How To Get Polyunsaturated Fatty Acids Out Of The Body

Dietary suggestions contained in this blog post are based on the Thermogenic lifestyle. Not all dietary suggestions are suitable for each individual.  Please consult your healthcare professional before making any changes to your dietary or supplement routine.

 

 

Out of everything that is hurting your health and metabolism, polyunsaturated fatty acids, or “PUFAs”, probably rank as number 1.

When we discussed carbs and sugar in the other metabolism articles, the end recommendation was that sugar was better, but that all carbs were more or less good for your metabolism.

But when it comes to fats in your diet, it is a much different story.

PUFAs are all around terrible for your health and metabolism, as we will soon discuss.

They even cause dysregulation of sugar metabolism, which can make sugar falsely look like the culprit if you do not look closely enough.

Table Of Contents:

• Why Does The Mainstream Believe PUFA Are Healthy?
• How To Fatten Up Livestock With Less Food
• What Are Fatty Acids?
• The Damaging Effects Of Polyunsaturated Fatty Acids
• Nature Gives Us Clues
• The Detoxification Of Polyunsaturated Fatty Acids
• But Aren't the "Essential Fatty Acids" Unsaturated?
• The Metabolic Power Of Shorter Chain Fats
• Fatty Acid Recommendations
• Key Points

Why Does The Mainstream Believe PUFA Are Healthy?:

Much of the confusion around PUFAs revolves around very shaky evidence that was never questioned or analyzed, and unfortunately, a big part of this has to do with marketing.

Around the 1970s, the introduction of petroleum based paints made the old vegetable oil-based varnishes obsolete.

Needing a new market, the companies that produced these oils quickly jumped on research showing that PUFAs reduced cholesterol levels, which at the time we believed to have meant that they protected the heart and prevented cardiovascular disease.

Of course, this turned out not to be true, and low cholesterol blood levels are actually heavily associated with a much higher mortality rate, suicide/depression, reduced survival from heart failure, and increased violence.

In reality, these fats are lowering blood cholesterol by preventing the liver from exporting its fat, resulting in accumulation of liver fat and liver damage.

Regardless, these companies began promoting these oils as healthy, and it stuck.

The problem is, these fats are incredibly unstable and peroxidize incredibly easily, causing free radical damage. In fact, this is precisely why they worked as paint varnish.

Their effect on cholesterol levels were viewed out of context and without regard to the whole picture, but it was enough to sway public opinion.

Despite newer evidence showing that PUFAs are actually terrible for heart health and cause cardiovascular disease, the public has not quite made a shift to believing it yet.

In reality, there is a lot of evidence that PUFAs, and their breakdown products, are a major contributor to a whole ton of diseases, like cardiovascular disease (the disease that they are said to “cure”), hypertension, Type II diabetes, obesity, cancers, ulcerative colitis, and Crohn’s disease.

In fact, the introduction of more PUFAs is correlated with the increase in all the big diseases that we have seen over the past few decades, including heart disease and obesity.

PUFA and their breakdown products have also been shown to slow wound healing, increase estrogen while decreasing SHBG (making the estrogen more “active”), suppress your immune system, reduce fertility and health of offspring, increase allergies, and increase neurodegenerative disorders like Alzheimer’s and dementia.

Since PUFA and their breakdown products lower your metabolism and your cells’ ability to produce the energy they need to function through their increases in inflammation and oxidative stress, this makes perfect sense.

“Polyunsaturated fats offer you absolutely nothing except an earlier grave. If you doubt that, go to the autopsies done among the Bantu, among the Japanese and you will find that their arteriosclerosis before the age of thirty is far greater than it is on the American diet, or on the Austrian diet, very similar to ours. This is a fake. Polyunsaturated fats, when this story is finally written is going to make Watergate look like a church social. This is a lie that has been forced on the public. Originally, they were in earnest. They thought it was true. But they know better today.”
- Dr. Broda Barnes

 

 

How To Fatten Up Livestock With Less Food:

But that is not all we have to look at.

In the 1940s, farmers were looking for a way to get their livestock fatter without having to buy a bunch of extra feed.

In other words, they wanted to lower the animals’ metabolic rates so that the same amount of food would add more mass to their bodies’, making it cheaper to raise livestock.

At first, they used the most concentrated, natural source of saturated fat: Coconut oil.

