ranged from a 114% reduction
own unique complex and varied diet. Complex statistical and bio- to an 88% increase, demonstrating that the statistically significant
informatics modelling is required to integrate information on nu- reduction in the mean did not result in an improved outcome for
merous genes, biomarkers, nutrients and foods for nutrigenetics to all individuals. Similarly, the mean change for plasma low-density
deliver on its promise of improving health outcomes. lipoprotein was a 7% increase, but with the variance of change

110 DOI: 10.14218/ERHM.2017.00027 | Volume 2 Issue 4, December 2017

Beckett E.L. et al: Nutrigenetics in personalized nutrition Explor Res Hypothesis Med

ranging from a 61% increase to a 50% reduction.38,39 In the same Gene variants involved in gene-diet interactions in cancer are
cohort,38 and independently,40 it was determined that the APOE2 namely those involved in detoxifying carcinogens and repairing
genotype was related to the magnitude of response, and this re- DNA damage. The majority of these are specific to colorectal can-
sponse may also be related to sex.41 cer, which has clear links to dietary risk factors.60,61 Increased risk
Together these data suggest that while fish oil supplementation of colorectal cancer has been shown with high red meat consump-
may improve cardiovascular biomarkers for a subset of individu- tion in combination with variants in CYP2E1, CYP1B1, SULT1A1
als this is not true for all, and in some cases, it may actually be and other members of the cytochrome P450 family of detoxifying
detrimental. As such, this may be an example of where it is not ap- genes.62–64 Several other gene variants have also been implicated
propriate to produce population-based recommendations, whether in gene-diet interactions that have been shown to decrease colo-
they are public health guidelines, or used for the marketing of sup- rectal cancer risk. Notably, common variants in the vitamin D re-
plements. However, there is a lack of evidence to link the variance ceptor gene and MTHFR which codes for an important enzyme
in responses to genotype,42 and further prospective studies includ- in folate metabolism; both have been shown to decrease risk of
ing genotyping are needed to understand how personalized recom- colorectal cancer when combined with diets high in calcium/vita-
mendations could be used to overcome the variance in responses min D and folate respectively.65–67 Whilst the majority of reported
and to assess whether this ultimately impacts disease risk, as these gene-diet interactions are specific to colorectal cancers, gene-diet
interactions remain poorly understood. interactions have also been reported in progression of gastrointes-
tinal, stomach, breast, lung and prostate cancer.57
Another well-studied gene-nutrient interaction involves cruci-
Diabetes ferous vegetables, which have been linked by systematic review
with reduced lung cancer in individuals with polymorphisms in
It is known that type 2 diabetes has both dietary and genetic risk the GSTT1 and GSTM1 genes, which code for glutathione s-trans-
factors and that outcomes are dependent on the combined and/or ferases, but not in individuals without these variants.68,69 However,
interactive influence of these, and other lifestyle risk factors.43–45 it is unclear how clinically relevant these findings will prove to be,
The majority of genes implemented in the progression of type 2 as the standard public health message to eat less meat and more
diabetes relate to pathways influencing fat distribution and insulin vegetables applies regardless of genotype and is likely to be in-
sensitivity. Genetic risk scores for type 2 diabetes are robust pre- volved in the reduction of risk of multiple diseases. The benefit
dictors of disease and have been shown to interact with western of these findings, however, may be found in the development of
diets (high fat and sugar) to further predict outcomes.46 nutraceuticals for intervention in genetically at-risk individuals,
Genome-wide association studies (GWAS) have identified should a mechanism for this interaction be identified. Interac-
nearly 100 gene variants associated with modified risk for type tions have also been shown between genes and diet in measures of
2 diabetes,47 with a recent review suggesting 27 of these inter- DNA damage,70 prostate cancer risk and levels of the glutathione
act with diet to modify progression of type 2 diabetes.48 Notably, s-transferase alpha.71,72
the transcription factor 7-like 2 gene (TCF7L2), involved in Wnt
signaling, has the strongest influence on risk for type 2 diabetes.
Common variants in this gene have been shown to interact with Cognitive decline
high intake of both carbohydrate and fiber to modify risk for type
2 diabetes.49,50 Due to the direct association between obesity and APOE has been identified as a susceptibility gene for Alzheimer’s
type 2 diabetes risk, a number of gene-diet interactions modifying disease, with the e4 variant increasing risk for disease. The Risk
risk of obesity have been identified that are of relevance to type Evaluation and Education for Alzheimer’s Disease (commonly
2 diabetes. Examples include the interactions between genotypes known as REVEAL) study examined how knowing APOE e4 sta-
for the fat mass and obesity associated gene (FTO),51 PPARG,52,53 tus impacted behavior change in the adult offspring of parents with
PLIN,54 and MC4R and diet,55 which influence disease-related out- Alzheimer’s disease.73 Having a parent who suffered from the dis-
comes, such as insulin sensitivity. ease, all study participants showed a higher-than-average risk for
GWAS has also identified more than 40 independent polymor- Alzheimer’s disease, regardless of genotype; however, those car-
phisms associated with type 1 diabetes; however, the loci identi- rying the APOE e4 variant were at higher risk. Participants were
fied do not fully explain the heritability component estimated from given a numerical estimate of their risk and were then randomly
familial studies,56 suggesting that dietary and other lifestyle factors allocated into groups. Controls were not given any genotypic data,
are also involved in pathogenesis. Additional studies are needed to and the intervention groups were genotyped for APOE e4 and their
fully elucidate the role of gene-nutrient interactions in the etiology status revealed to them. Participants who were APOE e4-positive
of diabetes. had a higher overall numerical risk score.73,74 One year later, simi-
lar proportions of positive behavior changes were reported among
controls and among participants who were told that they were
Cancer APOE e4-negative; however, additional positive behavior changes
were reported approximately twice as often among participants
A plethora of genes have been linked to cancer risk and outcomes. who were told that they had the APOE e4 risk variant.73
However, few associations between gene variants and cancer risk
remain robust, or reproducible, likely due to the interactive influ-
ence of diet and other environmental factors in epidemiological Obesity
studies.57 Genome instability is a hallmark feature of cancers, with
hundreds of genes involved in maintaining genome integrity.58 Obesity is related to both dietary and genetic variables, and again
The interactions between these genes and diet indicate potential the interaction between the two are likely to be important in deter-
mechanisms by which personalized nutrition may influence cancer mining phenotype, both in terms of risk for obesity and risk for dis-
outcomes.59 eases where obesity is a known risk factor.75 GWAS has revealed

