DNA Health® is a genetic test that provides unique insights into your health and your susceptibility to chronic diseases. Personalise your diet, supplement, and lifestyle recommendations for optimal health, improved longevity, and prevention of disease.
About This Test
The selection of genes included in the DNA Health test have multiple peer review studies examining how variations in these genes contribute to cellular health, and ultimately risk for chronic diseases of lifestyle.
The DNA Health report enables the personalisation of diet, nutritional and supplement recommendations according to your own unique genetic profile.
The DNA Health test is designed to optimise well-being and health by personalising lifestyle and diet choices and, where necessary, using supplements tailored to offset any particular nutritional deficit based on specific gene variants.
The DNA Health approach assists the healthcare practitioner in establishing the optimal nutrition necessary for good health, longevity and disease risk mitigation. Diet is a key factor in determining genomic stability as it impacts on all relevant pathways: exposure to dietary carcinogens, biotransformation, DNA repair and synthesis, and apoptosis. Current recommended dietary allowances for vitamins and minerals are based largely on the prevention of diseases of deficiency. However, because diseases of lifestyle are partly caused by damage to DNA it stands to reason that we should focus our attention on defining optimal requirements of key minerals and vitamins for preventing genomic instability.
Additional attention should be paid to individuals with genetic polymorphisms that alter the bioavailability of specific micro-nutrients and the affinity of specific key enzymes for their micro-nutrient co-factor.
- Highlights specific metabolic pathways that may require extra support
- Provides recommendations that involve optimisation of quantities of certain nutrients, vitamins and minerals
- Suggests whether an individual is better able to reduce their cholesterol levels through diet, as opposed to through medication
- Provides an indication of the degree of susceptibility to the harmful effects of carcinogens ingested in the diet
The DNA Health Test Report provides:
- The level of impact of any genetic variants identified
- An explanation of their impact on health
- Appropriate nutritional and lifestyle recommendations
The results are divided in sections of key metabolic function, so that genetic weaknesses and strengths within a functional area can be easily identified.
DNA Health® analyses 45 different genes to build individual health profiles based on genetics, determine unique needs and predispositions to disease, and create precise requirements unique to each person.
The test offers information to build tailored gene-based diet plans, including specific dietary goals for vitamins, minerals, phytochemicals, foods, and unique supplementary recommendations.
The 45 genes tested offer insight into seven different biological processes to identify health and predisposition to disease. These include heart disease, B vitamins (cell renewal and DNA), oxidative stress, bone health, detoxification, inflammation and insulin resistance. The results provide clear interpretations for useful lifestyle and dietary responses.
Gene variations associated with metabolic and biological processes
LPL: Removes lipids from the circulation by hydrolysing triglycerides into free fatty acids.
CETP: Plays a key role in the metabolism of HDL and mediates the exchange of lipids between lipoproteins.
APOC3: Plays an important role in cholesterol metabolism.
APOE: Is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. Affects antioxidant requirement.
MTHFR: Directs folate from the diet either to DNA synthesis or homocysteine re-methylation.
MTR: Catalyses the re-methylation of homocysteine to methionine.
COMT: Catalyses the transfer of a methyl group from S-adenosylmethionine to catecholamines, including the neurotransmitters dopamine, epinephrine, and norepinephrine.
MTRR: Catalyses methylcobalamin, which is essential for maintaining adequate intracellular pools of methionine. It is also responsible for maintaining homocysteine concentrations at non-toxic levels.
CBS: Catalyses the conversion of homocysteine to cystathionine and is directly involved in the removal of homocysteine from the methionine cycle.
CYP1A1: The cytochrome P450 enzyme converts environmental pro-carcinogens to reactive intermediates, which are carcinogenic.
GSTM1: Influences Phase II detoxification. It is responsible for the removal of xenobiotics, carcinogens, and products of oxidative stress.
GSTP1: Influences the metabolism of many carcinogenic compounds.
GSTT1: A member of a super family of proteins that catalyses the conjugation of reduced glutathione.
NQO1: Quinone Reductase is primarily involved in the detoxification of potentially mutagenic and carcinogenic quinones derived from tobacco smoke, diet and oestrogen metabolism.
IL-6: Plays a crucial role in inflammation by regulating the expression of C reactive protein (CRP).