Unfortunately, their plan backfired. The animals all wound up lean and hungry.

So they looked into some other possibilities, and found one anti-thyroid drug that seemed to work, until it was shown to be highly carcinogenic.

Scratch that one. What else could they try?

At this point, they decided to go with a different type of fat: Polyunsaturated fat from vegetable oil.

And guess what? Eureka! The animals all got fat and plump with the same amount of food.

In other words, the polyunsaturated fatty acids effectively lowered their metabolic rates, allowing more fat to get stored from the same amount of food.

The case is pretty clear that PUFAs damage your health and metabolism, but why?

In order to explain why PUFAs are so harmful, we first need to understand exactly what a PUFA is.

What Are Fatty Acids?:

At the very basic level, a fatty acid is essentially a carboxyl group attached to a chain of carbon atoms, which can be anywhere from 2 to 28 carbons.

The chain length is incredibly important, as there seem to be a lot of pro-metabolic features for short- and medium- chain lengths, but we will come back to that in a bit.

A carbon atom can make four bonds, and in the chain of a saturated fat, it is bound to a carbon on either side and a hydrogen atom above and below (“above and below” being used simplistically to make this easier to understand). The final carbon in the chain is bound to one carbon and 3 hydrogens.

Now, a saturated fat is called “saturated” because it is saturated with hydrogen atoms. Every carbon molecule has the maximum amount of hydrogens possible, which is 2 for all carbon molecules in the middle of the chain and 3 for the carbon molecules on the edge of the chain.

But when we look at the unsaturated fats, we see fewer hydrogens.

That is because in these fats, two or more of the carbons are “double bonded” to each other. Since carbon can only have 4 total bonds and double bonds account for 2 of these, that means it can no longer bond to 2 hydrogens, only 1. This makes the fat “unsaturated” with hydrogens.

If the chain has one double bond in it, we call it a “monounsaturated fatty acid”, or MUFA for short.

If the chain has two or more double bonds in it, we call it a “polyunsaturated fatty acid”, or PUFA for short.

The problem with these fats is that exposing these double bonds to heat, light, or oxygen will cause them to peroxidize and form free radicals.

To explain this, understand that each bond between carbons is essentially two electrons that both carbon atoms are sharing with each other. At each bonding site, molecules want to have electrons in pairs, which is far more stable than single electrons are. When they bind to each other, both carbons get to have two electrons by sharing them.

If a molecule only has one electron, we call this a “free radical”, and it will attack other molecules to steal an electron.

Now, single bonds are very strong, but double bonds are far weaker.

When exposed to the energy of heat and light, or the reactivity of oxygen, these double bonds are weak enough to fall apart, splitting so that each carbon only has one electron instead of two.

These single electrons are hungry to find other electrons to stabilize them and will react with other molecules to steal their electrons.

This creates a huge chain reaction that causes damage to every molecule it comes in contact with, creating more and more free radicals.

To stop this process, we have a built-in system of “antioxidants”, which can donate an electron to the free radical to stop the chain reaction, without turning into a free radical itself.

Nutritionally, there are many antioxidants, but the main ones we use in our own defense system are vitamin E and vitamin C. These work together with glutathione to shut down the damage that free radicals can create.

The unsaturated fats, having double bonds, are far more unstable than the saturated fats, especially when exposed to heat, light, and oxygen (and our bodies are full of heat and oxygen). The more double bonds they have, the more “reactive” they are to peroxidation.

Since PUFAs have many double bonds, this explains the damage they can cause.

For A step by step guide on how to eat to avoid these toxic fats and promote overall health of the body, make sure to check out The Thermo Diet inside of UMZUfit!

The Damaging Effects Of Polyunsaturated Fatty Acids:

So how exactly do the unstable PUFAs affect your metabolism?

As we mentioned previously, your cells primarily create energy through the mitochondria. Whenever the mitochondria cannot keep up with energy production, the cell turns on the stress metabolism, which increases the anaerobic glycolysis that produces lactic acid instead of CO2, as we discussed previously.

Fatty acids are also burned in the mitochondria, and this includes the unsaturated fats.

If they have not already peroxidized (either before you consumed them or once they got into your body), they now get exposed to lots of oxygen and heat that the mitochondria are using and creating. This causes the double bonds to break and the mitochondria to get damaged by free radicals, which lowers their ability to produce energy (again, this is precisely why they work as paint varnish).

