Reference for Lipids and Fats

Below is a list of saturated, monounsaturated and polyunsaturated fats showing alternate names, the isomer, and the most common food sources.

After the list follow a few notes on the basic properties of different fats and basic interactions.

Omega 3 fatty acids are in blue, omega 6 fats in red and omega 9 fats in green.

Essential fatty acids are marked with a *.

The list shows the main fats encountered in diet but is not a complete list - have chosen to miss out some of the very unusal lipids to save space.

Saturated Fats

Short Chain Saturated Fats (SCFAs or SCTs)

Butyric acid or butanoic acid (4:0)
butter, cheese

Medium Chain Saturated Fats (MCFAs or MCTs)

Caproic acid or hexanoic acid (6:0)
butter, diary, goat & sheep’s milk

Caprylic acid or octanoic acid (8:0)
baby milk formula, nuts, coconut oil, vegetable oil

Capric acid or decanoic acid (10:0)
baby milk formula, cheese, vegetable oil, coconut oil

Lauric acid or dodecanoic acid (12:0)
coconut oil, palm oil, breast milk

Long Chain Saturated Fats (LCFAs or LCTs)

Tridecanoic acid (13:0)
cheese, chicken, tomato

Myristic acid or tetradecanoic acid (14:0)
milk, dairy

Pentadecanoic acid (15:0)
cheese, meat

Palmitic acid or hexadecanoic acid (16:0)
palm oil, meat, poultry, fish

Margaric acid or heptadecanoic acid (17:0)
lamb, beef, pork

Stearic acid or octadecanoic acid (18:0)
meat, poultry, cocoa butter

Arachidic acid or eicosanoic acid (20:0)
peanuts, nuts, vegetable oils

Very Long Chain Saturated Fats (VLCFAs or VLCTs)

Behenic acid or docosanoic acid (22:0)
peanuts, nuts, veg oils

Lignoceric acid or tetracosanoic acid (24:0)
nuts, seeds, veg oils, seed oils

Monounsaturated Fats

Myristoleic acid or tetradecenoic acid 14:1
whale meat, red meat, dairy

Pentadecenoic acid (15:1)
tofu, miso, whale meat, poultry

Palmitoleic acid or hexadecenoic acid (16:1 undifferentiated)
whale, seal, nuts, avocado, poultry

Heptadecenoic acid (17:1)
tofu, cheese, meat

Oleic acid or octadecenoic acid (18:1 undifferentiated)
avocados, veg oil, nuts, goose fat, margarine

Gadoleic acid or eicosenoic acid (20:1)
seal, whale, fish

Erucic acid or docosenoic acid (22:1 undifferentiated)
veg oil, fish, mustard, watercress

Nervonic acid or cis-tetracosenoic acid (24:1c)
mustard, fish, margarine, nuts

Polyunsaturated Fats

Linoleic acid (LA) or octadecadienoic acid (18:2 undifferentiated)
poultry, avocado, eggs, cereals, veg oils, grains

Alpha-linolenic acid (ALA) or octadecatetraenoic acid (18:3 n-3 c,c,c)*
hemp, soya, flax

Gamma-linolenic acid or octadecatetraenoic acid (GLA) (18:3 n-6 c,c,c )*
primrose, hemp, blackcurrant oils

Octadecateraenoic acid (18:4 undifferentiated)
fish, molluscs

Eicosadienoic acid (20:2 n-6 c,c)
pine nuts, seal, poultry

Arachidonic acid or eicosatetraenoic acid (20:4 undifferentiated)
fish, meat, poultry

Eicosapentaenoic acid (EPA) or timnodonic acid (20:5 n-3)
fish, seal, molluscs

Docosapentaenoic acid (DPA) or clupadondonic acid (22:5 n-3)
seal, meat, poultry

Docosahexaenoic acid (DHA) 22:6 n-3
fish, seal, caviar

General Comments

Saturated Fats of between 12:0 and 18:0 raise LDL cholesterol

Myristic acid (14:0) increases HDL cholesterol

Trans saturated Fats (not listed) increase LDL cholesterol and lower HDL cholesterol