TNF-A: TNFa is a pro-inflammatory cytokine, secreted by both macrophages and adipocytes, which has been shown to alter whole body glucose homeostasis, and has been implicated in the development of obesity, obesity-related insulin resistance and dyslipidemia.
Food Responsiveness and Sensitivity
MCM6: Associated with adult hypolactasia.
FADS1: Influences blood fat concentrations by affecting desaturase enzyme efficiency.
CYP1A2: This detoxification enzyme influences the ability to metabolise caffeine.
ACE & AGT: Part of the renin-angiotensin system and response to salt.
HLA DQ2/DQ8: Major genetic predisposition for coeliac disease
BC01: Catalysing carotenoids to retinal (vitamin A)
CYP2R1: Conversion of vitamin D to 25(OH)D
FUT2: Vitamin B12 absorption and transport
GSTT1: Contributing to glutathione-ascorbic acid (vitamin C) antioxidant cycle
HFE: Regulates iron absorption by regulating the interaction of the transferring receptor with transferrin. Hereditary haemochromatosis results from defects in the HFE gene.
eNOS: Influences vascular tone and peripheral vascular resistance. It also has vaso-protective effects by suppressing platelet aggregation, leukocyte adhesion and smooth muscle cell proliferation.
MnSOD/SOD2: Has vital anti-oxidant activity within the cell, especially within the mitochondria. It destroys the radicals that are normally produced within cells.
VDR: Has a profound influence on bone density.
COL1A1: Influences the ratio of collagen-alpha chains produced by bone cells, affecting bone mineralisation of bone and bone strength.
PPARG: Involved in adipocyte differentiation. It is a transcription factor activated by fatty acids, and is also involved in the regulation of glucose and lipid metabolism.
TCF7L2: Influences blood glucose homeostasis – both insulin secretion and resistance.
FTO: Influences susceptibility to obesity and risk for type 2 diabetes.
SLC2A2: Facilitates glucose induced insulin secretion and is involved in food intake and regulation.
In order to assist interpreting the DNA Health report in a succinct manner, we have developed a protocol as well as summary outcome tables highlighting priority areas on which to focus. With regards to the protocol for report interpretation, this can be described as the “3-3-3 rule”.
The first step in the protocol is to identify the top three biological areas where there is the most amount of genetic variation. This can be done by focusing on the genotypes in each area that reflect moderate and high impact factors.
The second step is to provide the top three personalised diet and lifestyle interventions based on the priority areas identified.
Next, is to establish any supplementation that may be required based on the priority areas. Lastly, the practitioner can be guided on the follow up phenotypic, or biochemical tests, to recommend based on the genetic weaknesses and priority areas that were established. This protocol can then be used in a holistic manner to provide personalised recommendations.
Priority Table – Biological Area
The priority table offers a guideline to practitioners to assist in identifying the key biochemical pathways on which to focus their intervention.
Based on the genetic variations the patient carries in each biological area, an algorithm determines the significance of the area as either low, moderate, or high priority. Some genetic variations carry a stronger weighting compared to others.
This table provides a summarised overview of the biological pathways based on the genetics of the patient.
Report Summary – What should I do?
In this section of the DNA Health report, the top priority area’s are listed, based on the patients’ genetics results that led to ‘high priority’ biological area outcomes, or ‘moderate priority’ if no high priority areas are noted.
Each priority area is briefly explained, and practical, patient-friendly diet and lifestyle recommendations are summarised.
The report summary translates the DNA Health test information into the key take-home messages for the patient, based on their unique genotype results.
The summary table provides a snapshot of all the genes tested in the DNA Health test. The genes are categorised according to biological pathway, and the impact factor according to genotype is also shown. This is a useful table to be able to quickly identify where the focus of the intervention is going to be.
The genes in the DNA Health test are divided according to the main biological pathways in which they function, thus providing some guidance and insight for the practitioner when identifying which areas require support.
In the “gene name” column, the gene name is listed. Further on in the report, the full name of the gene is given and describes the protein for which it encodes.
The genetic variation column provides the name of the specific genetic variation that is being analysed. The name of the variation is given according to that found in the literature.
In this column, the patient’s genotype result is given, according to what was analysed in the laboratory.