On the other hand, saturated fats, which have no double bonds and are quite stable, can get burned for energy without creating these free radicals that damage the mitochondria.

Saturated fats actually reduce stress and promote metabolism, while PUFAs increase stress and oxidative damage.

 

Nature Gives Us Clues:

Now after all of that science on the molecular level, we can zoom back out and look at organisms from a broader view and consider the evolutionary aspects of this.

To set this up, understand that saturated fat is solid at room temperature, while unsaturated fats are liquid.

The more double bonds present in fat, the lower the melting point.

Since saturated fat has no double bonds, it melts at around 75-80 degrees F and is solid at temperatures below that.

Oleic acid, found in olive oil and avocados, is a MUFA and melts at around 22 degrees F, meaning that even when water freezes at 32 degrees F, olive oil will still be liquid.

The highly unsaturated fish oils, on the other hand, won’t solidify until somewhere between -50 to -60 degrees F.

The different melting/freezing points of the oils is incredibly important because all plants and animals have evolved a certain way, for specific reasons, and nature has given us clues as to why - if we look.

Specifically, oils need to be liquid for an organism to make use of it. If it is solid, the plant or animal would stiffen up, and problems would arise.

And as you would expect, the higher the unsaturation of the fat, the colder it is found in nature.

The fish oils that have an extremely low freezing point are found in cold-water fatty fish like salmon. If these salmon had pure saturated fat in them, they would stiffen up and be unable to swim.

The seed and nut oils are found in moderate climates, where the seeds stay buried deep in the cold soil for much of the time. The oils are more saturated than fish oils, but still unsaturated to handle the moderately cold temperature. These seeds also contain lots of vitamin E, which helps prevent peroxidation of the unsaturated oils when the temperature does increase a bit. In general this acts to delay the double bonds from breaking.

And finally, the most saturated fat, coconut oil, is found in a plant that lives in the tropics and is exposed to the highest temperatures. For these plants, unsaturated oils would peroxidize and cause damage, so they have evolved to only have saturated fats.

While unsaturated fats are used to prevent stiffening at cold temperatures, saturated fats are used to prevent peroxidation at high temperatures.

In other words, saturated fats cannot be used in cold temperatures because they harden, while PUFAs cannot be used in hot temperatures because they peroxidize.

Humans maintain a body temperature close to 100 degrees F, very similar to the temperatures that coconuts grow in. It only makes sense on a biological basis that we evolved to eat primarily saturated fats.

Paired with what we have seen about how bad polyunsaturated fats are for our hormonal and metabolic health, not to mention the health of the mitochondria in all of our cells that create the energy we need in order to function, eating PUFAs makes very little sense.

The Detoxification Of Polyunsaturated Fatty Acids:

So the case is clear that we should eat more saturated fat while cutting out the unsaturated fats (some MUFA is okay, but should be kept minimal and never cooked with).

But unfortunately, we are not done yet.

That is because your body still has a lot of PUFA stored in fat stores from the years of eating PUFA in the past. Because the half-life of fat stores is around 400-600 days, the fatty acid composition in your body reflects the fatty acid composition of your diet over the past 2-3 years.

This means you could be slowly clearing yourself of these PUFAs for up to 2-3 years. The more fat you have, the more likely you are to be dealing with stored PUFA.

However, this is where saturated fat really shines.

By eating more saturated fat, you can prevent too much PUFA from being released all at once, which would lower your metabolic rate and cause all the negative side effects.

Instead, you can limit PUFA release through a higher intake of saturated fat, which helps to lower and prevent their free radical production as your liver slowly gets rid of them.

As an example, coconut oil has about 4% unsaturated fat in it. Yet after a sitting for a year at room temperature, there is no rancidity (ie. breakdown, peroxidation, etc.), whereas a vegetable oil is highly rancid by this point.

By preventing the PUFAs from interacting with each other in the chain reaction fashion of free radicals, the toxic effects of PUFA can be minimized.

In fact, I have a theory that testosterone seems to be boosted from saturated fat intake for precisely this reason - more saturated fat dilutes PUFA in the body, prevents the damage, and allows thyroid to rise, which is used to turn cholesterol into the steroid hormones like testosterone (assuming adequate vitamin A intake).

