What will DNA testing tell me?
Our DNA test analyses genes that affect how you:
- Transform (aka detoxify)
Important chemicals for your body.
Genetic analysis can give insight into where your metabolism needs support. This is hugely important because what we mean by metabolism is all the chemical processes that go on continuously inside your body to keep you alive and healthy, such as respiration, digesting food, and repairing cells.
We also give clear advice on how you can compensate for genetic weakness though diet, exercise, health and (when required) optimising supplement choices.
We have partnered with Atlas Biomed, the leading genetic analysis company based in the UK. As well as the humanpeople report you will receive a detailed health report from Atlas Biomed.
What is nutrogenomics?
Nutritional genomics is the relationship between nutrients, what we eat and how our genes determine how our body will respond. It gives hints, as to how we can improve health through food.
Nutrogenomics is just a part of the jigsaw, an extra insight into our health. It is of most use when integrated into the general health picture, genetics are tendencies not absolutes and when taken in this context it can give answers to complex problems and help us to understand root cause that lead to better health today and tomorrow.
For example nutrogenomics might help with:
- Understanding weight gain or a struggle to lose weight- certain genes will affect our satiety (how full we feel after eating), how quickly we “put down” fat and how easily we release (lose) that fat in response to exercise.
- Inflammation causing tiredness or aches and pains – nutrients such as omega 3 and vitamin D reduce inflammation, genetic variation will affect the levels of both of these. Some of us produce higher levels of inflammatory messengers, due to our genes, so making sure our nutrients are balanced is essential to good health.
- Struggling with low energy- high levels of antioxidants, coenzymes, B vitamins and minerals like magnesium, selenium and zinc are essential for the normal production of energy. All of these are affected by our genetics.
What is the benefit of looking at my DNA?
Our cells, the stages on which the biochemical dance of life performs, rely on tiny molecular machines called proteins to carry out their day to day activities.
The instructions to properly make these molecular machines (proteins) are found in our DNA. Like building flatpack furniture, if one piece goes missing this can cause issues building the entire structure. This is when errors can occur.
That means that small changes can lead to significant impacts if just one character in our “code of life” changes. The difference between deed and dead is only one letter!
Producing energy for life is both an essential and damaging process. humanpeople’s DNA test analyses genes involved in both the production of energy and which protect the body from the toxic byproducts created when producing energy. This energy production occurs inside our mitochondria.
Imagine trying to rinse out water from a wet towel.
Your three major biochemical pathways take food molecules and squeeze out as much energy as possible. These pathways need specific / specialised ingredients to work at their best, including vitamins such as B12 and minerals such as magnesium. DNA testing allows us to look for variants that weaken the links in the energy production line.
Toxicity in energy production can be analogised to toxic waste produced by a nuclear power plant. Supplying the ingredients to make sure the protection system works and stabilising the bioenergetic environment is beneficial for overall health. One example is the gene NQO1 that helps to prevent free electrons damaging delicate molecular structures. Deficiencies in this gene are linked to hematotoxicity (toxicity of the blood), various forms of cancer, and Alzheimer’s (1).
Detoxification (also known as biotransformation) is a commonly misunderstood and mis-used phrase.
What is detoxification?
Detoxification as used scientifically in the body refers to the essential process of breaking down and removing malicious molecules or substances that have performed their purpose.
Detoxification is mostly done in two different phases in the liver.
Phase I detoxification: this stage makes it easier for the excretory system to ‘grip’ on the molecule by increasing its polarity whilst simultaneously trying to reduce the danger the molecule poses (however sometimes it can make it more dangerous). Most importantly, it lays the groundwork for the molecule to be targeted for the ‘knock out punch’ by Phase II enzymes.
Phase II detoxification is when the body attaches molecules that inactivate it. This ensures it passes out of the body by the excretory system.
COMT: neurotransmitters and stress
COMT is a gene within the DNA that codes an enzyme that acts as molecular scissors that target and break down a trio of messaging molecules called catecholamines; examples are adrenaline, noradenaline, and dopamine.
COMT is important for our mood, causing both anxiety and depression when it over- and under-active. Chronically raised catecholamines are what causes stress.
Catecholamines in the brain are the chemical equivalent of a red flashing light on a fire alarm. They are the chemical messengers that move our body into the fight or flight response.
Once the danger has passed these molecules need to be broken down. Otherwise we exist in a state of chronic stress that can contribute to disease.
COMT also breaks down oestrogen (a sex hormone produced by both males and females) that has been linked to a series of cancers if the intermediate breakdown product builds up and “hangs around” for too long as it signals cells to grow and divide (2).
These reasons make it very useful to know if you have a fast or slow acting COMT gene because there are ways of speeding it up and slowing it down through diet, behaviour and supplementation.
