Balancing your client’s omega-3 and omega-6 intake can be a task and a half. Science comes to the rescue by revealing another variable in the equation: recent studies show that certain gene variants impact omega-3 and omega-6 conversion in the body.
This week’s blog has been written by Dr Eve Pearce (PhD), an experienced geneticist and myDNAhealth’s Scientific Officer. Dr Pearce talks about how understanding your client’s essential fatty acids metabolism genotype can offer insights when balancing optimal omega ratios.
Omega 3 and omega 6 levels – How to personalise Essential Fatty Acid intakes
Most dietary fatty acids can be synthesised in the human body with the exception of omega-3, a-Linolenic acid (ALA) and omega-6, Linoleic acid (LA). These are then metabolised into other important polyunsaturated fatty acids (PUFAs), which have a range of important roles in human biology such as being substrates for the synthesis of inflammatory eicosanoids, components of cell membranes and acting as signalling molecules and regulation of gene expression. It is known that ALA and LA PUFAs may only be obtained from dietary sources and are therefore referred to as ‘essential fatty acids’.
The two families of omega-3 and omega-6 PUFAs are physiologically distinct and are metabolised through a series of desaturases and elongases. Both ALA and LA use the same enzymes and compete with each other for enzyme availability.
As PUFAs have powerful effects on human biochemistry, it is important to ensure that we have appropriate and balanced amounts in the body. Not only is this highly determined by diet and lifestyle, but also by our genetic capacity to metabolise the essential fatty acids (EFAs) to eicosanoids and very long chain PUFAs.
Omega-6 is necessary for our immune system function as it is a key contributor of pro-inflammatory hormones. A prolonged immune response might lead to chronic inflammatory states (as we know inflammation can be the underlying cause of many unpleasant symptoms and conditions). Anti-inflammatory mediators are needed to counteract the activity of pro-inflammatory ones; an important component of these are omega-3 fatty acids.
What can our genes tell us?
The key enzymes in this pathway are the Delta-5 (D5D) and Delta-6 desaturases (D6D), responsible for the formation of double bonds, encoded by FADS1 and FADS2 genes respectively. See Figure 1 via this link.
Therefore, conversion of omega-3 (dependent on D5D enzyme encoded by FADS1 gene) and omega-6 (dependent on D6D enzyme encoded by FADS2 gene) suggests that individuals will require different amounts of dietary PUFAs depending on their genetic variants. Indeed, studies of the FADS gene cluster indicate that these genetic variants are, in fact, associated with changes in PUFA plasma levels1.
D5D is encoded by FADS1 gene and the presence of genetic variants within this has been associated across European and Asian populations with lowered D5D activity. Research has indicated that reduced D5D activity is related to inflammatory states and associated with cardio-metabolic risk factors including cardiovascular disease, obesity and insulin resistance2.
A functional SNP in the FADS2 promoter gene region has been identified as increasing D6D activity by allowing binding of ELK1 transcription factor3. Increased D6D activity has been correlated to inflammatory states such as obesity, insulin resistance and T2DM which contributes to this risk2,4.
What does this mean in practice?
A variation on FADS1 gene indicates reduced D5D activity which impacts downstream production of omega 3 precursors; these individuals may need to consider supplementing with EPA and DHA.
A variation on FADS2 gene, indicating an increased activity of the enzyme and omega-6 conversion, might mean a decreased need for dietary omega-6 in order to avoid associated potential inflammatory states.
Knowing these genetic variants, taking into account your client’s current dietary habits and any possible symptoms of imbalance can help you establish the necessary omega-3 to omega-6 ratio for them. Genes are quite a fundamental factor: always remember that genes are not a health destiny, but merely a predisposition. Alongside genetic predispositions, it is crucial to consider diet, lifestyle, and other functional tests for the most precise approach to health and wellness.
Clinical Application – Case Study
The client is female, aged 39, with a BMI of 29 and symptomatic for EFA deficiency including dry ‘bumpy’ skin, brittle hair, brittle nails, excessive thirst and frequent urination. The client was experiencing pain generally in the joints which limits exercise. Her family history includes cancer and dementia. The client was a vegan for a few years and is now mainly gluten and dairy free. The diet appeared healthy at first glance, but there were too many unhealthy evening habits including a few glasses of wine most nights with dinner as a mechanism to cope with work stress followed by snacking on chocolate – she was also having business meals out about two to three times a week.
Presenting symptoms and Functional Test Results
The client’s main presenting issues were: difficulty sleeping, feeling emotional often with mood swings, concentration/memory issues, fatigue, digestive issues, inflammation, stress and feeling cold all the time.
Thyroid was checked by GP and was reported in the normal range.
Further functional tests also show undesirable levels of omega-3 and her AA to EPA ratio is in the suboptimal range, which shows that her omega-3 to omega-6 ratio is off balance.
DNA Test Results
The Essential Fatty acid pathway DNA test result indicates an impairment whereby a homozygotic (two allele copies) genetic variance indicates a reduction in D5D activity. This linked to a reduction in ETA to EPA conversion by the Omega 3 metabolism pathway.
Epigenetic Questionnaire Results
When considering a DNA test result for genetic variances, it is always important to assess the epigenetic impact alongside this, for environmental and lifestyle factors can have profound effects on gene expression. This should always be considered before implementing recommendations to a client as, otherwise, you are treating the SNP alone. The myDNAhealth’s approach uses an extensive Fatty Acid Questionnaire designed to highlight epigenetic factors which, in this case, indicates the client being at moderate risk of impaired fatty acid metabolism.
The client’s DNA results show a wildtype FADS2, indicating a normal functioning D6D enzyme, but a reduced D5D enzyme (FADS1) activity. This means an impaired conversion pathway from omega-3 alpha linolenic acid (ALA), making endogenous production of crucial PUFAs such as EPA and DHA slower. In addition, the EFA questionnaire result indicates lifestyle deficiencies in essential fatty acids. The bloodspot fatty acid functional test also confirms that the levels of omega 3 can be improved. Put together, these results point to a potential cause of imbalance.
Clinical Application Framework: Integrated Approach to Client treatment
Using our genetic testing we can advise the client to ensure an adequate intake of EPA and DHA omega-3 PUFAs to support the FADS1 variant. It is important to note that advice to increase intake of sources of ALA (as possibly suggested by the bloodspot analysis alone) may be ineffective as the client has a reduced capacity to convert them and a more targeted approach is required. Also, to limit dietary omega-6 to improve ratios (as omega-6 pathway will likely have precedence over omega-3) due to D6D enzyme being more active than the impaired D5D.
Introducing a supplement high in a pure and stable form of EPA and DHA to support the client initially could be beneficial. This should help to rebalance omega ratios and dampen the inflammatory response while the client adjusts their diet and lifestyle to reduce other inflammatory factors. The need for a supplement should be reviewed after 3 months, if the client has adjusted their diet sufficiently, the supplement may be stopped or reduced.
In addition, saturated fats often block absorption in the D5D pathway, making it difficult to convert plant fats such as ALA into the more active forms of essential omega fats EPA and DHA. Cutting down on fatty foods in the client’s diet such as cooked breakfasts and mayonnaise/milk chocolate (as recorded in the client’s weekly diet) would help improve absorption.
Don’t forget that…
For overall EFA pathway support, the client’s environment should be addressed. Contributing factors such as stress, toxins like alcohol and smoking, high saturated fat and high sugar intake should be reduced or removed. Prolonged stress can affect the gut, impacting digestion and even mood, through the gut-brain axis. Better managed stress and improved sleep patterns will also likely enhance absorption of omega-3, which are known to have a protective effect against anxiety and other stress-related symptoms.
myDNAhealth’s new Essential Fatty Acid Metabolism Panel includes the FADS genes and a questionnaire to assess symptoms of potential deficiencies. The overall result is fully interpreted and practitioners also receive additional nutrigenomic guidelines.
Dr Eve Pearce (PhD (Medicine), DipION, mBANT), an experienced geneticist and myDNAhealth’s Scientific Officer who has helped to develop the new EFA Metabolism Panel comments: ‘Understanding essential fatty acids metabolism genotype can offer insights when balancing optimal omega ratios. Practitioners can use the EFA Pathway alongside their client’s questionnaire result which indicates potential deficiencies contributing to inflammatory states. The overall results can inform targeted dietary and supplementation requirements.’
myDNAhealth is an award winning genetic testing company who continually researches genes and develops DNA test panels. myDNAhealth works with nutritional and healthcare practitioners to help them provide their clients with a personalised, science-based approach to nutrition, prevention and wellbeing programmes. Nutrigenomic and epigenetic testing includes a non-invasive cheek swab to obtain and analyse a person’s DNA combined with Lifestyle Analysis questionnaires in order to determine a person’s current environment and lifestyle to provide insights into gene expression.
Dr Eve Pearce (PhD (Medicine), DipION, mBANT)
Dr Eve Pearce is myDNAhealth’s Scientific Officer and a practicing clinician with over a decade of academic genetic and medical research experience. Eve’s passion for wellness and nutrition led her on to complete an ION Diploma in Nutritional Therapy. She works in both private practice and with a NHS weight management service and delivers bespoke nutrigenomic and biochemistry education to undergraduate and CPD audiences.
With many thanks to Dr Eve Pierce for this article, if you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time.
firstname.lastname@example.org, 01684 310099
The Cytoplan editorial team: Clare Daley and Joseph Forsyth
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- Schaeffer, L., Gohlke, H., Müller, M., Heid, I. M., Palmer, L. J., Kompauer, I., … Heinrich, J. (2006). Common genetic variants of the FADS1 FADS2 gene cluster and their reconstructed haplotypes are associated with the fatty acid composition in phospholipids. Human Molecular Genetics, 15(11), 1745–56. http://doi.org/10.1093/hmg/ddl117
- Warensjö, E., Rosell, M., Hellenius, M.-L., Vessby, B., De Faire, U., & Risérus, U. (2009). Associations between estimated fatty acid desaturase activities in serum lipids and adipose tissue in humans: links to obesity and insulin resistance. Lipids in Health and Disease, 8(1), 37. http://doi.org/10.1186/1476-511X-8-37
- Lattka, E., Eggers, S., Moeller, G., Heim, K., Weber, M., Mehta, D., … Adamski, J. (2010). A common FADS2 promoter polymorphism increases promoter activity and facilitates binding of transcription factor ELK1. The Journal of Lipid Research, 51(1), 182–191. http://doi.org/10.1194/jlr.M900289-JLR200
- Li, S.-W., Wang, J., Yang, Y., Liu, Z.-J., Cheng, L., Liu, H.-Y., … Liu, S.-M. (2016). Polymorphisms in FADS1 and FADS2 alter plasma fatty acids and desaturase levels in type 2 diabetic patients with coronary artery disease. Journal of Translational Medicine, 14(1), 79. http://doi.org/10.1186/s12967-016-0834-8