Difference between Omega-3, Omega-6, Omega-9 Fatty Acids

Why I wrote this post on essential fatty acids

This post is intense.  Not only is it intense, but you’re probably wondering why I’m bothering with it.  I mean, come on, I offer skincare products not dietary supplements or culinary oils.

Here’s the thing, an oil is not just an oil. 

It’s a complex blend of fatty acids that exist in different ratios depending on the plant that oil is pressed from and the part of the plant that oil is harvested from (fruit, flowers, stems, bark, etc.).

Even the region where a plant grows and the climate it experiences in any given year creates a very distinct oil composition – a vintage (and you thought that word was just for wine). 

Aside from the fatty acid composition of oils, a number of oil soluble compounds comprise the oil harvested from different plants, and this composition of oil soluble compounds is another reason why different oils have different characteristics. 

For instance, tamanu oil, a thick oil with a rich green color is rich in flavonoids and exhibits a unique fatty acid profile.  Compare that with pumpkin seed oil, a light orange oil, which gets that coloration from its high beta-carotene content.

Don’t worry, we’ll cover the characteristics of a wide variety of oils in future posts, but I really want to spend more time showing you what our body does with essential fatty acids (which are such an important part of the healing properties of certain oils).

The products we put on our skin get absorbed by our bodies.

So, understanding what happens when those ingredients get absorbed by my skin and by your skin is part of my job.  So, of course the question I ask myself is “What does it look like if we both use these products for life?”

And, I totally recognize that you don’t need to know this information. 

But, I'm thinking you may be just like me and have an innate curiosity.  And, since I already had the information at hand, I figured, what the heck, I might as well assemble it into one tidy blog post and at the very least make it available to you if you are interested.

After all, transparency is like, 100% of what Return to Eden is about.


This post is part two in a foundational series on essential fatty acids, polyunsaturated fatty acids (PUFAs), and monounsaturated fatty acids. 

We’re going deep here. 

We’re talking about how our body metabolizes omega-3 and omega-6 fatty acids all the way to forming arachidonic acid, eicosapentaenoic acid (better known as EPA, one of the magical fatty acids in fish oil), and docosahexaenoic acid (you’ll see this one listed as DHA in those fish oil supplements), and we aren’t stopping there.

We’re introducing eicosanoids – signaling molecules made from C20 PUFAs (polyunsaturated fatty acids), and then we’re talking about a specific subfamily of eicosanoids, prostaglandins.  We can’t very well talk about prostaglandins without mentioning the enzymes responsible for converting C20 PUFAs into prostaglandins, namely cyclooxygenase enzymes (you likely know them as COX-1 and COX-2).

Then, we’re talking about everybody’s favorite pain pills – NSAIDs (non-steroidal anti-inflammatory drugs). 

Why NSAIDs? 

Well, prostaglandins play a role in our body’s inflammatory responses, and NSAIDs impact which prostaglandins are made because they inhibit enzymes responsible for creating those particular prostaglandins.

So, what’s my obsession with prostaglandins? 

These molecules impact many aspects of our health, and they’re interwoven with our immunity, our ability to carry a pregnancy to term, our ability to detect abnormal cells within our body before they have a chance to turn into a cancerous growth, AND the unsaturated fatty acids we eat and apply to our skin can potentially impact which prostaglandins our body makes.

Sounds pretty important, right?

While this post is mostly for the girls out there who need to understand everything, more than anything it’s a foundational post, a reference article for future (lighter) posts.  If you don’t understand everything here, don’t worry.  I encourage you to read (or skim) it anyway as I’m sure you’ll find parts of this article fascinating.

Without further intro, let’s get into it.

Starting with a recap of Omega-3 and Omega-6 Fatty Acids

Omega-3 fatty acids include alpha-linolenic acid (ALA), which can be converted by our body to eicosapentaenoic acid (you’ll recognize this fatty acid as EPA), which can be further converted by our body to docosahexaenoic acid (DHA). 

Omega-3 fatty acids are essential to our diets because our body cannot make this class of fatty acids by itself. 

While it’s a good idea for us to include DHA and EPA in our diets, at the very least we need to receive alpha-linolenic acid (ALA) from the foods we eat to provide the nutrient necessary to create EPA and DHA internally.