As you continue depleting your body of PUFA, you can eventually lower your fat intake, as there will simply be less PUFA to worry about and less of a need to “dilute” the PUFAs with a high saturated fat intake. Lowering fat intake makes more room for carbs and sugar, while potentially being even better for increasing your metabolism (especially if you become “EFA deficient” as we are about to discuss).

During this entire “PUFA Detox” period, however, it is important to get plenty of vitamin E.

As we mentioned earlier, vitamin E is one of the main antioxidants in the body and is especially important for the prevention of PUFA damage, since vitamin E is soluble in fat.

But Aren’t The “Essential Fatty Acids” Unsaturated?:

Several studies show that one of the “symptoms” of an “essential fatty acid (EFA) deficiency” is an increased metabolic rate.

Many of these studies view this as a bad thing - that the polyunsaturated omega fats that they consider as “essential” are causing negative adaptations when you do not eat enough of them (even though these same studies showed that the animals’ mitochondria were working just fine).

In reality, the entire idea that these fats are essential in the first place is very flawed.

The idea originally came from a study in 1929 where they fed rats a fat-free diet and saw certain symptoms arise, like increased metabolic rate and certain skin issues.

They concluded that certain fatty acids were essential, because your body developed these symptoms if you do not eat enough.

The problem was, this was before the B vitamins and many of the minerals were discovered.

As soon as these were discovered, researchers easily saw that the “EFA deficiency” was actually a vitamin B6, vitamin B5, and zinc deficiency (probably some others as well). They later proved this in several studies.

So back to the first study, why did the group of EFA deficient rats experience these side effects, but not the control group that was still getting EFAs?

The answer is simple: the “EFA deficient” rats had  far greater metabolic rates and therefore higher nutritional requirements.

When metabolic rate is increased, your nutritional requirements are increased from a faster turnover of energy, especially in nutrients important for energy production, like the B vitamins and minerals. The rats that did eat the “essential” fats did not develop this deficiency because the unsaturated fats were lowering their metabolic rates,therefore also lowering their nutritional requirements for vitamins and minerals.

With this idea, I am extremely curious how many other studies have been taken out of context, not considering the effect of EFA on metabolic rate and nutritional requirements.

The reality of the situation is that because “EFA deficiency” can be cured with increased intake of certain B-vitamins and minerals, these fatty acids are, by definition, not essential.

Instead, they simply lower the metabolic rate and therefore decrease nutritional requirements.

On top of this, when your body is not dealing with these toxic fatty acids, a certain group of enzymes will stop being suppressed that start creating an unsaturated fat called “Mead” acid.

Some people view the presence of Mead acid as a problem (indicating EFA deficiency), but in reality, Mead acid is incredibly anti-inflammatory and has many positive benefits, far beyond the supposed health benefits of the EFAs, including the omega-3s (which appear to only have short-term benefits, mostly by suppressing your immune system).

And while Mead acid is unsaturated, it is far more stable than the EFAs due to its structure and fewer number of double bonds.

So essentially, without the EFAs, your metabolic rate increases, as does your resistance to many diseases and toxins, and you produce your own incredibly healthy fatty acids without any negative side effects (assuming adequate nutrition).

“EFA deficiency” is not a deficiency, but rather a key to optimal health.

There was even a human study done by a man named William Brown, where all fat was cut from the diet. It resulted in far increased energy levels and elimination of all the ailments he had been dealing with.

“Inducing an essential fatty acid deficiency in an adult human proved much more difficult than curing one…Each day, he consumed three quarts of defatted milk, a quart of cottage cheese made from it, sucrose, potato starch, orange juice and some vitamin and mineral supplements. His blood lipids became more saturated and their concentrations of linoleic and arachidonic acids were cut in half. He experienced a marked absence of fatigue, his high blood pressure returned to normal, and the migraines he had suffered from since childhood completely disappeared.”

- Chris Masterjohn, PhD

The Metabolic Power Of Shorter-Chain Fats:

Now, there is one final point before we dive into the specific recommendations.

Remember when we first dove into what fatty acids actually are, and I described how there are different lengths of carbon chains in fats?

As it turns out, the short- and medium- chain fats act metabolically different than the long fats, in both digestion and utilization.

For starters, they first go to the liver, much like fructose, rather than getting packaged into triglycerides like the long-chain fats do.

Once inside the cell, they do not need to use the carnitine-transport system that long-chain fats do, meaning they can quickly be absorbed into the mitochondria of the cell, forming into acetyl-CoA, an important molecule for kicking off the aerobic respiration pathway.

These short- and medium- chain fats have been studied for their pro-metabolic, anti-obesity, insulin sensitizing, inflammation reducing effects, and they are a big reason why coconut oil is so effective for boosting your metabolism - coconut oil is primarily made up of short- and medium- chain fatty acids.

On top of this, the very short chain fats like butyric acid, propanoic acid, and acetic acid have strong anti-inflammatory and insulin sensitizing effects, which is why the acetic acid in vinegar (for example), has been shown to massively reduce the insulin and glucose response to a high carb meal.

By including more of these fatty acids, you can help spark the aerobic pathways in the cells, similar to the way that fructose does, but by a completely different mechanism.

 

Fatty Acid Recommendations:

So taking all of this information into effect, how does this affect the way you should eat in daily life?

In essence, we want to avoid ALL polyunsaturated fats like the plague, eat more saturated fats, and keep monounsaturated fats low, while trying to include more short- and medium-chain fats.

Luckily, these shifts are not only very easy and affordable, but actually make your food taste better (which is a common theme of this program - your body has a preference for certain foods for a reason).

Oils like coconut oil, butter, ghee, cream and beef fat will be your staple sources of fats.

This is easily accomplished by cooking with any of them, or adding them to any hot meal.

Personally, I like to make the majority of my fat come from coconut oil, since it has the highest proportion of saturated fat and the highest amount of short- and medium-chain fats. I cook with it for every meal and sometimes add it to my coffee (see the Metabolism Coffee bonus).

If you do not like the flavor of coconut, do not worry - I do not either. If you get the refined coconut oil, you will not get any coconut flavor, just the increased palatability and texture it adds to any food.

Most likely, when you first start eating more coconut oil, you will feel your body warming up, which is an indication that it’s helping your thyroid jump up and creating body heat by reducing the PUFA concentration and/or stimulating oxidative phosphorylation in the cells.

Now, as far as what you should avoid, stay away from all vegetable oils and seed oils.

That means no soybean oil, canola oil, safflower oil, sunflower oil, peanut oil, rapeseed oil, or any other kind of vegetable oil.

Just stay away from them at all costs, especially if they are used for cooking.

This is relatively easy when eating at home, but becomes much more problematic when eating out at restaurants or friends’ houses.

Some restaurants are catching on and starting to use coconut oil, but many still use vegetable oils.

I certainly do not recommend avoiding restaurants - having a social life is also incredibly healthy and there is no point in optimizing your metabolism and health if you are miserable.

Instead, simply strive to limit your PUFA consumption when out, and take a good dose of vitamin E any time when you know that you will be eating some PUFAs. This helps to mitigate the damage (although it is NOT a cure-all).

It is also easy to ask what oils they use to cook with, and see if they have options. One restaurant I was at recently was able to substitute the oil they used with olive oil. While it is still generally not a good idea to cook with olive oil, it is far better than cooking with the PUFA oils.

On top of this, you will want to generally avoid foods that have PUFAs as well, like nuts, seeds, fatty fish, fatty poultry, and fatty pork.

Nuts, seeds, and fatty fish all naturally have PUFAs, while poultry and pork tend to have more PUFA from the feed that they given.

Unfortunately, this does mean that bacon has a high amount of PUFAs. HOWEVER, there is a great way to exchange the PUFAs for saturated fats, allowing you to still eat bacon, and it is simple to do (check out the Metabolism Hacks bonus to learn how).

Now, one of the more controversial recommendations of mine is to cut out fish oil supplementation as well.

There seems to be a lot of confusion around these oils, as they possibly seem to show potential for benefitting health in certain ways.

However, a lot of these benefits are often short-sighted improvements that result from decreased mitochondrial functioning and immune suppression, without understanding the overall context.

In very similar ways, doctors used to recommend X-Rays as therapy for their immunosuppressive and anti-inflammatory effects on the body, only to find out they were actively damaging the cells and causing cancer in many people. I think that the improvements from fish oil are working by the same mechanism (reduced immune function and therefore less inflammation, rather than curing the cause of the inflammation to begin with, or naturally helping your body fix it).

It is more likely that the benefits are from improving the omega-3 to omega-6 ratio, but that does not mean that cutting both out is not even more beneficial. Given the research around “EFA deficiency” and the benefits of Mead acid over fish oil, I think this is precisely the case.

After seeing how negative PUFAs are, and how PUFAs with more double bonds are even worse (the fish oils have many double bonds - 5 for EPA and 6 for DHA), I recommend cutting them out entirely.

Since cutting out fish oil and eating for amplified metabolism, the improvements that I have seen personally are far greater than I ever experienced while taking fish oil, so it is not something that concerns me in the slightest.

This includes things like lack of fatigue, better sleep, and improved memory and learning. There is simply no way that I will go back to eating these toxic oils, and I think that research in the coming years will elucidate their negative effects (the research connecting omega-3 to Alzheimer's is already heading in that direction).

Finally, the major sources of MUFAs are olive oil, macadamia nuts, and avocados. These foods are fine to include in your diet, but sparingly. Do not cook with them if you have the choice (heat will break the double bonds).

As far as your total fat intake goes, I recommend initially going a bit higher in fat to help with the PUFA detoxification. Somewhere around 30% of total Calories is a good bet.

After avoiding PUFAs for a few months to a year, you can start dropping fat down to 20%, then eventually 10%. This may be too low for you in a practical sense, so feel it out and experiment with what works best for you.

If you want a step by step guide on exactly how to eat to avoid pufas and skyrocket the metabolism then check out The Thermo Diet only inside of UMZUfit!

Key Points:

• Cook all foods in coconut oil, butter, or ghee
• Beef fat and cream are also good sources of saturated fat
• Avoid all vegetable oils and never cook with them
• Be careful when eating out at restaurants and supplement with vitamin E to minimize the damage
• Avoid eating nuts, seeds, fatty fish, fatty poultry, and fatty pork
• Stop supplementing with fish oil
• Limit avocados and olive oil, and never cook with them

