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Genetically personalised nutrition has been shown to improve physical performance, help lose fat faster and motivate an individual to make long-term dietary changes that lead to an improvement in the health of that individual.

Clinically proven to improve performance

Female athlete exercising

Frontiers in nutrition journal: Sport Nutrigenomics: Personalized Nutrition for Athletic Performance. Front. Nutr., 19 February 2019

Female athlete exercising in park

Nutrition Journal: Arkadianos, I., Valdes, A.M., Marinos, E. et al. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J 6, 29 (2007).

Male and Female athletes exercising

Nutrition Journal: Arkadianos, I., Valdes, A.M., Marinos, E. et al. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J 6, 29 (2007).

DNA base Pairs

Your genetic variants impact your nutrition requirements

Our genes play an important role in how well we process, metabolise, use and store nutrients. When following a normal or ‘balanced’ diet (i.e. nutrient quantities prescribed by NRV and DRI), specific genetic variants can reduce your body’s ability to absorb or make active forms of certain nutrients, which may potentially lead to lower levels or deficiencies and reduced physical and mental performance as a consequence.

References

Genomics in Personalized Nutrition: Can You “Eat for Your Genes”?
Veronica A. Mullins 1, William Bresette 1 , Laurel Johnstone 2, Brian Hallmark 2 and Floyd H. Chilton 1,2

Your genetic variants impact your nutrition requirements

Our genes play an important role in how well we process, metabolise, use and store nutrients. When following a normal or ‘balanced’ diet (i.e. nutrient quantities prescribed by NRV and DRI), specific genetic variants can reduce your body’s ability to absorb or make active forms of certain nutrients, which may potentially lead to lower levels or deficiencies and reduced physical and mental performance as a consequence.

Illustration of how a key variant in the MTHFR gene reduces folate (vitamin B9) bio-availability*

*the proportion of nutrient that enters into blood circulation, so is able to have an active effect

References

Homocysteine and MTHFR Mutations, Stephan Moll, Elizabeth A. Varga 7 Jul 2015 Circulation. 2015;132:e6–e9.

Guinotte CL, Burns MG et. Al.. Methylenetetrahydrofolate reductase 677C-->T variant modulates folate status response to controlled folate intakes in young women. J Nutr. 2003 May;133(5):1272-80. doi: 10.1093/jn/133.5.1272. PMID: 12730409.

Solis C, Veenema K, Ivanov AA, et al. Folate intake at RDA levels is inadequate for Mexican American men with the methylenetetrahydrofolate reductase 677TT genotype. J Nutr. 2008;138(1):67-72. doi:10.1093/jn/138.1.67

Find out more about how NGX and genetically personalised nutrition can help achieve your goals

What do your genes say about you?

Take our DNA Nutrition Test and discover what your personal nutrition should ideally look like for your genes and body type with this comprehensive genetic test and 30-page personal nutrition report.

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The genes we test for

To understand your unique nutritional requirement, our DNA Nutrition test analyses the following panel of genes.

Find out more about the genes and related nutrients below:  

MTHFR

Description:
The MTHFR gene plays an important role in folate (vitamin B9) metabolism. The test is used to identify variations in two specific regions of the MTHFR gene - C677T and A1298C that determine the level of MTHFR enzyme activity and the corresponding ability to utilise folate.

MTHFR – C677T

  • TT: May reduce MTHFR function by nearly 80%
  • CT: May reduce MTHFR function by 40%
  • CC: Normal MTHFR Activity

MTHFR – AA1298C

  • CC: May significantly reduce MTHFR activity
  • CT: May slightly reduce MTHFR activity
  • TT: Normal MTHFR activity

RFC1

Description:
The RFC1 gene is a transporter of folate and is involved in the regulation of intracellular concentrations of folate. Variants on this gene are associated with reduced ability to take up, retain, and metabolise folate.