Omega-6 fatty acids include linoleic acid (LA), which can be converted by our body to gamma-linolenic acid (GLA), further converted to dihomo-gamma-linoleic acid (DGLA), and even further converted to arachidonic acid in our body. 

Like omega-3 fatty acids, omega-6 fatty acids (at the very least linoleic acid) are essential to our diets because our body cannot make this class of fatty acids by itself.

We’ll talk about Omega-9 fatty acids in a minute, but before we get there, let’s take a look at the structure of an omega-3 and omega-6 fatty acid.

 structure of alpha-linolenic acid, an omega-3 fatty acid

Figure 1.  The omega-3 fatty acid, alpha-Linolenic Acid (ALA), with the formula C18H30O2

structure of linoleic acid, an omega-6 fatty acid and essential fatty acid

Figure 2.  The omega-6 fatty acid, linoleic Acid (LA), with the formula C18H32O2

Interpreting Molecular Drawings

If you’re not used to looking at chemical structures this way, I know you’re thinking “What am I looking at?” and more importantly “Why do I care?”

Well, here’s why you should care. 

The location of that first double bond makes the difference in whether the fatty acid is classified as an omega-3 or an omega-6 fatty acid.

Double bond?  Okay, let’s take a step back and talk about just what we’re looking at with those figures.

We’re going to start out with the simplest fatty acid structure, a saturated fatty acid.

saturated fatty acid, palmitic acid

Figure 3.  Palmitic acid (saturated fatty acid) with the formula C16H32O2.

In organic chemistry, it’s very common to draw the chemical structure as shown in this figure.

Each line of the zig-zag in the figure represents a connection between two carbon atoms, so essentially, the point of each zig or zag represents a carbon atom. 

Atoms that are not carbons are labeled as “O” for oxygen and “OH” for an oxygen atom bound to a hydrogen atom.  Each carbon atom can have a total of four bonds (each line leaving a point is one bond, and a double line represents two bonds to a neighboring carbon atom). 

The bonds not shown in the figure are bonds between carbon atoms and hydrogen atoms, and it just gets too messy to show ALL those bonds.

For palmitic acid, a single bond joins each carbon atom with the carbon atom on either side of it.  As mentioned above, this type of fatty acid is known as a saturated fatty acid.  Why? 

Because every carbon along the carbon chain of the molecule is saturated with hydrogens and there’s only a single bond between neighboring carbon atoms.

Back to the omega-3 and omega-6 fatty acids

For alpha-linolenic acid and linoleic acid, you’ll see two lines between some of those carbon atoms.  Here’s alpha-linolenic acid (ALA) again with the double bonds circled in blue.

omega-3 fatty acid alpha-linolenic acid with the double bonds circled in blue

Figure 4.  The omega-3 fatty acid, alpha-Linolenic Acid (ALA), with the formula C18H30O2

Any fatty acid with double bonds between neighboring carbons in the carbon chain is an unsaturated fatty acid.

If there’s only one double bond in that carbon chain, the fatty acid is classified as a monounsaturated fatty acid. 

If there are two or more double bonds (as you can see there are for alpha-linolenic acid, ALA and linoleic acid, LA), then the fatty acid is classified as a polyunsaturated fatty acid.

You’ll notice the Greek letter, ω, omega in red in to the far right in the figures above and below.  That’s the omega end of the molecule.

And, you’ll also see red numbers, which correspond to the number of carbons in the chain when we start numbering at the omega end of the molecule. 

Here’s the structure of ALA and linoleic acid (LA) again.

 structure of omega-3 essential fatty acid, alpha-linolenic acid (ALA)

Figure 5.  Omega-3 fatty acid alpha-Linolenic Acid (ALA) with the formula C18H30O2

the structure of the essential fatty acid omega-6, linoleic acid (LA)

Figure 6.  Omega-6 fatty acid linoleic Acid (LA) with the formula C18H32O2

Notice where the first double bond (counting from the omega end) is located in both these molecules. 

For omega-3 fatty acids, the first double bond is between the 3rd and 4th carbon of the molecule if we’re counting from the omega end (red numbers). 

For omega-6 fatty acids, the first double bond is between the 6th and 7th carbon of the molecule if we’re counting from the omega end (red numbers).