Monounsaturated Fats raise HDL cholesterol

Omega 3 Polyunsaturated Fats raise HDL cholesterol

Smoking lowers HDL cholesterol

Essential fatty acids (cannot be synthesised within humans) are:
Alpha-linolenic acid (omega 3 polyunsaturated)
Gamma-linolenic acid (omega 6 polyunstaurated)

Near essential fatty acids (can be synthesised within human but usually not to adequet levels) are:
Eicosapentaenoic acid (EPA) (omega 3 polyunsaturated)
Docosahexaenoic acid (DHA) (omega 3 polyunsaturated)
Oleic acid (omega 9 monounsaturated)

The omega 9 monounsaturated fat Oleic acid reduces total and LDL cholesterol

The saturated fat Myristic acid (14:0) increases HDL cholesterol as well as LDL cholesterol

The omega 6 polyunsaturated fat Linoleic acid prevents the LDL raising effects of palmitic acid when at a 1/5 ratio or better (such as in coconut oil), and may also do the same for other saturated fats although the ratio at which this may occur is not not known.

That bastard list took me ages to compile and double check. No cut and paste job.

There's no 'thanks' button on this forum but i'd click it if i could.

Excellent reference article there mate!

excellent post mate.

Top work!

I will add one thing tho:

The general comments:

Saturated Fats of between 12:0 and 18:0 raise LDL cholesterol

Myristic acid (14:0) increases HDL cholesterol

Trans saturated Fats (not listed) increase LDL cholesterol and lower HDL cholesterol

Monounsaturated Fats raise HDL cholesterol

Omega 3 Polyunsaturated Fats raise HDL cholesterol

I feel are a bit generalised for what is a very complex mechanism.
And often any studies into which fatty acids effect cholesterol are 'ratio changes', i.e substituting satured for polyunsatured or whatever.
The effect will differ depending on the fatty acid too, for example someone who is totally deficient in EFA's will see massive changes in physiology upon consumption of small amounts, whereas a much larger change in a non essential saturated fat will see barely any effect on physiology.
Obviously this is because the EFA's have a structural use in the cell membranes phospholipids, which is also why trans fats are so destructive in small quantities because they are often omega 3/6 fats that have been hydrogenated and their structure changed.

Another factor is displacement, adjusting one fatty acid changes how much of another is used, due to enzyme function

Dietary ω-3 decreases tissue concentrations of AA. Animal studies show that increased dietary ω-3 results in decreased AA in brain and other tissue. Linolenic acid (18:3 ω-3) contributes to this by displacing linoleic acid (18:2 ω-6) from the elongase and desaturase enzymes that produce AA. EPA inhibits phospholipase A2's release of AA from cell membrane. Other mechanisms involving the transport of EFAs may also play a role.

The reverse is also true – high dietary linoleic acid decreases the body's conversion of α-linolenic acid to EPA. However, the effect is not as strong; the desaturase has a higher affinity for α-linolenic acid than it has for linoleic acid

increasing certain saturated fats is known to reduce omega 3 : omega 6 ratio in cell membranes (which is one of the reasons they have nock on effects, even tho they are not directly used)
It actually gets crazy complicated, which is why i've basically followed the rule of 'a good mix of natural foods that people have thrived on' interests me deeply nontheless.

There's even large differences on health depending on DHA/EPA ratio, DHA can be produced from EPA but is limited by an enzyme, thus changing the ratio changes enzyme usage and has nock on effects.
Then there's likelyhood of lipid peroxidation etc etc etc.....

Excellent post Det. Really good.

I never knew the Tridecanoic acid in tomatoes one.

I have also stopped eating peanuts (which was mostly peanut butter) for the past year. As must as I like the taste of peanuts and peanut butter I don't like some of the fats in them. Plus they're very acidic lol

Pain wrote:i've basically followed the rule of 'a good mix of natural foods that people have thrived on'

So easy and simple, yet most people just don't get this.

