Polyunsaturated fatty acids (PUFAs) are fatty acids which have more than 1 double bond in their structure, whereas saturated fats have no double bonds (only single bonds).
The more double bonds a fatty acid has, the more fluid it is, and the longer the saturated fatty acid chain is, the more solid it is. For instance, seed oils are liquid at very low temperatures, whereas coconut oil is hard at room temperature and cocoa butter is much more solid than coconut oil, due to it having more longer chain fatty acids.
Monounsaturated fatty acids only have one double bond in their structure, which is why they are also liquid at room temperature.
- Methyl head/omega head
- The first double bond is found at the 6th carbon, that’s why it’s an omega 6.
- Carboxyl head
- The first double bond is found at the 3rd carbon, that’s why it’s an omega 3.
- The first double bond is found at the 7th carbon, that’s why it’s an omega 7.
- The first double bond is found at the 9th carbon, that’s why it’s an omega 9.
- There is a lone hydrogen between two double bonds. The carbons which have the double bond, only have one hydrogen per carbon. The carbon between two double bonds have two hydrogens. This is what makes PUFAs so easily damageable (oxidizable), because this hydrogen is very susceptible to free radicals.
Conjugated linoleic acid doesn’t have this lone hydrogen (as shown above), and this analog of linoleic acid competes with the linoleic acid in tissues, which protects against cancer, atherosclerosis, inflammation and other effects of the non conjugated PUFA.
Fats are incorporated into phospholipids, which are considered to be “membrane lipids”, which are incorporated into the formation of cell membranes. Because SFAs are more rigid, and PUFAs are more bendable (due to their double bonds), SFA will decrease the cells’ fluidity and permeability, and increase order. Whereas PUFAs, will increase fluidity and permeability, and decrease order. This more fluid and permeable state is thought to be better, or so the myth goes. However, more permeable cells allow more access to a broader range of substances (toxins, estrogens, etc.) and have an increased affinity for water. An increase in intracellular water causes swelling of the cell (including the mitochondria), and this reduces oxidative metabolism and CO2 production, allowing calcium to enter the cell.
This activates excitatory processes which decrease energy production, increase inflammation, and can lead to cell death and/or unstructured cell growth (tumor/cancer cells). SFAs however, have the opposite effect and increase cell integrity, survival, resistance to toxins, function, energy production, etc.
Cell membranes exist out of fat: true or false?
It’s been found that when a cell is cleansed with a solution that removes all lipids, it still has a membrane. Fats (in the form of phospholipids) just accumulate around the membrane and have been demonstrated to be involved in cell division, and other cellular functions (such as polarity, stability, permeability, catalytic actions, etc.) (1, 2), rather than in membranes themselves. Yet, it is thought and taught that fats form cellular membranes, which is a myth, yet everyone believes it as if it is common knowledge.
The reason I bring this up, is because many myths exist, such as cell membranes, proteins can’t enter a cell, membrane pumps and receptors, omega 3 is healthy, omega 6 is essential, etc. Many people just accept these “facts” because fraudulent studies have “proven” them to be true.
So let’s start at the very beginning…
The “essentiality” of PUFAs, was first “proved” by a study done in 1930, by Burr.
He fed his rats a fat free diet, consisting of purified sugar and casein, and added a vitamin/mineral mix (only two B vitamins were known back then), which was lacking in a lot of minerals and vitamins that were only discovered years later. After a few months the rats who were given the fat free diet started getting eczema, dandruff, hair loss, edema, and some even died with serious organ damage. Burr reversed these health effects by giving the rats a tiny amount of linoleic acid (linseed oil, corn oil and poppy seed oil), whereby he concluded that PUFAs are essential for life. However, years later other researchers replicated Burr’s study, but added vitamin B6, and found that the rats didn’t develop any of the same symptoms as Burr’s rats did with a PUFA deficient diet. Prior to Burr’s study, Germans did a similar study, and showed that rats which were deficient in linoleic and linolenic acid were perfectly healthy and were remarkably resistant to cancer, tumors, shock, trauma and many toxins (3). The rats that were deficient in PUFAs had a significant faster metabolism, >50%, and their requirements for nutrients increased as a result. Giving them inadequate nutrients, such as in the case of Burr’s study, would result in health issues.
When the body is deficient in the “essential fatty acids”, Mead acid (an omega 9 unsaturated fatty acid) is produced endogenously. Mead acid, contrary to the other PUFAs, is anti-inflammatory. The body can also make other unsaturated fats, such as palmitoleic acid, oleic acid and nervonic acid. However, fatty acids such as Mead acid and nervonic acid (which is important in brain development) has yet to be studied more in depth (4).