ALL omega-3 and omega-6 fatty acids are polyunsaturated fatty acids, which is a key distinguishing feature between these types of fatty acids and omega-9 fatty acids.

Omega-9 fatty acids are any mono-unsaturated fatty acid.  Oleic acid is one of the most common in our diet, so here’s the structure of oleic acid for comparison with ALA and LA above.

 structure of monounsaturated fatty acid, oleic acid (cis structure)

Figure 7.  An omega-9 fatty acid, oleic acid, with the structure C18H34O2 (the cis structure, instead of the trans structure is shown above)

Unlike omega-3 and omega-6 fatty acids, our body can make omega-9 fatty acids from the foods we eat. 

How our body uses omega-3 and omega-6 fatty acids

Now that we know the basic structure of omega-3, omega-6, and omega-9 fatty acids, let’s have a look at what our body does with omega-3 and omega-6 fatty acids.

metabolic pathway of omega 3 and omega 6

Figure 8.  How our body creates other fatty acids from ALA and LA (Reference 1).

We use two different classes of enzymes, elongase and Δ5 or Δ6-desaturase, to create longer chain fatty acids from the essential omega-3 fatty acid, ALA, and the essential omega-6 fatty acid, LA.  We also use elongase and those same two desaturase enzymes along part of the omega-9 pathway. 

Since we use the same enzymes to process omega-3 and omega-6 fatty acids, the ratio of omega-3 to omega-6 in our diets is really important! 

Most experts recommend a 4 to 1 ratio of omega-6 to omega-3, and it’s been shown that risk of certain cancers is improved by changing that ratio to 2 to 1 omega-6 to omega-3 fatty acids (Reference 11). 

The American diet is more along the lines of 16 to 1 ratio of omega-6 to omega-3.  What do all these ratios look like? 


Omega-6 Intake

Omega-3 Intake

Modern American diet

5 Tablespoons (Tbsp., the big spoon)

1 teaspoon (tsp., the little spoon)

Recommended diet

1 Tbsp. + 1 tsp.

1 tsp.

Preferred diet for reducing risk of developing certain types of cancers

2 tsp.

1 tsp.


Why a 4:1 or 2:1 ratio of omega-6:omega-3?  Well, what I haven’t mentioned yet is that these particular desaturase enzymes have a higher affinity for omega-3 fatty acids than they do for omega-6 fatty acids. 

They also have a higher affinity for omega-6 fatty acids than for omega-9 fatty acids.  So, the enzymes prefer to bind with the omega-3 over the omega-6 or the omega-9 fatty acids.

How much ALA gets converted to EPA and DHA?

It’s been shown that healthy young men convert about 8% of dietary ALA to EPA and convert between 0% and 4% of ALA to DHA.  The conversion in healthy young women is higher with about 21% of dietary ALA converted to EPA and about 9% converted to DHA (Reference 2). 

Aside from gender, genetics and age play a big role in how much of the essential fatty acids are converted to these conditionally essential fatty acids. 

As we age, conversion rates tend to drop, and depending on your genes, you may convert ALA and LA better (or worse) than other people.  The low conversion rate is also why EPA and DHA are considered conditionally essential.

The same holds true with our body’s ability to convert the omega-6 LA to gamma-linolenic acid (GLA) and then onto DGLA and finally to arachidonic acid (AA).

We talked in our previous post about why EPA, DHA, and AA are important for our health.  These fatty acids get incorporated into our cellular membranes and are important for our vision, our mind, fetal development, and our skin’s health.

Here, we’re going to go a step further and talk about what our body does with EPA, DHA, and AA.

EPA, DHA, and AA – precursors for signaling molecules

What the heck is a signaling molecule?  These ever so important molecules are how the cells of your body communicate with one another.  Signaling molecules play important roles in local inflammation (for example, when we get a cut or scrape), pregnancy (all the way from ensuring the body recognizes the fetus as part of itself to instigating contractions at the time of delivery), regulating cell growth, controlling blood pressure, fighting infections such as a cold or flu, etc.).

Signaling molecules are incredibly important for our health.

Eicosanoids are a class of signaling molecules made by the oxidation of PUFAs that are 20 carbon units long. 