  • AA: Associated with higher levels of folate
  • GA: Associated with higher levels of folate
  • GG: Associated with reduced levels of folate

TCN2

Description:
The TCN2 gene provides instructions for making a protein called transcobalamin. This protein transports vitamin B12 from the bloodstream to cells throughout the body.

  • GG: May significantly reduce the efficiency of B12 transport
  • CG: Can slow down the transport of B12 into cells
  • CC: Normal TCN2 function

VDR

Description:
The VDR gene provides instructions for making the Vitamin D receptor (VDR) receptor, which allows the body to respond to vitamin D. This test is used to identify variations in two specific regions of the VDR gene to determine the level of response.

VDR – rs731236

  • TT: Reduced ability to absorb vitamin D
  • CT: Reduced ability to absorb vitamin D
  • TT: Normal ability to absorb vitamin D

VDR – rs1544410

  • GG: Good Vitamin D Receptor sensitivity
  • GA: Reduced Vitamin D receptor sensitivity
  • AA: Reduced Vitamin D receptor sensitivity

CYP1A2

Description:
CYP1A2 plays an important role in the body detoxification process and how we process and eliminate caffeine.
Individuals who carry one or more CYP1A2*1C alleles are slow caffeine metabolisers.

  • AA: Fast metaboliser of toxins and caffeine
  • AC: Intermediate metaboliser of toxins and caffeine
  • CC: Slow metaboliser of toxins and caffeine

CAT, SOD2 & GXP1

Description:
CAT, SOD2 and GPX1 genes provide instructions for making proteins and enzymes (such as antioxidants) that protect against and breakdown free radicals, which cause damage to healthy cells and DNA.

CAT

  • TT: Reduced capacity to neutralise free radicals
  • CT: Moderately reduced capacity to neutralise free radicals
  • CC: Normal capacity to reduce free radicals

SOD2

  • GG: Reduced capacity to neutralise free radicals by 39%
  • GA: Moderately reduced capacity to neutralise free radicals
  • AA: Normal capacity to reduce free radicals

GXP1

  • TT: Reduced capacity to neutralise free radicals
  • CT: Moderately reduced capacity to neutralise free radicals
  • CC: Normal capacity to reduce free radicals

IL6

Description:
The Interleukin-6 (IL-6) gene is associated with the synthesis of IL-6, a multifunctional cytokine that regulates immune responses such as inflammation by secreting substances to influence other cells.

  • GG: Increased cytokine levels
  • CG: Moderately increased cytokine levels
  • CC: Normal cytokine levels

TNF

Description:
Tumour Necrosis Factor (TNF) helps regulate the immune response involved in inflammation. Variants on TNF are associated with an overactive immune response and susceptibility to a range of inflammatory health conditions.

  • AA: Increased risk of producing excessive Tumour Necrosis Factor
  • AG: Moderately increased risk of producing excessive Tumour Necrosis Factor
  • GG: Normal TNF activity and immune response

APOA5

Description:
Apolipoprotein A5 (APOA5) is involved in the regulation of triglyceride (the most common form of fat in the body) blood plasma levels and the subsequent levels of α-tocopherol (a form of vitamin E).

  • CC: Significantly reduced levels of a-tocopherol in plasma
  • CA: Slightly reduced levels of a-tocopherol in plasma
  • AA: Normal levels of a-tocopherol in plasma

CYP4F2

Description:
CYP4F2 is one of the enzymes known to mediate vitamin E metabolism in humans.

  • CC: Significantly reduced levels of a-tocopherol in plasma
  • CA: Slightly reduced levels of a-tocopherol in plasma
  • AA: Normal levels of a-tocopherol in plasma

BC01

Description:
The BC01 gene converts beta-carotene (a precursor of vitamin A) into vitamin A so that it can be used by the body.
Variants on the BCO1 gene can reduce your ability to convert beta-carotene by more than 50 percent. This test is used to identify variations in two specific regions of the BC01 gene to determine how well you convert beta-carotene.

