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Unlocking Disease PreventionThrough Your Genes: The Role of FADS1 in Modern Nutrition

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Imagine this: two friends embark on the same new “superfood” diet, excited to transform their health. One feels energized and radiant, while the other is plagued by fatigue and inflammation.

How could the same diet lead to such dramatically different results?

The answer isn’t found in the food itself but hidden within their DNA—carefully shaped over thousands of years. This genetic mystery, quietly influencing how our bodies respond to food, holds the key to understanding why one-size-fits-all diets often fail. The truth lies in our evolutionary past, where dietary survival shaped the genes we still carry today.

In the first part of this article, we uncovered how the diets of our European ancestors left a permanent mark on our genes—particularly through adaptations like the FADS1 gene, which determines how efficiently we process essential fatty acids.

Now, let’s explore how this powerful gene continues to influence not just what we should eat today, but how it can unlock the prevention of chronic diseases—helping you design a diet that’s written into your very DNA.

The FADS1 Gene: A Critical Player in Fatty Acid Metabolism

The FADS1 gene is responsible for producing enzymes that convert short-chain polyunsaturated fatty acids (PUFAs) from plant sources—such as alpha-linolenic acid (ALA) and linoleic acid (LA)—into their long-chain forms, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)(1). These long-chain fatty acids are vital for brain development, inflammation control, and heart health(2).

However, the ability to efficiently convert plant-based fatty acids into their long-chain counterparts varies significantly across populations due to genetic adaptations shaped by ancient diets.

Prevalence of the FADS1 Allele That Converts Plant-Based Fats

Genetic adaptation in the FADS1 gene is not uniform across populations. In fact, the prevalence of the derived allele—which enhances the conversion of plant-based short-chain fatty acids into long-chain essential fatty acids—varies greatly depending on geographical and historical factors. Let’s take a look:

  • Southern Europe: In Southern European populations, where plant-based foods were more common historically, the derived allele of FADS1 is highly prevalent. Up to 70% of individuals in Southern Europe carry this allele(3). This reflects the long history of agricultural practices in the region, where grains, legumes, and vegetables were incorporated into the diet.
  • Northern Europe: In contrast, Northern Europeans—whose ancestors consumed more animal products, including wild fish, game, and dairy—show a lower prevalence of the derived allele. Only about 40-50% of individuals in Northern Europe carry the derived allele, with the ancestral allele (less efficient at converting plant-based fats) being more common(4). This aligns with their diet, which historically provided direct sources of EPA and DHA through meat and seafood.
  • East Asia: In East Asian populations, where seafood has traditionally been a major part of the diet, the derived allele is found in 30-40% of individuals(5). The reliance on direct sources of long-chain fatty acids, such as wild fish, reduced the need for enhanced conversion of plant-based fatty acids.
  • Africa: African populations, which have the highest genetic diversity, tend to have the lowest prevalence of the derived FADS1 allele, with only about 20-30% carrying it(6). This is consistent with their ancestral diets, which were rich in animal-based sources of long-chain fatty acids. Traditional hunter-gatherer societies, such as the Hadza in East Africa, exemplify this. The Hadza have historically consumed a diet rich in game meat, organ meats, and foraged foods like honey and tubers, relying heavily on direct sources of EPA and DHA from their diet. This reduced the need for genetic adaptations to convert plant-based fats into their long-chain forms. Such diets reflect a long evolutionary history of obtaining essential fats from animal products rather than plants.
fresh fish and seafood dha

This variation illustrates how our ancient diets shaped our genetic ability to process fats.

Populations with longer histories of plant-based agriculture developed a greater frequency of the derived FADS1 allele, enhancing their ability to convert plant-based omega-3 and omega-6 fatty acids into their long-chain forms.

Meanwhile, populations that relied more heavily on animal-based diets didn’t require this adaptation, as their food provided direct sources of these essential fats.

FADS1 and Inflammation: How Your Genes Impact Chronic Disease Risk

The fatty acids produced through the FADS1 gene play a direct role in regulating inflammation.

EPA and DHA, for example, are known to produce anti-inflammatory compounds called resolvins and protectins, which help calm the body’s inflammatory response(7). If your body is inefficient at producing these critical long-chain fatty acids, you could be at a higher risk of chronic inflammation—a key driver of chronic diseases like heart disease, arthritis, and Alzheimer’s(8).

Research shows that individuals with the less efficient version of the FADS1 gene are more likely to have higher levels of inflammatory markers and a greater risk of developing these diseases(9). On the other hand, those with the more efficient version of FADS1 have lower inflammation and are better protected against these chronic conditions.

Understanding your FADS1 profile not only explains why certain diets work better for you but also provides the roadmap for making smarter choices to reduce disease risk and optimize wellness.

Fine-Tuning Your Diet Based on Your FADS1 Profile: Ancestral or Derived Allele

So how do you use this information to fine-tune your nutrition?

It starts by understanding which version of the FADS1 gene you carry. Genetic testing is becoming more accessible, offering insights into your ability to convert plant-based omega-3s into their essential long-chain forms(10).

If you carry the ancestral allele and struggle with this conversion, it’s important to focus on direct dietary sources of EPA and DHA—primarily from fatty fish like wild salmon, mackerel, Alaskan halibut, Alaskan cod (sablefish) and sardines, as well as grass-fed meats. Supplements derived from fish oil can also help ensure you get enough of these critical fats.

If you have the derived allele and are better able to convert short-chain PUFAs into long-chain PUFAs, you will still benefit from EPA- and DHA-rich foods, while also having the ability to get some of your requirements met from plant-based omega-3 sources, like flaxseeds, chia seeds, and walnuts(11).

Remember, the conversion of short-chain omega-3s like ALA into their long-chain forms, EPA and DHA, is still inefficient, with only a small percentage successfully converted. This means that while you can obtain some benefits from plant-based sources, incorporating direct sources of EPA and DHA from animal sources remains critical for disease prevention and optimal health.

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FADS1, Cardiovascular Health, and Omega-3s

The link between FADS1 and heart health is well-established. Omega-3 fatty acids, especially EPA and DHA, have been shown to lower triglyceride levels, reduce blood pressure, and decrease the risk of cardiovascular disease(12). For individuals with the less efficient version of FADS1, a deficiency in omega-3 intake can significantly increase the risk of heart disease.

The good news is that ensuring an optimal intake of omega-3s can help lower inflammation, reduce arterial plaque buildup, and improve overall heart function. This is particularly important for those with a family history of cardiovascular disease, where genetic predisposition might play a role(13).

From Genetics to Personalized Nutrition: Designing Your Optimal Diet

Your genes provide a roadmap, but you are in control of how to navigate it. Personalized nutrition based on genetic insights is a powerful tool for improving your health, preventing disease, and optimizing well-being.

  1. Get Tested: Start by finding out which version of the FADS1 gene you carry. Many at-home genetic testing kits can provide this information.
  2. Prioritize Omega-3 Intake: If you carry the ancestral allele, focus on direct sources of EPA and DHA from fatty fish, grass-fed meats, and clean-sourced fish oil supplements. If you have the derived allele, ensure you incorporate both plant-based and marine sources of omega-3s to optimize your fatty acid balance.
  3. Monitor Inflammation: Controlling inflammation is key to long-term health. Include anti-inflammatory, ancestral foods rich in long-chain omega-3s and clean protein while avoiding processed foods, sugars, and refined carbohydrates that can spike inflammation.
  4. Work with a Professional: Consider consulting with a healthcare professional who specializes in nutrigenomics to help you create a tailored diet that aligns with your genetic profile and health goals.

By aligning your diet with your genetic makeup, you’re not just feeding your body—you’re optimizing it for longevity and vitality. This approach honors the legacy of your ancestors while embracing the science of modern nutrition and biochemical individuality.


 

For this and more delightfully nutritous articles from trusted sources make sure to visit our US Wellness Meats Discover Blog today! 

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References

  1. Ye, K., Gao, F., Wang, D., Bar-Yosef, O., & Keinan, A. (2017). Dietary adaptation of FADS genes in Europe varied across time and geography. Nature Ecology & Evolution, 1(0167), 1-7.
  2. Simón, M. I., White, P. J., Lichtenstein, A. H., Lamon-Fava, S., Van Rompay, M. I., & Ordovás, J. M. (2020). Genetic modulation of the response to omega-3 fatty acids supplementation in humans: A systematic review. Nutrients, 12(5), 1376.
  1. Mathias, R. A., Pani, V., Chilton, F. H., & Blangero, J. (2012). Genetic variants in the FADS gene: implications for dietary recommendations for omega-3 fatty acid intake. Journal of Nutrigenetics and Nutrigenomics, 5(1), 43-64.
  2. Chilton, F. H., Dutta, R., Reynolds, L. M., Sergeant, S., Mathias, R. A., & Seeds, M. C. (2017). Precision nutrition and omega-3 polyunsaturated fatty acids: A case for personalized supplementation approaches for the prevention and management of human diseases. Nutrients, 9(11), 1165.
  3. Fenech, M., El-Sohemy, A., Cahill, L., Ferguson, L. R., French, T. A., Tai, E. S., … & Milner, J. (2011). Nutrigenetics and nutrigenomics: viewpoints on the current status and applications in nutrition research and practice. Journal of Nutrigenetics and Nutrigenomics, 4(2), 69-89.
  4. Serhan, C. N., & Chiang, N. (2008). Resolution phase lipid mediators of inflammation: agonists of resolution. Current Opinion in Pharmacology, 8(3), 286-293.
  5. Calder, P. C. (2017). Omega-3 fatty acids and inflammatory processes: from molecules to man. Biochemical Society Transactions, 45(5), 1105-1115.
  6. Blekhman, R., Man, O., Herrmann, L., Boyko, A. R., Indap, A., Kosiol, C., … & Gilad, Y. (2008). Natural selection on genes that underlie human disease susceptibility. Current Biology, 18(12), 883-889.
  7. Fenech, M., El-Sohemy, A., Cahill, L., Ferguson, L. R., French, T. A., Tai, E. S., … & Milner, J. (2011). Nutrigenetics and nutrigenomics: viewpoints on the current status and applications in nutrition research and practice. Journal of Nutrigenetics and Nutrigenomics, 4(2), 69-89.
  8. Chilton, F. H., Dutta, R., Reynolds, L. M., Sergeant, S., Mathias, R. A., & Seeds, M. C. (2017). Precision nutrition and omega-3 polyunsaturated fatty acids: A case for personalized supplementation approaches for the prevention and management of human diseases. Nutrients, 9(11), 1165.
  9. Mozaffarian, D., & Wu, J. H. (2011). Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. Journal of the American College of Cardiology, 58(20), 2047-2067.
  10. Ordovás, J. M., & Mooser, V. (2004). Nutrigenomics and nutrigenetics. Current Opinion in Lipidology, 15(2), 101-108.
  11. Mozaffarian, D., & Wu, J. H. (2011). Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. Journal of the American College of Cardiology, 58(20), 2047-2067.