DOI: 10.14218/ERHM.2017.00027 | Volume 2 Issue 4, December 2017 111

Explor Res Hypothesis Med Beckett E.L. et al: Nutrigenetics in personalized nutrition

that body fat patterns have large genetic components, with 97 loci younger adults are the most likely to take part.96
related to fat accumulation and an additional 49 loci relating to Health has been identified as a primary motivator for undergo-
body fat distribution.76,77 Implicated genes in these loci have di- ing genetic testing,96,98 which may facilitate the uptake of nutrige-
verse roles and are involved in pathways such as those regulating netics, given that diet is a major modifiable determinant of disease.
satiety, food intake, energy metabolism and adipogenesis.76 Mo- Acceptance may also be linked to current health; for example, re-
nozygotic (i.e. identical) twins have strong similarities in the adap- spondents with high blood cholesterol or central adiposity were
tation to long-term overfeeding and in terms of weight gain and fat more likely to identify as willing than those without to undergo
distribution,78 demonstrating genetic concordance. genetic testing, in general, and specifically for dietary modifica-
Insight into genes that influence obesity has led to the calcula- tion.98 However, several possible outcomes to this are possible.
tion of genetic risk scores, the sum of obesity risk conferred by Joost et al.99 suggested that individuals identified as having a
multiple gene variants. Diet (particularly fat and energy intake) higher disease risk through genetic testing may be more motivated
has been shown to interact with genetic risk scores to alter the obe- to comply with a dietary intervention; however, it was also noted
sity risk.79 Genes implemented in diet-gene interactions in obesity that knowledge of a genetic predisposition may result in a fatalis-
namely include FTO, MC4R, APOA2, PLIN and PPARG genes. tic attitude and reduced compliance. Furthermore, Hunter et al.100
FTO is regarded as the first identified obesity gene. Common ge- reasoned that a negative result may lead to reduced motivation as
netic variance in FTO is strongly associated with increases in body individuals become reassured that they will not develop disease.
mass index, with this association shown to be enhanced by diets Communicating the nuanced nature of risk and risk modification
high in dietary fat and protein.80,81 Similar associations have been through nutrigenetics will be vital to ensure responses to informa-
found for the MC4R gene, involved in appetite regulation.82,83 tion are not detrimental to outcomes.
Gene-diet interactions in obesity have also been shown between Interestingly, in a study of familial hypercholesterolemia, par-
high saturated fat intake and APOA2, which codes for an apolipo- ticipants with the at-risk polymorphisms were less likely to believe
protein,84 and variants in PPARG, which codes for a nuclear tran- that eating a lower fat diet would reduce their cholesterol levels,
scription factor.52,85 Notably, a common polymorphism in PLIN, and more likely to believe that medication would.101 Acceptance of
which is involved in the regulation of lipid storage in adipocytes, genetic testing and personalized nutrition may not depend on the
has been shown to decrease risk of obesity when combined with actual science but on the consumers’ understanding of its implica-
a high carbohydrate intake, but increases obesity risk when com- tions for their personal health. However, following a systematic re-
bined with a low intake of this macronutrient.86 These data dem- view, Marteau et al.101 argued in addition to significant gaps in the
onstrate the difficulty in the “one-size fits all” approach to weight relevant science, there is limited evidence that nutrigenetic dietary
management, and in particular, weight loss. advice will motivate appropriate behavior changes.
In a study conducted on patients with a history of weight loss
failures, it was found that nutrigenetic screening resulted in in-
creased compliance and longer-term body mass index reductions, Technology and regulation
when compared with standard weight-loss advice.87 However, it
was also shown that the high-risk individuals had lower perceived Web-based and smartphone technologies increase product reach
behavioral control over their eating and hence felt less able to and ease of delivery, but also raise issues of data security and accu-
change their dietary habits.88 Another study found that genetic racy of information. However, the technology for offering direct-
