If you follow our nutrition discussions online, you may have noticed a certain lack of nuance. You know the drill, eggs are either a super food or eggs are worse than cigarettes, it just depends on who you ask.
The same applies to vegetable oils.
The party line for a long time has been that vegetable and seed oils are problematic because they are high in omega 6 fats, and when eaten to excess, omega 6 fats drive inflammation.
However, a recent Harvard Health blog encourages people to replace saturated fats with polyunsaturated fats, like vegetable oils. Harvard says omega 6 fats have significant health benefits, but does this research apply to everyone?
In this post, I am going to show you why Harvard’s nutrition advice is wrong for 80% of the African American population and for people like me, who don’t metabolize omega 6 fats like everyone else. But before we discuss why a personalized approach to polyunsaturated fats is necessary, let’s first explore why vegetable oils, and omega 6 fats generally, are thought to be pro-inflammatory.
Why omega 6 fats can be pro-inflammatory
Some of the fats we eat are burned for energy, while others form our cell membranes. 1 Cholesterol and polyunsaturated fats make their way into cell membranes whereas MCT fats are largely burned as fuel.
In the Western diet, more of our cell membranes are made up of polyunsaturated omega 6 fats as the amount of canola, sunflower, safflower and peanut oils we eat increases.
This 2018 review does a good job of summarizing the current thinking on why omega 6 fats can trigger inflammation. One the side of the omega 6 fats are inflammatory camp – the Western world is seeing a greater share of cell membranes made up of arachidonic acid (ARA), an omega 6 fat that is known drive inflammation when produced in excess. Think of it this way: Americans eat so much omega 6 fats that they have become the oil our human engines run on.
When we have more omega 3 fats in the diet, they form the bulk of our cell membranes and the immune system quiets down, which means lower inflammation. By contrast, when the ratio of omega 6 fats goes up, the immune system gets irritated, which stimulates the production of inflammatory markers called eicosanoids. 2
However, despite biochemical evidence of omega 6 driving inflammation, many studies simply don’t show an uptick in inflammatory markers when ARA and linoleic acid is increased in the diet. Further, omega 6 fats are viewed by many as preferable to saturated fats because saturated fats tend to increase LDL.
This is why you have the Harvard Health blog recommending people use vegetable oils rather than avoid them.
But here’s the problem. The Harvard Health blog assumes that most of us won’t convert meaningful amounts of linoleic acid into the pro-inflammatory ARA. Consider this quote:
It turns out that the body converts very little linolenic acid into arachidonic acid, even when linolenic acid is abundant in the diet. The AHA reviewers found that eating more omega-6 fats didn’t rev up inflammation. Instead, eating more omega-6 fats either reduced markers of inflammation or left them unchanged. Many studies showed that rates of heart disease went down as consumption of omega-6 fats went up.
The above quote is the problem with one-size fits all diet advice and with a lot of clinical research in general. It tends to put all of us against the template of the healthy white male. And I happen to be a healthy white male, but I also carry a genetic variant, that is more common in the Black and Mexican communities, that results in the increased conversion of linoleic acid into ARA.
Omega 6 rich diets and the Black community
As I wrote about in my post on omega 3 deficiency in the Vegan community, variants in the FADS1 gene (rs174537) are much more common in the Black community than in European populations. Carriers of the G allele convert much more of the linoleic acid they eat into ARA, and 80% of African Americans carry two copies of this “mutation.” It’s not clear to me how we can continue to say things like “the body converts very little linoleic acid to ARA” as if we all metabolize these fatty acids in identical fashion when there is solid scientific research indicating that the response is highly personalized based on nutrigenomics.
Consider this study, published in BMC Genetics, titled The impact of FADS genetic variants on ω6 polyunsaturated fatty acid metabolism in African Americans. To quote the study:
the impact of FADS genetic variants on PUFA metabolism, specifically AA levels, is likely more pronounced in African Americans due to the larger proportion of individuals carrying the genotype associated with increased FADS1 enzymatic conversion of LA to AA.
Sadly, there is a scarcity of research looking at polyunsaturated fat metabolism in African American and Hispanic populations. Even this meta-analysis of 15 studies, which concluded, as Harvard has, that greater consumption of linoleic acid in the diet didn’t result in an increase in inflammatory markers looked at almost exclusively European populations. The one study (out of 15) that was done in South Africa did not disclose its racial makeup.
This is why we must personalize nutrition and why articles claiming DNA diets “don’t work” are unbelievably premature. The research is mounting, but most still ignore it.
In the case of omega 6 fats, the determining factor as to whether they are to be included as part of a healthy diet could be genetics and how much of the linoleic acid we eat converts into ARA.
We have strong evidence that certain communities would be better served limiting these types of fats because they could have a greater inflammatory impact. To quote a review published in Current Nutrition Reports:
What if 6-8% of energy from LA were converted to ARA in African Americans? Would this change the dietary recommendations for PUFAs? We certainly believe it should given the role ARA and its eicosanoid product plays in human diseases and the link between FADS variants to a variety of human disease and particularly heart disease.
We know that some of the standard advice on heart health, such as maintaining a good triglyceride to HDL ratio doesn’t apply to the Black community because African Americans typically have naturally low levels of triglycerides.
The standard advice on omega 6 fats is that they are healthy substitutes for saturated fats because most people don’t convert omega 6 fats into inflammatory byproducts. However, that advice is predicated on certain genotypes and much of the research has failed to address genetic differences in the Black and Hispanic communities.
While it is clearly not a good idea to suggest that people should go load up on ketogenic style, high saturated fat foods, it’s also not prudent to offer one size fits all diet advice for a diverse, multi-ethnic population.
We need further research to see how omega 6 rich diets may affect the Black and Hispanic populations in ways that are different from European populations where most of the research has been conducted to date.