You've probably been told that polyunsaturated fats is good for your heart. I'm here to tell you they're not.
Rather than being a heart healthy, they're likely implicated in a range of chronic diseases like cancer, alzheimer's, and diabetes, among others.
Polyunsaturated fats (PUFAs) are found primarily in oils: soybean oil, sunflower oil, safflower oil, grape seed oil, flaxseed oil, sesame seed oil, fish oil, and cod liver oil. They can also found in margarine.
The key to understanding how PUFAs cause damage is understanding their chemical structure.
A saturated fat is a molecule that has carbons "saturated" with hydrogen.
A monounsaturated fat is a molecule whose carbon is not fully saturated with hydrogen. It has one carbon double bond instead of full saturation.
A polyunsaturated fat is a molecule that is even more unsaturated. It has two or more carbon double bonds.
Below are the different chemical structures of the fats. Notice the additional double bonds.
The double carbon bonds make the molecule more "kinky". This is why polyunsaturated fats such as canola oil are liquid at room temperature and why saturated fats are mostly solid at room temperature. The molecules don't stack nicely when they're "kinky".
But why does this matter? It's because the chemical composition of polyunsaturated fats makes them liable to Lipid Peroxidation. This occurs when free radicals attacks the lipid and cause it to degrade.
When you have a double bonds on either side a "methylene bridge" (-CH2-), such as in PUFAs, the hydrogen on the "methylene bridge" is very reactive. Monounsaturated and Saturated fats not having this methylene bridge makes them much more stable and less prone to Lipid Peroxidation.
Please notice the methylene bridge on PUFA below.
Imagine this scenario. You're having a nice day at the beach and you're soaking up lots of UV light from the sun. Your skin cells are full of polyunsaturated fat because you've been using "heart healthy" canola oil as a frying oil for years.
The UV light beating down on you is an ionizing radiation. It reacts with the water in your cells to produce a Reactive Oxygen Species known as hydroxyl radical (OH-). A Reactive Oxygen Species is an unstable molecule that contains oxygen. As the name suggests, they are reactive with other molecules. They want to steal a hydrogen so that they can turn into water again (H2O), which is much more stable. The methylene bridge of our polyunsaturated fat is one of the most reactive, and so the Reactive Oxygen Species (OH-) will easily react with it.
This is how Lipid Peroxidation is initiated. A reactive species like OH- will steal the hydrogen from the polyunsaturated fat.
The byproducts of Lipid Peroxidation are also very reactive, so they propagate a chain reaction of even more lipid peroxidation, until they are stopped by an antioxidant, like Vitamin E. Vitamin E and Vitamin C are both very important in in stopping the Lipid Peroxidation chain reaction.
One might ask, if there's adequate vitamin E, then why even worry about the Lipid Peroxidation reaction with polyunsaturated fats? The reason is because Vitamin E only neutralizes the lipid radicals in the Propagation step of Lipid Peroxidation (circled below), not the Initiation step. There is still ample damage to be done to cells from Initiation step.
Now, why are we told polyunsaturated fats are healthy? Let's review some quotes about Lipid Peroxidation in the organism.
The growing body of evidence for the involvement of lipid peroxidation and general oxidative stress as a driving force of Alzheimer's disease has generated much interest in using antioxidants as therapeutics. (R)
There is ample evidence supporting a causative role of lipid peroxidation in selected human cancers, including kidney, liver and skin, and in degenerative diseases. (R)
There is considerable evidence that hyperglycemia represents the main cause of complications of diabetes mellitus (DM), and oxidative stress resulting from increased generation of reactive oxygen species plays a crucial role in their pathogenesis. (R)
The results of this study indicate that lipid peroxidation, determined by breath ethane and pentane outputs and F2-isoprostane, was significantly higher in Crohn's Disease patients than in healthy control subjects. (R)
Recently, oxidative stress has also been implicated in depression, anxiety disorders and high anxiety levels. (The lipid peroxidation chain reaction causes oxidative damage). (R)
Those are quotes from highly cited papers, in high impact journals, that I was able to pull from PubMed within 10 minutes.
The current consensus is that PUFAs are healthy because they lower LDL cholesterol and increase HDL cholesterol. Since there have been some studies showing reduced LDL and increased HDL resulted in lower incidence of heart disease, PUFAs are therefore healthy.
Harvard Health says
Omega-6 fatty acids have been linked to protection against heart disease.
The Mayo Clinic says
Evidence shows that eating foods rich in polyunsaturated fatty acids instead of saturated fats improves blood cholesterol levels, which can decrease your risk of heart disease and may also help decrease the risk of type 2 diabetes.
But an article from the Mayo Clinical Proceedings says the opposite. (R)
Meta-analyses of the dietary trials have found only trivial or no benefit at all from decreasing the intake of SFAs and/or increasing the intake of PUFAs
They go even further
Associations have been found between omega-6 PUFAs and prostate, pancreas, colon, and in particular breast cancer. In an in vitro study, the growth of human breast cancer cells was stimulated by linoleic acid; several cohort studies have found that women with a high intake of omega-6 PUFAs run a higher risk of breast cancer.
Why is there so much inaccuracy and controversy? Unfortunately, that's pervasive across all nutritional research, but I think there's one additional variable..
We may not be designing observational experiments long enough, and this may be contributing to the confusion and contradictory results. An 8-year controlled clinical trial followed 846 men living in a veterans home in Los Angeles and put them into a control (low PUFA) and experimental (high PUFA) groups. They found that only after 2-5 years was there significant difference in cancer mortality. (R)
And only after 7 years was there any significant increase in deaths due to other causes. (R).
However, these studies are rare. It's difficult to accurately control the diets of people over a number of years unless of course you're in prison, a mental institution, or a live-in veterans association.
While not always the most accurate or reliable, I should mention two epidemiological paradoxes, which are useful when we're thinking about very long timeframes. The Israeli paradox and the French paradox.
The Israeli paradox is that Israeli jews have relatively high incidence of coronary heart disease (CHD), despite eating a diet high in PUFAs and low in saturated fats. The opposite of what is expected.
The French paradox is that the French have relatively low incidence of coronary heart disease despite having a diet low in PUFA and high in saturated fats. Very curious.
We have two different paradoxes around PUFAs that are the same, but in reverse. Instead of reassessing base assumptions about the role of PUFAs in the diet, complex and fanciful hypotheses have been made such as – "the French drink a lot of wine, that must have something to do with it!". And if the complex wine hypothesis doesn't hold up, the final cop-out is simply to say it comes down to genetics.
These paradoxes will become less absurd once we understand the relation between PUFA intake and LDL lipid oxidation (which leads to heart disease).
Atherosclerosis is the narrowing of the arteries due to plaque buildup on the artery walls. Eventually the arteries can become so narrow that a clot can form and block the flow of blood, leading to heart attack or stroke.
Let's ask now, what causes the plaque buildup? It happens when HDL and LDL cholesterols enter the tunica intima of the artery and LDL becomes oxidized (pictured below). (R) This oxidation attracts macrophages from the blood. Macrophages are specialized cells used to clean up pathogens and dead cells. The macrophages ingest the oxidized LDL and turn into foam cells. These foam cells are what form the plaque in the arterial wall.
But when and why do LDL particles get oxidized?
The LDL particles are responsible for transporting lipids through the blood. They contain a phospholipid (fat) layer. This fat layer can be comprised more or less of saturated or unsaturated fat depending on the diet.
If the diet is mostly PUFAs, the lipids on the LDL particles will be mostly PUFAs. We already know from when we learnt about Lipid Peroxidation, that PUFAs are more likely to oxidize. The same is true when they are in the layers of the LDL particle -- they LDL particles with higher PUFA content are much more prone to oxidation! (R, R)
The fact that PUFAs enable greater oxidation is not great, since there is a direct connection between oxidation of LDL particles and plaque formation that causes heart disease.
This information on LDL oxidation should help us understand the paradox of Israel and France.
The Electron Transport Chain is a system comprised of proteins that produces the majority of the ATP in the body. The proteins is comprises sit in the inner membrane of the Mitochondria. The fats in this membrane can be more or less saturated based on diet.
It's been found that increasing unsaturation of the inner membrane can disrupt the function of the Electron Transport Chain, this results in lower ATP production and impaired mitochondrial respiration. (R,R) We want our Electron Transport Chain to produce the most ATP possible for the best health.
... an increase in n–3 PUFAs disorganizes the mitochondrial membrane and can potentially alter protein function...
One interesting tidbit is that PUFAs are essential to hibernating animals. Animals fed diets lacking in PUFAs have a much higher metabolic rate and thus shorter bouts of hibernation.
Hibernators lacking essential fatty acids in their diet, or on a diet high in saturated fat, had significantly higher metabolic rates than hibernators fed a control or fed a diet high in polyunsaturated fatty acids while in deep hibernation (R)
PUFAs are required to reduce the metabolism for hibernation. Do you want to have a high metabolic rate so that you can maintain or lose weight easily? You can cut back on PUFAs
There's one more paradox I'd like to introduce related to metabolic rate. The Australian Paradox. In Australia, sugar consumption has dropped since the 1980s, but obesity continues to rise.
In America the same can be found. Per-capita consumption of sweeteners peaked in 1999 in the U.S and has been on the decline since.
However, obesity continues to rise.
A puzzling paradox. I think we may be able to understand this paradox if we understand the role of PUFAs in decreasing metabolic rate. A decreased metabolic rate makes it much easier to gain weight, contributing to obesity.
And indeed we see that Americans are consuming increasing amounts of vegetable oils containing PUFAs. Maybe this isn't much of a paradox after all.
When I tell people about PUFAs and their effects, most people say that they don't use canola oil very often to fry foods at home, and that they don't eat out very much either. In response, I give them this challenge.
The next time you're at the supermarket. Grab 5 different items. Maybe 1 from the soup aisle, 1 from the chips aisle, one from bread aisle, etc.
Make a count of how many of the items have at least one of: canola oil, soybean oil, safflower oil, or sunflower oil. I can guarantee it's nearly 100%. Even the products you might not considered processed: a simple can of soup, raisins, locally baked bread, salad dressing.
People are eating far more vegetable oils than they realize, simply because it's an additive in most commercial foods.