testing increased self-confidence in the participant’s ability to lose to-consumer genetic testing has out-paced regulation for its provi-
weight, regardless of the actual result.89 sion, at times out-pacing the scientific evidence. Therefore, there
needs to be a progression of regulation and technology to ensure
consumer privacy is protected, data is appropriately stored, and
Consumer acceptance that consumers are not misled. Early practitioners of nutrigenetics
need to be mindful that inaccurate information offered prematurely
The utilization and advancement of nutrigenetics, and personal- can damage the reputation of the field. This may be exacerbated
ized nutrition more broadly, is not just dependent on the strength by the delivery of genetic information outside of a clinical setting.
of the data, elucidating mechanisms and defining the appropriate Several studies have documented concerns regarding the tech-
level of evidence required for implementation but requires public nology used to provide nutrigenetic information. These include on-
acceptance to facilitate uptake. Motivating individuals to change line privacy concerns, and the potential for information to be mis-
dietary behaviors is one of the biggest challenges for any nutri- used by insurers, employers, governments or other entities for profit
tional intervention.90 There must be ease of use and access, and a or exploitation.102–104 Advances in technology have driven the rise
perception of benefit. Genetic testing, in general, has a unique set of personalized nutrition in general and nutrigenetics specifically.
of barriers to uptake, and several of these remain in the context of This includes the advances in genetic testing technology and the
nutrigenetics, regardless of outcomes. reduction in cost, as well as the use of technology for the collection
Numerous studies have been conducted into the acceptance and dissemination of information. The expansion of internet deliv-
of genetic testing in general.91–95 Whilst testing is well accepted ery systems needs to be considered in personalized nutrition. As
and becoming routine in the cases of high penetrance single poly- oversight and regulation varies by jurisdiction, it is reasonable for
morphisms, such as the BRCA1 gene in breast cancer risk, in nu- consumers to be cautious about their privacy and future use of their
trigenetics, however, the associations are often weaker and less data. Additionally, provision of results directly to the consumer
clear.92,95 Although, attitudes vary by demographics and results may be harmful without the input of a genetic counselor.105
have been mixed. It has been reported that men are more will-
ing to undergo genetic testing,96,97 but the opposite association has
also been reported.98 It has also reported that age is a factor in Ethical considerations for implementation
acceptance of genetic testing; yet, some studies have found that
older people are more willing,97,98 while others have reported that There is significant debate surrounding whether or not the current

112 DOI: 10.14218/ERHM.2017.00027 | Volume 2 Issue 4, December 2017

Beckett E.L. et al: Nutrigenetics in personalized nutrition Explor Res Hypothesis Med

knowledge base is sufficient for ethically responsible implementa- Training Program (RTP) Scholarship from the Australian Govern-
tion of nutrigenetic testing.23,25,106,107 While there is still much to be ment.
discovered, we need to consider if we are holding nutrigenetics to
a higher standard than generic population recommendations.23 The
ethics of implementation may need to be considered on a case-by- Conflict of interest
case basis. For some gene-nutrient interactions, there is significant
evidence that for some individuals with particular genotypes there The authors have no conflict of interests related to this publication.
could be a benefit from following dietary patterns other than those
recommended by the standard guidelines; however the strength of
evidence varies depending on the association in question. The key Author contributions
question is how to proceed in the face of uncertainty. Gorman et
al.23 argue that a precautionary approach should be adopted, sug-
gesting that personalized dietary advice should be offered only in Manuscript writing (EB, PJ), design and revision (ML, MV).
cases where there is strong scientific evidence for health benefits,
followed by continued stepwise evaluation to identify unforeseen
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