Arachidonic acid (AA), its precursor dihomo-γ-linolenic acid or DGLA, and eicosapentaenoic acid (EPA) are all PUFAs (polyunsaturated fatty acids) with 20 carbon units.

The term eicosanoid is pretty inclusive and encompasses signaling molecules in a variety of different families. 

For the remainder of this post, we’re going to talk about one particular family of eicosanoids: prostaglandins (PG).

Prostaglandins: A specific class of signaling molecule

All prostaglandins have the basic structure shown in the figure below.

basic structure of prostaglandins

Figure 9.  Basic structure for the prostaglandins.

Despite having a basic structure, there are three classes of prostaglandins (PG) and like 8 subclasses, so yeah, there are a lot of different prostaglandins, and each one does a different thing in the body, and sometimes, each one does different things in different parts of the body.

Class 1 prostaglandins have one double bond and are created from dihomo-γ-linolenic acid or DGLA (DGLA’s precursor is γ-linolenic acid (aka gamma-linolenic acid or GLA), which is derived from the omega-6 linoleic acid). 

DGLA, GLA, and LA are all omega-6 fatty acids if you’re tired of scrolling up to check.

Class 2 prostaglandins have two double bonds and are created from arachidonic acid (AA), which is derived from DGLA whose precursor is GLA whose precursor is LA.  Class 2 prostaglandins are also created from the omega-6 fatty acid metabolism pathway.

Class 3 prostaglandins have three double bonds and are created from eicosapentaenoic acid (EPA), whose precursor is alpha-linolenic-acid (ALA), the essential omega-3 fatty acid.

Each prostaglandin class is further broken down into categories depending on substitution on the cyclopentanone ring.  There’s subclass:  A, B, C, D, E, F, G, H, and I. 

So, you’ll often see prostaglandins written as PGE2, which means it’s a class 2 prostaglandin (2 double bonds) with a specific make-up and orientation of the cyclopentanone ring. 

If you want to read more about prostaglandin nomenclature and structure, check out this reference (Reference 3).

DGLA, AA, and EPA can all be metabolized in our body to create different prostaglandins.

Prostaglandins and other eicosanoids are rapidly metabolized, so they don’t hang around in our body for very long. 

Since prostaglandins aren’t stored, they’re manufactured as needed by releasing fatty acids from the cell membrane (remember, fatty acids are incorporated into the phospholipid cell membrane – if you want a refresher on that, check out our previous blog post here).

Inflammatory or Anti-Inflammatory… well, both

You may have heard that arachidonic acid is pro-inflammatory.  Well, that’s not the whole story.  And, here’s where we’ll introduce yet more terms. 

Don’t leave, you’ll likely recognize these guys:  COX-1, COX-2, and LOX. 

All three of these terms are acronyms for enzymes.  COX stands for cyclooxygenase, and you recognize this because common NSAIDs (non-steroidal anti-inflammatory drugs like ibuprofen and meloxicam) are COX inhibitors.  LOX stands for lipoxygenase.

Our body always has COX-1 hanging around, in fact, it’s called a constitutional enzyme because it’s ever present.  In times of stress and inflammation, our body generates COX-2, which is why it’s known as an inducible enzyme. 

Let’s look at how DGLA, AA, and EPA are converted in the presence of COX enzymes (LOX pathways are also shown, but those pathways are beyond the scope of this post). 

how fatty acids get converted to prostaglandins COX-1, COX-2, and LOX pathways

Figure 10.  Metabolism of PUFAs arachidonic acid, DGLA, EPA, and DHA (Reference 2).

Different tissues in our body can generate COX-2 when those tissues receive certain signals. 

For instance, COX-2 is generated in our skin in response to the presence of radical oxygen species (ROS) and UV exposure.  Arachidonic Acid (AA) gets metabolized to PGE2 (Prostaglandin E2) in the presence of COX-2, and this is a potent pro-inflammatory molecule that is the major contributor to UV-induced inflammation (hello sunburn!). 

EPA (omega-3) is converted to PGE3 (Prostaglandin E3) another pro-inflammatory molecule, but much less potent than PGE2 (Reference 2 and Reference 5).

Are you telling me fish oil can help protect me from sunburn?