The fact that everyone knows how “healthy” omega 3s are, just shows the effectiveness of the fish oil companies’ lobbying. As Adolf Hitler said, “If you tell a big enough lie and tell it frequently enough, it will be believed.” This is most likely one of the only times that I would say that he was right.
If PUFAs are bad, why are they present in natural food sources?
Let’s start with a good example… cold water fish have high amounts of PUFAs in their tissue, whereas warm water fish have lower amounts. This is because PUFAs prevent the fish from becoming stiff in very cold water, thus increasing their survival. The cold water and low UV exposure protect the PUFAs from being oxidized.
Similarly, seeds also contain PUFAs so that the fat can be used as an energy source during germination and so it won’t solidify during cold weather. Another reason why seeds are so high in PUFAs is because whenever an animal consumes the seed, the PUFAs inhibit proteolytic enzymes in the stomach of the animal (or human), which prevents the digestion of the seed, so that it can be excreted to germinate somewhere else.
At low temperatures and low oxygen concentrations these oils are not highly reactive; but in warm-blooded creatures such as ourselves, it becomes much more reactive.
This is also why tropical nuts such as coconuts and cocoa, mainly contain saturated fats and are very low in PUFAs.
Bears and other animals that eat lots of PUFA rich foods do so for their metabolisms to slow down for the wintertime; and once they have eaten enough, they can go into hibernation. An interesting fact is that when an animal eats SFAs instead of PUFAs, it cannot go into hibernation and will die. It is also shown that once a bear goes into hibernation after stocking up on PUFAs it becomes totally diabetic. But once it comes out of hibernation it consumes high glucose foods such as honey and fruits, which then cures its diabetes in about one week’s time. This was also shown to be true in humans, as in the olden days doctors actual treated and cured diabetic patients with sucrose and fructose. (why doctors don’t do it anymore is a whole different story).
This busts another myth on glucose being the cause for diabetes, but we’ll get into that a bit more in another following part of the PUFA Dangers series. We as humans don’t hibernate, but when we eat PUFAs our metabolism slows down in a very similar way to bears and other hibernating creatures.
The process of storage, mobilization and oxidation
Babies are born with their tissue consisting mostly out of SFAs. During life, as people eat foods containing PUFAs, it starts to accumulate in all body tissue.
The body absorbs unsaturated fats more easily than SFAs, and this will contribute to faster unsaturation of bodily tissue. The absorption efficiency for stearic, oleic, and linoleic acid is 78.0%, 97.2%, and 99.9%, respectively. (5)
The storage of fatty acids differs. Fatty acids store in the following order, from most stored to least stored in adipose tissue: MUFAs>omega 6>SFAs>omega 3 (6) and this also contributes to a faster increase in unsaturation over time. Oleic acid, linoleic acid and palmitic acid gradually increased and accounted for the greatest proportions of MUFAs, PUFAs and SFAs respectively. (7) It can even take up to 2 weeks before ingested fats are finally incorporated into adipose tissue for long term storage (8).
Longer chains are more likely to be incorporated into phospholipids (18% and 33% for palmitic and stearic acid respectively), whereas shorter chains are oxidized. (9)
The area where fats are stored can also vary, for instance, saturated fats are more abundantly stored in the upper body, whereas unsaturated fats are more abundantly stored in the lower body.
Buttocks fat: (10)
- Oleic acid – 46.7%
- Linoleic acid – 11.9%
- Palmitic acid – 9.1%
- Palmitoleic acid – 8%
- Stearic acid – 3.7%
- Myristic acid (14:0) – 3.1%,
- SFAs: Lower back > lower abdominal > butt
- MUFAs: Butt > lower abdominal > lower back
- PUFAs: Butt > Lower back = lower abdominal (11, 12, 13, 14)
There is about 1kg of linoleic acid stored in the adipose tissue, and even more if someone has >20% of bodyfat. That’s pretty scary, as this means that you’ll still have a pretty big supply of linoleic acid, even after having stopped ingesting it.
PUFAs don’t just accumulate in the adipose tissue, but also in the lenses of the eyes, skin, brain, heart, blood vessels, etc. They react with heat, light (UV) and moisture, and produce a variety of reactive particles, which damage cellular proteins and DNA. This forms lesions (lipofuscin) in the brain, liver, heart, blood vessels, lenses of the eyes and age spots on the skin. (15)
Mobilization. Fatty acids are mobilized from adipose tissue via lipolysis (the mobilization of fatty acids from fat stores). Preferential mobilization increases with unsaturation and decreases with an increase in chain length. The relative mobilization for PUFAs are in the order of:
EPA (20:5 n-3) > arachidonic acid (20:4 n-6) > α-linolenic acid (18:3 n-3) > DHA (22:6 n-3) > linoleic acid (18:2 n-6) (16).
This isn’t just from adipose tissue, but also from chylomicrons after digestion and absorption.
