How Nutrition Manipulates Our Genes

Evolutionarily speaking, every genetic polymorphism that exists must have conveyed evolutionary advantage at some point or it would not exist. For example, in the context of food scarcity, a gene that encourages calorie-dense food consumption may be an advantage.

The Human Genome Project

We have known since the 1950’s that certain inherited conditions are due to genetics such as cystic fibrosis, and it’s mostly this led to the hypothesis that all disease was due to genetics. So, the ‘Human Genome Project’ that commenced in 1990 was considered by many to be the best tool the human race would have in battling chronic disease – If genes could be identified that were causative in chronic disease, then drugs could be developed to act on these genes, preventing or mitigating conditions such as cancer, autoimmune disease or even obesity (1).

Unfortunately, this is not what transpired. As it turns out, whilst certain genes may increase your risk of specific conditions, they do not guarantee them. Individuals with high-risk disease genes may go a lifetime and never get the disease in question and those with low-risk genetics may, in fact, develop it.

So what is the determining factor?


Good or Bad Genes Depends on Context

Genes are often presented as negative or positive depending on disease outcome. But nothing is that simple – certain polymorphisms or SNPs cannot be simply “bad” or “good”, there is only biological context relative to the polymorphisms.

Evolutionarily speaking, every genetic polymorphism that exists must have conveyed evolutionary advantage at some point or it would not exist. For example, in the context of food scarcity, a gene that encourages calorie-dense food consumption may be an advantage. However, in the context of calorie abundance may be more likely to lead to metabolic disease (2) – a situation we increasingly find ourselves in today.

APOE4 is a polymorphism of the APOE gene that carries an increased risk of cardiovascular disease and cognitive decline in western populations. But the exact same polymorphism is protective of cognitive decline and carried no increased risk for heart disease within developing countries (3) or indigenous populations with a high parasitic load. It is clear that genes are only part of the picture – context is everything.

So how can we manage genes?


Why Epigenetics is Important

This refers to the expression of your genes as opposed to what is set in stone.

For example, a great epigenetic mediator is exercise. We know that if you have high-risk genes for obesity, diabetes, or heart disease your risk for all these diseases is reduced by partaking in regular appropriate exercise (4).

So genes alone don’t determine outcomes, they signal for specific biochemistry that may be pathological in certain settings. Though your genes can never be changed, how they express themselves can be. I like to think of it like this – whilst your genes may load the gun, your environment (context) pulls the trigger.

So where does nutrition come in?


How Nutrition Affects Epigenetics

Your genetics determine how much of a specific protein, enzyme, lipid, neurotransmitter, receptor, or other molecules are produced and broken down within your body. But, the raw materials you give the body that make this possible, alongside your genetics determines your biochemistry. And how these 2 things interact is Epigenetic expression.

For example, SNP variants of the FADS1 haplotype gene may cause a low conversion of alpha-linoleic acid (ALA, an omega 3 fat found in vegetables or nuts which can’t be used by your body as it is) to eicosapentaenoic acid (EPA, an anti-inflammatory fat the body can use). This means that vegetable sources of ALA alone may not be sufficient for that individual’s omega 3 requirements (5), and animal sources of EPA may need to be included. This person on a vegetarian diet may not thrive but give them the right environment and this gene SNP is no longer a problem.

What can you do?


Eating and Living For Your Genetics

Although there is nothing you can do about your genes – even genes that give the highest risks for disease do not determine outcomes – how you live and eat is more important.

You want to eat a diet that exposes you to all the required macro and micronutrients in the forms and amounts that will enable your genes to best express themselves for health.

This sounds complicated but it needn’t be.

Taking a gene test with a practitioner who is literate in genetic polymorphisms and how this would relate to lifestyle and nutrition is ideal for formulating a plan that may optimise your epigenetics for the rest of your life.


  1. Marshall J. Human Genome Project. In: Encyclopedia of Applied Ethics. 2012.
  2. Liu X, Weidle K, Schröck K, Tönjes A, Schleinitz D, Breitfeld J, et al. Signatures of natural selection at the FTO (fat mass and obesity associated) locus in human populations. PLoS One. 2015;
  3. Abondio P, Sazzini M, Garagnani P, Boattini A, Monti D, Franceschi C, et al. The genetic variability of APOE in different human populations and its implications for longevity. Genes. 2019.
  4. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: Underlying causes and modification by exercise training. Compr Physiol. 2013;
  5. Smith CE, Follis JL, Nettleton JA, Foy M, Wu JHY, Ma Y, et al. Dietary fatty acids modulate associations between genetic variants and circulating fatty acids in plasma and erythrocyte membranes: Meta-analysis of nine studies in the CHARGE consortium. Mol Nutr Food Res. 2015;


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