The gene impact column will reflect an impact factor based on the patient’s genotype result. This impact factor could either be a ‘beneficial impact’ (designated by a tick), a ‘no impact’ (a clear circle), ‘low impact’ (one coloured circle), a ‘moderate impact’ (two coloured circles) or a ‘high impact’ factor (three coloured circles). The impact factor is a qualitative assignation by the laboratory, that has been assigned based on the scientific literature available. The ‘no impact’ factor means that, based on that genotype, the gene should be encoding for a ‘normal’ functioning protein and thus there is no change in intervention based on that genotype. When the impact factor is a moderate or high impact, it means that the genotype has been related to an altered function/expression of the protein and thus an increased risk for a weakness in the corresponding biological pathway, requiring a personalised intervention.
It is important for the practitioner to take note of the areas where there are moderate and high impact factors.
Biological Area Results
The DNA Health report goes on to give further detail on each biological area. For each biological area in the DNA Health report, a result table is given. The result table provides the genes, corresponding variations, the genotype result, as well as the impact factor per genotype.
The DNA Health report provides the practitioner (and patient) with detail of each gene tested. In this section, the gene being tested is described in more detail, thus offering insight into the importance of the gene in the biological pathway and its relevance to health.
In this section, the DNA Health report will provide the genotype result of the client and, when there is a variant detected that leads to a change in how the gene may affect an individual’s health, a description of the relevance of the variation will be given. Actionable, genotype-specific information to intervene appropriately is also given.
Based on the priority level of the biological area, according to an individual’s genotype results, a summary of personalised nutrigenetic and nutrigenomic recommendations is provided.
According to the individual’s genotype results and priority level of the biological area, appropriate biochemical and phenotypic tests will be recommended. These tests are helpful indicators of the patient’s ‘here and now’ and can be used to monitor the patient’s progress after the intervention is given.
Dron 2017. Genetics of Triglycerides and the Risk of Atherosclerosis.
Gibson 2018. Lipid and Non-Lipid Factors Affecting Macrophage Dysfunction & Inflammation in Atherosclerosis.
Song 2015. Associations of the APOC3 rs5128 polymorphism with plasma APOC3 and lipid levels, a meta-analysis.
Mirmiran 2017. Genetic variations of cholesteryl ester transfer protein and diet interactions in relation to lipid profile. v2.
Pirim 2013. Lipoprotein Lipase Gene Sequencing and Plasma Lipid Profile.
Mahley 2009. Apolipoprotein E, structure determines function, from atherosclerosis to Alzheimerʼs disease to AIDS.
Luo 2019. Associations of PON1 rs662 polymorphism with circulating oxidized low-density lipoprotein and lipid levels, a systematic review and meta analysis.
Liu 2013. Role of One-carbon Metabolizing Pathway Genes and Gene-Nutrient Interaction in the Risk of Non-Hodgkin Lymphoma.
Kang 2014. Association of the A1298C polymorphism in MTHFR gene with ischaemic stroke.
Ganz 2016. Genetic impairments in folate enzymes increase dependence on dietary choline.
Mandaviya 2014. Homocysteine and DNA methylation.
Stover 2011. Polymorphisms in 1-Carbon metabolism epigenetics & folate related pathologies.
Gonzales 2018. Gene-environment interactions and predictors of breast cancer in family-based multi-ethnic groups.
Colsen 2017. The impact of MTHFR 677 CT genotypes on folate status.
Zahid 2014. Unbalanced Estrogen Metabolism in Ovarian Cancer.
Wu 2016. Role of SNPs as related to 1-carbon metabolism Vitamin B6 & gene nutrient interactions in maintaining genomic stability.
Wang 2015. Role of IL6 SNPs in the risk of CAD.
Tan 2018. Nutrients & oxidative stress.
Cormier 2016. Expression and Sequence Variants of Inflammatory Genes; Effects on Plasma Inflammation Biomarkers Following a 6-Week Supplementation with Fish Oil. v2.
Verdile 2015. Inflammation & Oxidative stress. The molecular connectivity between insulin resistance, obesity & AD.
Kornman 2006. Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging.
Kakkoura et al. 2015 MnSOD and CAT polymorphisms modulate the effect of the Mediterranean diet on breast cancer risk among Greek-Cyp
Avelar 2015. Oxidative stress in the pathophysiology of metabolic syndrome
Karunasinghe 2012. Serum selenium and single-nucleotide polymorphisms
Zheng 2018. Replication of a gene diet interaction at CD36 NOS3 & PPARG in response to n3 FA supplements on blood lipids. Double blind RCT.
Saha 2017. Correlation between Oxidative Stress, Nutrition and Cancer Initiation
Da Costa 2012. Nutrigenetics and Modulation of Oxidative Stress.
Abellan 2019. Sorting out the Value of Cruciferous Sprouts as Sources of Bioactive Compounds for Nutrition and Health. v2 (1).
Yuan 2016. 2-Phenethyl isothiocyanate, glutathione S-transferase M1 and T1 polymorphisms, and detoxification of volatile organic carcinogens and toxicants in tobacco smoke.
Lee 2008. Cruciferous vegetables, the GSTP1 Ile105Val genetic polymorphism, and breast cancer risk.
Lajin & Alachkar 2013. The NQO1 polymorphism C609T (Pro187Ser) and cancer susceptibility, a comprehensive meta-analysis.
Hodges & Minich 2015. Modulation of Metabolic Detoxification Pathways Using Foods and Food-Derived Components
Ding 2018. Cytochrome P450 1A1 gene polymorphisms and cervical cancer risk A systematic review and meta-analysis.
Grygiel-Gorniak 2014. Peroxisome proliferator-activated receptors and their ligands, nutritional and clinical implications – a review. v2.
Wagner 2014, Untangling the interplay of genetic and metabolic influences on beta-cell function.
Barucija, 2018. Decade of the Common FTO Rs9939609 Polymorphism A Systematic ReviewIndira.
Michau 2013. Mutations in SLC2A2 Gene Reveal hGLUT2 Function in.
Konig 2018. Specific Collagen Peptides Improve Bone Mineral.
Thakkinstian 2004. Haplotype analysis of VDR gene polymorphisms. A meta-analysis.
Kanis 2013. European Guidance For The Diagnosis and Management of Osteoporosis in postmenopausal women.
Senderovich 2017. The Role of Exercises in Osteoporotic Fracture Prevention.
Tye-Din 2015. Appropriate clinical use of human leukocyte antigen typing for coeliac disease, an Australasian perspective.
Lukito 2015. From lactose intolerance to lactose nutrition.
Oniki 2016. The longitudinal effect of the aldehyde dehydrogenase 2 variant and non-alcoholic fatty liver disease.
Freire 2018. Daily sodium intake influences relationship between angiotensin converting enzyme gene insertion,deletion polymorphism and hypertension. v2 (1).
de Caterina 2016. Moving towards Specific Nutrigenetic Algorithms – Caffeine, Genetic Variation and Cardiovascular Risk.
Chilton 2014. Diet-Gene Interactions and PUFA Metabolism-A Potential Contributor to Health Disparities and Human Diseases.
Radford-Smith 2018. Haemochromatosis – A clinical update for the practicing physician.
Turner 2018. Interactions between Bitter Taste, Diet and Dysbiosis, Consequences for Appetite and Obesity.
Cahill 2009. Functional genetic variants of glutathione S-transferase protect against serum ascorbic acid deficiency.
Feigl 2014. The Relationship between BCMO1 Gene Variants and Macular Pigment Optical Density in Persons with and without Age-Related Macular Degeneration. v2.
Nissen 2014. Common Variants in CYP2R1 and GC Genes Predict Vitamin D Concentrations in Healthy Danish Children and Adults.
Ganz 2012. Vitamin D binding protein rs7041 genotype alters vitamin D metabolism in pregnant women.
Allin 2017. Genetic determinants of serum vitamin B12 and their relation to body mass index.
The DNA and the original sample material are destroyed after 3 months, so that there are no names or other identifiers on the samples. The samples are analysed only for the SNPs that are included in the tests at DNALife, and no other research or analyses are performed without a separate permission from the patient. We do not give or sell the results to any third parties.
Please note, the price of this test includes home delivery of test kit and a DHL home collection and shipping to Nordic Laboratories OY in Finland where the samples are processed.
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