When the diet chronically contains more PUFAs than what the body can immediately oxidize or detoxify, the PUFAs will be stored in tissue. As seen in this study, a high linoleic acid diet increased adipose linoleic acid levels from 11% to 32% in 5 years. The half life of fats in adipose tissue is 350-750 days. Meaning that if you stop consuming PUFAs, your tissue can still contain a significant amount of PUFAs after 2+ years. (17)
Losing weight/fat however can significantly speed up this process once the intake of PUFAs are limited to lowest amounts.
Oxidation. Short chain fatty acids are oxidized the fastest, but the speed of oxidation decreases with an increase in chain length. The more unsaturated the fat is, the faster it is oxidized. The longer chain fats, such as stearic and arachidonic acid, are preferably used in phospholipids, instead of being used for energy.
The body oxidizes fatty acids as follows:
Octanoic acid (5x faster than oleic acid) > Lauric acid = Oleic acid > linolenic acid (α/γ) > linoleic > arachidonic > stearic acid (18, 19, 20, 21, 22, 28)
Linolenic acid is oxidized about 50% faster than palmitic acid and 3 times faster than stearic acid. While α-linolenic acid is oxidized almost twice as fast as linolenic acid, about three times faster than palmitate, and six times faster than stearate.
Oleic acid’s average rate of oxidation in various reports are 6% slower than linoleic acid and about 50% slower than α-linolenic acid. (23)
Children’s metabolisms are also shown to be almost double more effective at burning fats than adults’. In this study children burned 61% of ingested palmitic acid over 24 hours, whereas adults only burned 35%. (24) I thought this was just interesting to mention because children with healthy metabolisms burn saturated fat much faster than adults who have damaged metabolisms and a build up of PUFAs. This also just confirms the findings that reverting back to a low PUFA diet repairs, and speeds up the metabolism to work smoothly as it should.
Excretion. The body can also excrete PUFAs, unlike SFAs, which indicates that the body sees it as a liability. The liver detoxes PUFAs (ω3 and 6) via glucuronidation (25).
Oleic acid is able to increase the activity of the glucuronidation process by 8 fold, which speeds up the detoxification process (26). However, this system is inhibited by PUFAs, arachidonic acid and linoleic acid (27). This will lead to an increase in PUFA levels over time, if dietary PUFAs are not drastically reduced.
The body either stores, burns or excretes PUFAs to prevent it from doing harm.
Having PUFAs in your body is directly associated with disease, inflammation, aging, cellular damage, low energy state, stress, etc., which is definitely not good.
The requirements for PUFAs are grossly overestimated; the maximum intake should actually only be 1-2g daily, if you believe that they are essential, which I do not. But whether you believe it to be essential or not, you won’t be able to avoid PUFAs entirely even if you eat a very low fat diet, as PUFAs are just about in everything, even vegetables contain small amounts thereof. The point however, is that PUFA consumption becomes detrimental to the body once you start consuming too much thereof in your daily diet.
So in order to prevent a metabolic slow down, oxidative stress and inflammation and risk of all diseases, I would highly advise to keep your daily PUFA intake as low as possible.
Foods high in PUFAs
All vegetable oils, nut oils and seed oils except for macadamia nut oil and olive oil (which should still be used in moderation – 1 tablespoon per day).
Best and lowest PUFA oil to use is coconut oil and second best would be MCT oil (but make sure that it’s derived from coconut oil and not palm oil) and then butter.
MCT is second to coconut oil, because it’s not a complete fat, such as coconut oil or butter, but is still a great oil to use.
- Coconut oil 1.7% PUFA
- MCT 0% PUFA
- Macadamia nut oil 2.5% PUFA
- Butter 3% PUFA
- All seeds and all nuts; with macadamia nuts having the lowest content of PUFAs: 1.5g per 100g.
- Eggs (1-2 eggs daily can be exceptional; being aware that 1 egg contains 0.7g of PUFAs).
- Fatty meat, especially fatty chicken and fish (with beef, lamb and wild game being more safe as they have a favorable SFA to PUFA ratio).
- Grains, legumes (lentils, beans etc.).
- Dairy such as cheese and milk is still safe (with a favorable ratio and SFA to PUFA) but when consumed in high amounts could easily lead to too much PUFA intake.
So it’s best to consume low to no fat dairy products.
Next (in Part 2 of PUFA Dangers) we’ll be discussing lipid peroxidation and prostaglandins.
1 thought on “PUFA Dangers Part 1: storage, mobilization and oxidation”
Great article! But I’m confused about a recent 2021 meta-analysis on the effects of PUFAs in Humans and their metabolism.
Their research shows PUFAs increase metabolism more so then saturated fats. And on top of that Omega-6 was better at doing so then Omega-3.
Will you please help clear up this confusion?
Here is the link: