Omega-3 vs. Omega-6 fats and your genes

Butter is evil.  Butter is the best!  Only cook with Canola oil.  Wait — everyone switch back to saturated fats. Olive oil, grapeseed oil, avocado oil, cold pressed, expeller pressed….  is palm oil now good?  Am I the only one who is confused by which kind of fat is the best?

It turns out, like most things, that the answer to the ‘best type of fat’ question partially depends on your genes.

My simplified overview of the genes involved in Omega-3 and Omega-6 fatty acids.
My simplified overview of the genes involved in Omega-3 and Omega-6 fatty acid elongation and desaturation.

Let’s start out with a simplified overview of polyunsaturated fats and how they are processed by your body. I’ll put links at the bottom for more in-depth information and better explanations.

Omega-6 fatty acids are named as such because they have a double carbon-carbon bond as the sixth bond, while omega-3 fatty acids have a double bond as the third bond.  Each one is metabolized in the body into other essential fatty acids.  Common sources of omega-6 (as linoleic acid) in the diet include corn, sunflower, cottonseed, and peanut oils.  Fats high in omega-3 as ALA include flaxseed and chia seed, while EPA and DHA can be found in fish oil.

Most nutritionists seem to agree that the ratio of omega-6 to omega-3 fatty acids is important to our health.  It is thought that our ancestors in the past ate a diet with a ratio of omega-6 to omega-3 was less than 4:1.  Currently, an average Western diet has a ratio of 16:1 or higher.  Omega-6 fats can have both inflammatory and anti-inflammatory properties, and it is thought that the higher ratio of omega-6 to 3 is causing an increase in inflammatory diseases such as heart disease and diabetes. [ref]

There isn’t just one “Omega-6” fat.  The term applies to a series of different chains of fatty acids that are changed in your body by enzymes called fatty acid desaturase (coded for by the FADS1 and FADS2 genes).  For example, if you eat a plant-based oil high in omega-6 fats (sunflower, cottonseed,  corn, etc), you are consuming it in the form of linoleic acid.  Linoleic acid can then be converted by FADS1 and FADS2 (in a couple of steps)  to arachidonic acid, which can be pro-inflammatory.

Similarly, omega-3 fatty acids from plant sources usually are in the form of alpha-linolenic acid. A small percentage of alpha-linolenic acid can be changed via the enzymes produced by FADS1 and FADS2 genes into eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).  DHA and EPA are touted for their effects on lowering the risk of heart disease and for their brain health benefits.

So notice that the same enzymes are involved in the metabolism of both the omega-6 and the omega-3 fatty acids.  This is where the ratio of the fats in your diet comes into play.  With only a limited amount of the desaturase enzymes available, a high ratio of omega-6 to omega-3 means that more of the omega-6 will be metabolized into arachidonic acid.

Genetics of Fatty Acid Metabolism:

Genes do come into play here.  The FADS1 (codes for delta-5 desaturase) and FADS2 (codes for delta-6 desaturase) genes have several different variants which slow down the production of the enzymes.

So what does a slowing of the production of these enzymes mean for your body? On the one hand, having less of the linoleic acid (omega-6) turning into the sometimes inflammatory arachidonic acid due to having less of the enzyme can be good.  But on the omega-3 side, this situation also produces less EPA and DHA if your diet is heavy on the omega-6 fatty acids.  One way around this is to eat very little omega-6 fat; another way is to directly get EPA and DHA from fish or fish oil.

Quite a few studies have found that those with variants that slow down the conversion of linoleic acid to arachidonic acid affect disease risks.  A 2008 study found that those with higher arachidonic acid to linoleic acid ratios had a higher risk of coronary artery disease.  [ref]  The opposite has also been found in that those with variants slowing down the FADS enzymes can have a lower risk of heart disease.

FADS1 Variants:
Note that some of these variants are considered linked, meaning that if you have the minor allele for one of them it is highly likely to have the minor allele for all of them.  

rs174546  (v.4 and v.5)(minor allele is T)  – those carrying the minor allele have lower enzyme activity[ref];  lower risk of coronary artery disease [ref]; lower conversion of LA to AA; minor allele benefits more from high intake of EPA and DHA to lower high triglycerides [ref]

rs174547 (v.4 and v.5 )(minor allele is C) – Lower gene expression for the minor allele [ref]

rs174537   (v.4 and v.5) ( minor allele is T) – Lower arachidonic acid and EPA levels [ref]; lower total cholesterol levels for the minor allele [ref] lower risk of type 2 diabetes [ref]

rs174548 (v.4 and v.5)(minor allele is G) – arachidonic acid and phosphatidylcholine is reduced in those with the minor allele[ref]

rs174550    (v.4 and v.5)(minor allele is C) – minor allele is associated with lower HDL and higher triglycerides [ref]

FADS2 Variants:

rs1535  (v.4 and v.5)(minor allele is G) – a lower rate of ALA to EPA conversion in adults with the minor allele [ref]; increased DHA levels in breastfed babies with the minor allele [ref];

rs174575  (v.4 and v.5)(minor allele is G) – part of a haplotype corresponding to higher linoleic acid and lower levels of arachidonic acid.  [ref]; several other studies on DHA in breastmilk that seem to possibly contradict each other.

Things to think about doing if you have FADS2 and FADS1 variants: 

  • Reducing your omega-6 to omega-3 ratio is a good idea (cut out the fried fast food!)
  • If you have a clean source of fish, increase your fish consumption.
  • If you are supplementing with flaxseed oil or chia seeds, you may be converting very little into DHA and EPA.  A fish oil supplement may be a better way to go.

More to read:

 

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