Benefats: The Truth About Fats and Genetics

More fat or less fat? Carb-free or Paleo?

Despite all the uninformative dietary advice out there, we have some good news. Understanding your genetic profile can help you eat smarter.

Not all people digest food the same way – your genetics can tell you how you do. Join our kit waitlist today!

The digestion of food in the human body is a complex process, and varies highly from person to person. Ever wonder why some people can tolerate immense amounts of fats while others balloon from a slight caloric increase? Our genetic makeup is one of several reasons why.

Hundreds of enzymes, receptors, and even your gut bacteria contribute to breaking down food on its journey from your mouth through the rest of your body. At each step of the process, loads of proteins play a role in the metabolism of macronutrients – carbs, protein, and fat. With a better understanding of your genes that code for these metabolic enzymes, you can make better dietary choices tailored to your body.

One particularly demonized macronutrient is fat. When looking for a reason for increased weight gain, many of us place the blame on this rich nutrient found in cheese, bacon, and oils. Although fat is the most calorically dense macronutrient (9 calories per gram of fat vs. 4 calories per gram of carbohydrate or protein) and therefore shunned by the calorically-conscious community, it is essential for your health and performance.

In fact, fat offers cardiovascular support, is vital in absorbing fat-soluble vitamins, and is an essential component of the membranes in each cell in our body. In order to harness the benefits of vitamins A, D, E, and K, at least some fat has to be consumed. However, like any nutrient, excess fat intake can lead to a host of unfavorable health effects. It is easy to overdo fat intake since even the smallest amount contains such a large amount of calories.

In knowing that you should be careful with your fat intake, it is important to note that all fats are not made equal.

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What are the different fats?

Fats are tiny organic molecules that consist of carbon and hydrogen atoms arranged in long chains. The shapes in which these molecules are constructed are responsible for the different types of fats and their respective chemical properties. In some cases it determines if a fat will be healthy or not.

Broadly, fats fall into categories of saturated and unsaturated. These terms refer to the how many hydrogen atoms are on the carbon chain, or how saturated the chain is.

Saturated fats are those that are fully saturated with hydrogen atoms attached to each carbon atom. Because of their molecular structure, they stack easily on top of one another and are solid at room temperature, like butter and bacon grease. They are commonly referred to as the “bad fatas a diet rich in these fats can induce a spike in the bad type of cholesterol (LDL) and can play a role in cardiovascular disease (1). However, saturated fat can raise both good and bad types of cholesterol, so its effects are not entirely clear.

saturated-fatty-acid

Saturated fat

 

unsaturated-fatty-acid

Monounsaturated fat

Unsaturated fats have one double bond (monounsaturated fat, above) or multiple double bonds (polyunsaturated fat) between carbons in the chain that introduce a kink in the fat molecule, making them more fluid at room temperature, like with olive oil. Unsaturated fats are the “healthy fats”, since they offer a wide range of health effects in the body.

Health benefits of unsaturated fats (especially omega-3 fish oils):

  • Improve heart health (2)
  • Reduces depressive symptoms (3)
  • May assist with weight loss vs saturated fat intake (8)
  • Joint health & arthritis alleviation (4) 

Sources of the different types of fats:

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That said, your body responds differently to different types of fat due to their different molecular properties, and differences within our genes. Depending on your genotype at markers in the APOA2 and PPARG genes, it may actually be beneficial for you to increase your intake of saturated or unsaturated fat, keeping within healthy guidelines.

Saturated Fat and Your Genes

Despite the popular opinion that saturated fat should be highly avoided, some people may not gain weight with an increased saturated fat intake, depending on their genetic profile at a marker in the apolipoprotein A2 (APOA2) gene (5, 6).  The APOA2 gene codes a protein that is a part of HDL cholesterol (“good” cholesterol), and variation at this gene has been proposed to affect the function of lipoprotein lipase, the enzyme that breaks down fats into a usable form for the body (11). People with a certain variant in the APOA2 gene may therefore be more sensitive than the average individual to weight gain as a result of increased saturated fat intake, like those from animal fats and butter (7). By using dietary guidelines alongside your genetic profile, you can make better decisions with your fat intake. See our quick saturated fat guide for more info:


Summary of outcomes for saturated fat sensitivity (APOA2 gene – rs5082 marker): 