Mood and cognitive performance
Mood is orchestrated by the levels and flow of messaging chemicals in the brain called neurotransmitters (NTMs). Some genes are well evidenced to alter neurotransmitter levels, therefore affecting mood and cognitive performance. The MTHFR gene is a good example. It is known to protect the brain from unbalanced NTM levels and is associated with Alzhmier’s (3), depression (4, 5) and effects mood (6). The chemical production line MTFHR participates in also produces chemical tags called methyl groups that activate the above-mentioned COMT gene. This enables it to break down alarm messaging molecules.
However a slow working version of this enzyme poses risks including depression, psychiatric disorders and a reduction in the capacity to form new neurons.
If the results of your DNA test identify that you have a slow MTHFR gene there are specific types of B vitamins that can help to boost the pathway to minimise the problems.
Food and appetite
The genetic impact of body weight is a very active research field. Currently it is thought genetics determine as much as ⅔ of weight variation. Rather than making you more hungry these genes tend to influence weight by destabilizing your satiety and appetite. That is to say how we react to food when we see or smell it, rather than the internal biological feeling of hunger. In an environment of plenty and endless opportunities for food these genes contribute to your resting weight level (7).
FTO gene influences your BMI
FTO is an example of one the genes we look at. A lot of research has gone into this gene and understanding how it works.
Large studies have demonstrated that it will influence your BMI (8) (Body Mass Index – measurement that compares how much someone weighs compared to their height) and is one of the most widely studied genes associated with weight. It influences energy balance, desire to eat, and whether you feel full after eating (potentially by influencing other hunger hormones).
However knowing which version of this gene you have will help to guide your food choices to keep at a healthy weight.
We will recommend food modifications that will work well with your personal genetics if you have a variant that predisposes you to a higher BMI.
- NCBI – Gene (2021). NQO1 NAD(P)H quinone dehydrogenase 1 [Homo sapiens (human)] – Gene – NCBI. [online] www.ncbi.nlm.nih.gov. Available at: https://www.ncbi.nlm.nih.gov/gene/1728 [Accessed 14 Oct. 2021].
- Caiazza, F., Ryan, E.J., Doherty, G., Winter, D.C. and Sheahan, K. (2015). Estrogen Receptors and Their Implications in Colorectal Carcinogenesis. Frontiers in Oncology, [online] 5(Article 19, 2). Available at: https://www.frontiersin.org/articles/10.3389/fonc.2015.00019/full#B2 [Accessed 14 Oct. 2021].
- Rai, V. (2016). Methylenetetrahydrofolate Reductase (MTHFR) C677T Polymorphism and Alzheimer Disease Risk: a Meta-Analysis. Molecular Neurobiology, 54(2), pp.1173–1186.
- Lewis, S.J., Lawlor, D.A., Davey Smith, G., Araya, R., Timpson, N., Day, I.N.M. and Ebrahim, S. (2006). The thermolabile variant of MTHFR is associated with depression in the British Women’s Heart and Health Study and a meta-analysis. Molecular Psychiatry, [online] 11(4), pp.352–360. Available at: https://pubmed.ncbi.nlm.nih.gov/16402130/ [Accessed 14 Oct. 2021].
- Lok, A., Bockting, C.L.H., Koeter, M.W.J., Snieder, H., Assies, J., Mocking, R.J.T., Vinkers, C.H., Kahn, R.S., Boks, M.P. and Schene, A.H. (2013). Interaction between the MTHFR C677T polymorphism and traumatic childhood events predicts depression. Translational Psychiatry, [online] 3, p.e288. Available at: https://pubmed.ncbi.nlm.nih.gov/23900311/ [Accessed 14 Oct. 2021].
- Peerbooms, O.L.J., van Os, J., Drukker, M., Kenis, G., Hoogveld, L., de Hert, M., Delespaul, P., van Winkel, R. and Rutten, B.P.F. (2011). Meta-analysis of MTHFR gene variants in schizophrenia, bipolar disorder and unipolar depressive disorder: Evidence for a common genetic vulnerability? Brain, Behavior, and Immunity, 25(8), pp.1530–1543.
- Brunner, E.J., Maruyama, K., Shipley, M., Cable, N., Iso, H., Hiyoshi, A., Stallone, D., Kumari, M., Tabak, A., Singh-Manoux, A., Wilson, J., Langenberg, C., Wareham, N., Boniface, D., Hingorani, A., Kivimäki, M. and Llewellyn, C. (2021). Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory. International Journal of Obesity, 45(4), pp.758–765.
- Dina, C., Meyre, D., Gallina, S., Durand, E., Körner, A., Jacobson, P., Carlsson, L.M.S., Kiess, W., Vatin, V., Lecoeur, C., Delplanque, J., Vaillant, E., Pattou, F., Ruiz, J., Weill, J., Levy-Marchal, C., Horber, F., Potoczna, N., Hercberg, S. and Le Stunff, C. (2007). Variation in FTO contributes to childhood obesity and severe adult obesity. Nature Genetics, 39(6), pp.724–726.