BCO1 - rs12934922

  • CC: Likely to be poor at converting beta-carotene to vitamin A
  • AC: Slightly reduced ability to convert beta-carotene to vitamin A
  • AA: Normal ability to convert beta-carotene to vitamin A

BCO1 - rs7501331

  • CC: Likely to be poor at converting beta-carotene to vitamin A
  • CT: Slightly reduced ability to convert beta-carotene to vitamin A
  • TT: Normal ability to convert beta-carotene to vitamin A

GSTT1 & GSTM1

Description:
GSTT1 and GSTM1 belong to the glutathione transferase (GST) gene family which use glutathione (a super antioxidant) to bind toxins for removal from the body in phase 2 of the detoxification process.

GSTM1

  • Deleted – gene deletion resulting in complete absence of GSTM1 activity
  • Inserted – normal function of GSTM1

GSTT1

  • Deleted – gene deletion resulting in complete absence of GSTT1 activity
  • Inserted – normal function of GSTT1

LCT

Description:
The LCT gene provides instructions for making an enzyme called lactase. This enzyme helps to digest lactose, a sugar found in milk and other dairy products.

  • CC – Likely to be lactose intolerant
  • CT – Likely to be lactose tolerant
  • TT – Likely to be lactose tolerant

HLA-DQA2/8

Description:
The HLA-DQA2/8 gene provides instructions for making a protein that plays a critical role in the immune system. Variants on HLA genes are associated with auto-immune conditions including Coeliac Disease, which is an inability to digest gliadin, the component of gluten found in wheat, rye and barley.

  • AA: Highest risk of developing Coeliac Disease and more likely to be gluten intolerant
  • AG: Slightly increased risk of developing Coeliac Disease and gluten intolerance
  • GG: Not likely to develop Coeliac Disease or gluten intolerance

Simply following government recommended dietary allowances is not going to give you what you specially need to best realise your health and fitness goals:

'Dietary reference values, e.g. recommended dietary allowance (RDA) are designed for the general population and based on different metabolic outcomes, are not optimised for genetic subgroups which may differ critically in the activity of transport proteins for a micronutrient and/or enzymes that require that micronutrient as a cofactor. Better health outcomes can be achieved if nutritional requirements are customised for each individual taking into consideration both his/her inherited and acquired genetic characteristics depending on life stage, dietary preferences and health status.'

Prof. Michael Fenech, of CSIRO Preventative Health National Research Flagship commented in his key 2011 paper:

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121546/

The power of nutrigenetics

We work with leading experts in the field of nutrigenetics. Together, we use the science to develop enhanced nutritional plans that put you in the strongest position to achieve your goals.

“The relationship between our genes and what we eat is becoming clearer through advances in the field of nutrigenetics - once an individual has had their genetic profile determined, they can optimise their daily nutritional intake and achieve enhanced physical and cognitive performance.”

— Dr. Vimal Karani, Associate Professor of Nutrigenetics & Nutrigenomics, University of Reading

OLGA HAMILTON

Registered Nutritional Therapist, FdSc, DipION, PGDip Nutritional Medicine, BA (Hons), mBANT,
CNHC Registered

PROFESSOR HELEN ROCHE

Human Nutrition & Molecular Medicine. Bsc, PHD, Msc

PROFESSOR MICHAEL MÜLLER

Professor of Nutrigenomics and Systems Nutrition.PHD, DipLON, Bsc

DR. VIMAL KARANI

Associate Professor of Nutrigenetics & Programme Director for Food and Nutritionial Sciences PHD

What do your genes say about you?

Take our DNA Nutrition Test and discover what your personal nutrition should ideally look like for your genes and body type with this comprehensive genetic test and report.

Sold out

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Happiness guaranteed!

We are confident that you will love NGX and experience real gains and benefits from using our products. However, if after 30 days you are not satisfied, we will give you your money back. No questions asked.