   GG (Opportunity) High sensitivity to saturated fat intake (5-7). Increased odds of weight gain and higher LDL cholesterol levels (11) when on a high saturated fat diet.  Less APOA2 protein in the blood, resulting in changes to fat metabolism (11).  Limit saturated fat intake to minimal amounts consumed from animal fats and oils. Choosing healthy unsaturated fats from a variety of plants (e.g. olive oil, avocado, sunflower oil, and nuts) and reducing saturated fat consumption can help you improve your body composition.     AG and AA (Adaptable) Normal sensitivity: Typical odds of weight gain on both a high and low saturated fat diet.   Although those with this phenotype may be less sensitive to saturated fat intake, a lower intake of saturated fats is advised by many. AG and AA individuals may be able to metabolize more saturated fat than GG individuals, but should still monitor their saturated fat intake.  The American Heart Association suggests an intake of 7% or less of total calories per day from saturated fats, or about 16 grams on a 2,000 calorie diet.

How do you metabolize unsaturated fats?

Similar inferences from genetic research can be made with respect to unsaturated fats. The PPARG gene, which is responsible for differences in unsaturated fat metabolism is a master regulator of fat storage and glucose (sugar) metabolism. Polyunsaturated fats directly bind to the PPARG protein in the body, which then turns on other genes that are responsible for fat metabolism, called beta oxidation. Those with the high responder genotype at this marker in the PPARG gene have a different efficiency of fat breakdown at the molecular level (12), explaining why they may be able to consume more unsaturated fat from sources like olive oil and almonds without gaining weight (8).

Summary of outcomes for unsaturated fat sensitivity (PPARD gene – rs1801282 marker):

Unsat Fat Table

The Nitty-Gritty of the Research

A study by Spanish researchers discovered that from their cohort of 1465 overweight individuals between 20 and 45 years old, some people lost more weight on the study than others, even though their diets were tightly controlled. The diet contained a macronutrient ratio of: 35% fat (10% or less saturated fat, 20% monounsaturated), 50% carbohydrates, and 15-20% protein (8). The participants were advised to consume an unlimited amount of vegetables, plentiful amounts of fruit, and use olive oil only for cooking fat, as advised by guidelines of the Mediterranean diet. Participants were also genetically screened for mutations at the PPARD gene and the results were striking.

The researchers found  that carriers of the G allele (gifted genotypes) lost more weight in the study when monounsaturated fat (MFA) intake was high (56% or more of total fat), but no differences were found between genotypes when MFA intake was low. It seems counterintuitive, but this means that those with the gifted genotypes lost more weight when they ate more unsaturated fats.

So what should I eat?

There is no magic percentage or ratio of macronutrient intake that is optimal for weight loss. Reducing calorie intake and increasing energy output is the primary factor in losing weight. By using calculators such as this one in addition to your genetic profile you can dial in your fat intake to suit your goals. Replacing unhealthy fats with more vegetable, protein and unsaturated fat intake, and not refined carbs or hydrogenated oils (like margarine, a source of trans fats) is likely the best course of action for your health (9).

It’s also important to note that the same diet will likely not affect two people the same. Due to small but meaningful differences in metabolism at the molecular level, some can tolerate more fat than others. The research discussed above with respect to fat sensitivities supports that an all-encompassing approach to nutrition may be an inefficient strategy for you. We should all be armed with our genetic information to properly formulate diets for optimal performance and body composition.

Learning more about your unique nutritional needs with an Athletigen profile may help you achieve your dietary goals faster. Join our exclusive kit waitlist today!

Fat Infographic-01

References:

  1. Hooper, L., Martin, N., Abdelhamid, A., & Davey Smith, G. (2015). Reduction in saturated fat intake for cardiovascular disease. The Cochrane Database of Systematic Reviews, (6), CD011737.
  2. Hammad, S., Pu, S., & Jones, P. J. (2016). Current Evidence Supporting the Link Between Dietary Fatty Acids and Cardiovascular Disease. Lipids, 51(5), 507–517.
  3. Sublette, M. E., Ellis, S. P., Geant, A. L., & Mann, J. J. (2011). Meta-analysis of the effects of eicosapentaenoic acid (EPA) in clinical trials in depression. The Journal of Clinical Psychiatry, 72(12), 1577–1584.
  4. Miles, E. A., & Calder, P. C. (2012). Influence of marine n-3 polyunsaturated fatty acids on immune function and a systematic review of their effects on clinical outcomes in rheumatoid arthritis. The British Journal of Nutrition, 107 Suppl 2, S171–184. http://doi.org/10.1017/S0007114512001560
  5. Corella, D., Tai, E. S., Sorlí, J. V., Chew, S. K., Coltell, O., Sotos-Prieto, M., … Ordovas, J. M. (2011). Association between the APOA2 promoter polymorphism and body weight in Mediterranean and Asian populations: replication of a gene-saturated fat interaction. International Journal of Obesity (2005), 35(5), 666–675. doi:10.1038/ijo.2010.187
  6. Smith, C. E., Tucker, K. L., Arnett, D. K., Noel, S. E., Corella, D., Borecki, I. B., … Ordovás, J. M. (2013). Apolipoprotein A2 polymorphism interacts with intakes of dairy foods to influence body weight in 2 U.S. populations. The Journal of Nutrition, 143(12), 1865–1871.
  7. Smith, C. E., Tucker, K. L., Arnett, D. K., Noel, S. E., Corella, D., Borecki, I. B., … Ordovás, J. M. (2013). Apolipoprotein A2 polymorphism interacts with intakes of dairy foods to influence body weight in 2 U.S. populations. The Journal of Nutrition, 143(12), 1865–1871.
  8. Garaulet, M., Smith, C. E., Hernández-González, T., Lee, Y.-C., & Ordovás, J. M. (2011). PPARγ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet. Molecular Nutrition & Food Research, 55(12), 1771–1779.
  9. Mozaffarian, D., Micha, R., & Wallace, S. (2010). Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLOS Med, 7(3), e1000252.
  10. Robitaille, J., Després, J.-P., Perusse, L., & Vohl, M.-C. (2003). The PPAR-gamma P12A polymorphism modulates the relationship between dietary fat intake and components of the metabolic syndrome: results from the Québec Family Study. Clinical Genetics, 63(2), 109–116.
  11. Noorshahi, N., Sotoudeh, G., Djalali, M., Eshraghian, M. R., Keramatipour, M., Basiri, M. G., … Koohdani, F. (2016). APOA II genotypes frequency and their interaction with saturated fatty acids consumption on lipid profile of patients with type 2 diabetes. Clinical Nutrition, 35(4), 907–911.
  12. Larsen, T. M., Toubro, S., & Astrup, A. (2003). PPARgamma agonists in the treatment of type II diabetes: is increased fatness commensurate with long-term efficacy? International Journal of Obesity and Related Metabolic Disorders, 27(2), 147–161.

Infographic References:

  1. Hammad, S., Pu, S., & Jones, P. J. (2016). Current Evidence Supporting the Link Between Dietary Fatty Acids and Cardiovascular Disease. Lipids, 51(5), 507–517.
  2. Sublette, M. E., Ellis, S. P., Geant, A. L., & Mann, J. J. (2011). Meta-analysis of the effects of eicosapentaenoic acid (EPA) in clinical trials in depression. The Journal of Clinical Psychiatry, 72(12), 1577–1584.
  3. Garaulet, M., Smith, C. E., Hernández-González, T., Lee, Y.-C., & Ordovás, J. M. (2011). PPARγ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet. Molecular Nutrition & Food Research, 55(12), 1771–1779.
  4. Miles, E. A., & Calder, P. C. (2012). Influence of marine n-3 polyunsaturated fatty acids on immune function and a systematic review of their effects on clinical outcomes in rheumatoid arthritis. The British Journal of Nutrition, 107 Suppl 2, S171–184. http://doi.org/10.1017/S0007114512001560
  5. Corella, D., Tai, E. S., Sorlí, J. V., Chew, S. K., Coltell, O., Sotos-Prieto, M., … Ordovas, J. M. (2011). Association between the APOA2 promoter polymorphism and body weight in Mediterranean and Asian populations: replication of a gene-saturated fat interaction. International Journal of Obesity (2005), 35(5), 666–675. doi:10.1038/ijo.2010.187

1 Comment

  1. You may want to look into rs1800206. Low percentage of heterozygotes but the consequences are meaningful.

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