I’m telling you that including fish oil or other oils high in omega-3 in your diet OR topically applying oils high in omega-3 can attenuate (alter/modify/reduce) the effects of UV exposure resulting in a less severe immediate response. 

In fact, one study shows the minimal erythemal dose (MED), which is the lowest dose of sun exposure that results in detectable redness 24 hours later was significantly increased (meaning the folks in the study could sunbathe longer without developing a sunburn the next day) in people who consumed 2.8 grams DHA and 1.2 grams EPA per day for four weeks before sun exposure. 

That’s right!  Including EPA and DHA in your diet might help you keep from getting sunburned… if you take enough of it for long enough before sunbathing – just so you know, this is NOT a pass to sunbathe (even though the sun just feels so darn good sometimes, and hey, we need it for Vitamin D synthesis, right?).

Another study showed topical application of sardine oil provided sun protection as well, but walking around smelling like fish oil seems like a pretty high price to pay for sun protection (Reference 2).

Inflammation is NOT a bad thing

Sometimes, acute inflammation can be just what you want (even if it’s painful).

As a society, we are so adverse to pain that we don’t realize pain can be a good thing. 

Inflammation causes pain, and acute inflammation is part of the healing process, which is a really good thing. 

You can see in the figure below that arachidonic acid can create beneficial eicosanoids (signaling molecules taking the pathway below towards tissue repair) and also pro-inflammatory eicosanoids (the prostaglandins fall into that category) that can lead to chronic inflammation.

role of arachidonic acid in tissue recovery and healing

Figure 11.  Metabolic pathways of arachidonic acid and DHA (Reference 7).

The problem with inflammation is that it’s a bad thing when it’s chronic. 

Arachidonic acid has gotten a bad rep because it’s associated with pro-inflammatory prostaglandins, but we forget that acute inflammation is the first step to recovery.

One last note before you go running for the ibuprofen because at this point it’s totally unclear what the point of this article is about, I’ve made your head hurt, and you’re worried about COX-2 and chronic inflammation. 

Balance is Key

Do you remember when Vioxx was pulled from the market back in the early 2000s? 

For a long time, pharma companies have been attempting to selectively inhibit COX-2 without inhibiting COX-1 expression because COX-1 is important in maintaining the stomach’s mucus lining that keeps us from getting ulcers due to reading unwieldy blog posts that seem to be going down a rabbit hole.

Vioxx worked wonders at selectively inhibiting COX-2 without messing with COX-1 levels, but after it was approved, pharmacovigilance teams started to see a pretty significant uptick in the number of cardiovascular events (heart attack and stroke).  In 2004, Vioxx was pulled from the market.

Why this association between selective inhibition of COX-2 and heart attack and stroke? 

Well, in addition to maintaining the stomach’s mucus lining, COX-1 is also responsible for vasoconstriction and platelet aggregation.  COX-2 counters (BALANCES) the effects of COX-1 by being an equally potent vasodilator.  COX-2 also reduces the potential for platelets to aggregate (Reference 2 and Reference 4). 

So, by reducing our body’s ability to produce COX-2 without also reducing its ability to produce COX-1, we wind up with an out of balance system and run the risk of cardiovascular events (events sounds so pleasant doesn’t it?  Not at all like something life altering/life threatening). 

If you’re wondering which NSAID you should be taking, well, it depends (What, you thought I was going to give you medical advice?  That’s between you and your doctor). 

You can reference these articles to see what researchers found regarding selective inhibition of COX-1 vs. COX-2 with different NSAIDs (Reference 3 and Reference 4).

Brief Summary

Alright, let’s recap what we’ve discussed here.

We started out talking again about the basic structure of omega-3 and omega-6 fatty acids.  We talked about the difference between these two classes of PUFAs and compared them to omega-9 (a class of monounsaturated fatty acids).

Then, we looked at how our body metabolizes (processes) these fatty acids.  We spent quite a bit of time talking about prostaglandins, the signaling molecules responsible for pro-inflammatory responses in the body (it’s unclear at this time whether prostaglandins are also involved in anti-inflammatory responses or if they just hasten the way towards anti-inflammatory responses). 

Since we were talking about inflammation anyways, we went on to talk a little bit about COX-1 and COX-2 enzymes.