Pain wrote:I will add one thing tho:

The general comments:

Saturated Fats of between 12:0 and 18:0 raise LDL cholesterol

Myristic acid (14:0) increases HDL cholesterol

Trans saturated Fats (not listed) increase LDL cholesterol and lower HDL cholesterol

Monounsaturated Fats raise HDL cholesterol

Omega 3 Polyunsaturated Fats raise HDL cholesterol

I feel are a bit generalised for what is a very complex mechanism.
And often any studies into which fatty acids effect cholesterol are 'ratio changes', i.e substituting satured for polyunsatured or whatever.
The effect will differ depending on the fatty acid too, for example someone who is totally deficient in EFA's will see massive changes in physiology upon consumption of small amounts, whereas a much larger change in a non essential saturated fat will see barely any effect on physiology.
Obviously this is because the EFA's have a structural use in the cell membranes phospholipids, which is also why trans fats are so destructive in small quantities because they are often omega 3/6 fats that have been hydrogenated and their structure changed.

Another factor is displacement, adjusting one fatty acid changes how much of another is used, due to enzyme function

Dietary ω-3 decreases tissue concentrations of AA. Animal studies show that increased dietary ω-3 results in decreased AA in brain and other tissue. Linolenic acid (18:3 ω-3) contributes to this by displacing linoleic acid (18:2 ω-6) from the elongase and desaturase enzymes that produce AA. EPA inhibits phospholipase A2's release of AA from cell membrane. Other mechanisms involving the transport of EFAs may also play a role.

The reverse is also true – high dietary linoleic acid decreases the body's conversion of α-linolenic acid to EPA. However, the effect is not as strong; the desaturase has a higher affinity for α-linolenic acid than it has for linoleic acid

increasing certain saturated fats is known to reduce omega 3 : omega 6 ratio in cell membranes (which is one of the reasons they have nock on effects, even tho they are not directly used)
It actually gets crazy complicated, which is why i've basically followed the rule of 'a good mix of natural foods that people have thrived on' interests me deeply nontheless.

There's even large differences on health depending on DHA/EPA ratio, DHA can be produced from EPA but is limited by an enzyme, thus changing the ratio changes enzyme usage and has nock on effects.
Then there's likelyhood of lipid peroxidation etc etc etc.....

Great post Sam. It's certainly a bitch of a subject because, as you perfectly highlight, the 'rules' of the interactions vary a fair bit according to ratios, not just between all the lipids but also possibly against other macros and activity. Fortunately most of the 'trends' seem to be fairly consistent.

If anyone has anything else to add or amend jump right in. Such a big subject it's easy to miss things... that's why I really wanted to do this 'reference thread', so that it's easier to find info.

Pain wrote:'a good mix of natural foods that people have thrived on'

Most definitely the diet to aim for.

^^ definitely.

Great posts guys.

Big ups Det, cheers for putting the effort in on this one.

Without meaning to cajole you into another post of similar length & detail, how does this info translate to your diet at the moment? Do you have some basic rules of thumb that you try and stick to when choosing dietary fats?

Getting the ratios of differing fats correct is another aspect that I'm not so up on.

Spit wrote:Big ups Det, cheers for putting the effort in on this one.

Without meaning to cajole you into another post of similar length & detail, how does this info translate to your diet at the moment? Do you have some basic rules of thumb that you try and stick to when choosing dietary fats?

Dammit, was hoping no one would ask me that! My diet is ok, and I do pay some attention to these things, but it's not engineered down to the last detail. Am pretty happy with it but it's not quite exactly where I want it to be yet. To avoid clogging this thread I'll start another one on 'dietary principals' or something, then everyone can chime in

More details hopefully coming soon into the specific fatty acids, but here's a smaller teaser of fats and their effects on leptin:

PUFAs
typically improve leptin sensitivity
typically increase leptin levels (significant).

Saturated Fats
typically reduce leptin sensitivity
typically reduce leptin levels.

MUFAs:
typically improve leptin sensitivity
typically increase leptin levels (minor) or cause no change.

Plasma Triglycerides (synthesised in vivo)
Direct correlation - higher triglycerdies, higher leptin production

The use of the word 'typically' is a caveat as most but not all of the studies show the result to statistical significance.