Again, this is a foundational post, and may not be of much interest to you here where it seems out of context… at least for now.  As you start reading more and more of our planned articles on PUFAs, you might just see us referencing this post more and more. 

Until then, if you’ve got a test on metabolomics of fatty acids, well, you know where to find me.


Reference 1.  https://www.tuscany-diet.net/tag/polyunsaturated-fatty-acids/

Reference 2.  Essential Fatty Acidshttps://lpi.oregonstate.edu/mic/other-nutrients/essential-fatty-acids#deficiency

Reference 3.  William W. Christie.  Prostanoids: Prostaglandins, Prostacyclins
and Thromboxanes.  https://www.lipidhome.co.uk/lipids/fa-eic/eicprost/index.htm

Reference 4.  Zreik, T, Behrman, H, Glob. libr. women's med., The Prostaglandins: Basic Chemistry and Action (ISSN: 1756-2228) 2008; DOI 10.3843/GLOWM.10313 Under review - Update due 2020.  https://www.glowm.com/section_view/heading/The%20Prostaglandins:%20Basic%20Chemistry%20and%20Action/item/312

Reference 5.  Hruza LL1Pentland APJ Invest Dermatol. 1993 Jan;100(1):35S-41S.  Mechanisms of UV-induced inflammation.  https://www.ncbi.nlm.nih.gov/pubmed/8423392

Reference 6.  https://www.researchgate.net/figure/2-Oxygenation-pathways-of-arachidonic-acid-AA-and-docosahexaenoic-acid-DHA-in-CNS_fig1_273133662

Reference 7.  https://images.app.goo.gl/RrZDJMvayctU98ka6

Reference 8. https://academic.oup.com/jn/article/128/2/427S/4724041

Reference 9.  Koletzko B: Human Milk Lipids. Ann Nutr Metab 2016;69(suppl 2):27-40. doi: 10.1159/000452819.

Reference 10.  https://www.dietobio.com/dossiers/en/nuts/fats.html

Reference 11.  The importance of the ratio of omega-6/omega-3 essential fatty acids. https://www.ncbi.nlm.nih.gov/pubmed/12442909

Reference 12.  February 2010.  Vegetarian’s Challenge — Optimizing Essential Fatty Acid Status.  By Brenda Davis, RD.  Today’s Dietitian.  Vol. 12 No. 2 P. 22

Additional References

Journal of Neuroscience 23 March 2005, 25 (12) 3032-3040; DOI: https://doi.org/10.1523/JNEUROSCI.4225-04.2005.




Are Neurodegenerative Disorder and Psychotic Manifestations Avoidable Brain Dysfunctions with Adequate Dietary Omega-3?  Letten F. SaugstadFirst Published July 1, 2006 Research Article Find in PubMedhttps://doi.org/10.1177/026010600601800302


Omega-3 for your eyes. https://www.health.harvard.edu/heart-health/omega-3-for-your-eyes

Fatty Acid Composition of Human Brain Phospholipids during Normal Development.  https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1471-4159.1998.71062528.x

Journal of Lipid Research.  Lipid composition of the normal human brain: gray matter, white matter, and myelin*John S. O'Brien and E. Lois Sampson.  October 1965.  Volume 6, pages 537-544.

Fatty Acids and the Aging Brain.  Alyssa Bianca Velasco, Zaldy S. Tan, in Omega-3 Fatty Acids in Brain and Neurological Health, 2014

Fatty Acid Composition of the Brain.  https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/lipid-composition


vegan sources of omega-3 and omega-6 fatty acids

Brandy Searcy founder Rain Organica

About the Author

Brandy's a formulation scientist and self-proclaimed health geek who loves hiking, gardening, bird-watching, and body boarding. 

Her struggle with acne during her teens and 20s led to a holistic and healthy approach to skincare, embracing skin as an organ to be loved and cared for rather than a canvas to wage war on. 

Since 2008, she's been developing all-in-one products for a simple routine at home, & Rain Organica started when her backpacking friends asked for a portable skincare routine to keep their skin healthy & happy on and off the trails.

You can try Rain Organica for yourself with The Essentials Kit, a complete skincare routine in just 3 steps.

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