References

• Schatz, Irwin J., et al. "Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study." The lancet 358.9279 (2001): 351-355.
• Muldoon, Matthew F., Stephen B. Manuck, and Karen A. Matthews. "Lowering cholesterol concentrations and mortality: a quantitative review of primary prevention trials." Bmj 301.6747 (1990): 309-314.
• Zureik, Mahmoud, Dominique Courbon, and Pierre Ducimetière. "Decline in serum total cholesterol and the risk of death from cancer." Epidemiology (1997): 137-143.
• Rose, Geoffrey, and M. J. Shipley. "Plasma lipids and mortality: a source of error." The Lancet 315.8167 (1980): 523-526.
• Zureik, Mahmoud, Dominique Courbon, and Pierre Ducimetiere. "Serum cholesterol concentration and death from suicide in men: Paris prospective study I." Bmj 313.7058 (1996): 649-651.
• Ulmer, Hanno, et al. "Why Eve is not Adam: prospective follow-up in 149,650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality." Journal of Women's Health 13.1 (2004): 41-53.
• Iribarren, Carlos, et al. "Low Serum Cholesterol and Mortality Which Is the Cause and Which Is the Effect?." Circulation 92.9 (1995): 2396-2403.
• Iribarren, Carlos, et al. "Serum total cholesterol and mortality: confounding factors and risk modification in Japanese-American men." Jama 273.24 (1995): 1926-1932.
• Wannamethee, Goya, et al. "Low serum total cholesterol concentrations and mortality in middle aged British men." BMJ 311.7002 (1995): 409-413.
• Anderson, Keaven M., William P. Castelli, and Daniel Levy. "Cholesterol and mortality: 30 years of follow-up from the Framingham Study." Jama 257.16 (1987): 2176-2180.
• Salmond, Clare E., R. Beaglehole, and I. A. Prior. "Are low cholesterol values associated with excess mortality?." Br Med J (Clin Res Ed) 290.6466 (1985): 422-424.
• Beaglehole, Robert, et al. "Cholesterol and mortality in New Zealand Maoris." Br Med J 280.6210 (1980): 285-287.
• Eichholzer, Monika, et al. "Association of low plasma cholesterol with mortality for cancer at various sites in men: 17-y follow-up of the prospective Basel study." The American journal of clinical nutrition 71.2 (2000): 569-574.
• Harris, Tamara, et al. "The low cholesterol-mortality association in a national cohort." Journal of clinical epidemiology 45.6 (1992): 595-601.
• Frank, John W., et al. "Will lowering population levels of serum cholesterol affect total mortality? Expectations from the Honolulu Heart Program." Journal of clinical epidemiology 45.4 (1992): 333-346.
• Fagot-Campagna, Anne, et al. "Serum Cholesterol and Mortality Rates in a Native American Population With Low Cholesterol Concentrations A U-Shaped Association." Circulation 96.5 (1997): 1408-1415.
• Seneviratne, S. L., et al. "Serum cholesterol concentrations in parasuicide." The Ceylon medical journal 44.1 (1999): 11-13.
• Marčinko, Darko, et al. "Are there differences in serum cholesterol and cortisol concentrations between violent and non-violent schizophrenic male suicide attempters?." Collegium antropologicum 29.1 (2005): 153-157.
• Vevera, J., et al. "Cholesterol concentrations in violent and non-violent women suicide attempters." European Psychiatry 18.1 (2003): 23-27.
• Alvarez, Jean-Claude, et al. "Low serum cholesterol in violent but not in non-violent suicide attempters." Psychiatry Research 95.2 (2000): 103-108.
• GARLAND, MALCOLM, et al. "Total serum cholesterol in relation to psychological correlates in parasuicide." The British Journal of Psychiatry 177.1 (2000): 77-83.
• Law, M. R., S. G. Thompson, and N. J. Wald. "Assessing possible hazards of reducing serum cholesterol." Bmj 308.6925 (1994): 373-379.
• Lindberg, Gunnar, et al. "Low serum cholesterol concentration and short term mortality from injuries in men and women." Bmj 305.6848 (1992): 277-279.
• Hulley, Stephen B., J. M. Walsh, and Thomas B. Newman. "Health policy on blood cholesterol. Time to change directions." Circulation 86.3 (1992): 1026-1029.
• Horwich, Tamara B., et al. "Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure." Journal of cardiac failure 8.4 (2002): 216-224.
• Rauchhaus, Mathias, et al. "The relationship between cholesterol and survival in patients with chronic heart failure." Journal of the American College of Cardiology 42.11 (2003): 1933-1940.
• Gordon, Bruce R., et al. "Low lipid concentrations in critical illness: implications for preventing and treating endotoxemia." Critical care medicine 24.4 (1996): 584-589.
• Wilson, Robert F., Jeffrey F. Barletta, and James G. Tyburski. "Hypocholesterolemia in sepsis and critically ill or injured patients." Critical Care 7.6 (2003): 1.
• Zhang, Jian, Matthew F. Muldoon, and Robert E. McKeown. "Serum cholesterol concentrations are associated with visuomotor speed in men: findings from the third National Health and Nutrition Examination Survey, 1988–1994." The American journal of clinical nutrition 80.2 (2004): 291-298.
• Golomb, Beatrice A. "Cholesterol and violence: is there a connection?." Annals of internal medicine 128.6 (1998): 478-487.
• Papassotiropoulos, A., et al. "The risk of acute suicidality in psychiatric inpatients increases with low plasma cholesterol." Pharmacopsychiatry 32.01 (1999): 1-4.
• Sarchiapone, Marco, et al. "Cholesterol and serotonin indices in depressed and suicidal patients." Journal of Affective Disorders 62.3 (2001): 217-219.
• Kunugi, Hiroshi, et al. "Low serum cholesterol in suicide attempters." Biological Psychiatry 41.2 (1997): 196-200.
• Kaplan, Jay R., et al. "Demonstration of an association among dietary cholesterol, central serotonergic activity, and social behavior in monkeys." Psychosomatic Medicine 56.6 (1994): 479-484.
• Kaplan, Jay R., et al. "Assessing the observed relationship between low cholesterol and violence‐related mortality." Annals of the New York Academy of Sciences 836.1 (1997): 57-80.
• Wardle, Jane. "Cholesterol and psychological well-being." Journal of psychosomatic research 39.5 (1995): 549-562.
• Weverling-Rijnsburger, Annelies WE, et al. "Total cholesterol and risk of mortality in the oldest old." The Lancet 350.9085 (1997): 1119-1123.
• Weverling-Rijnsburger, Annelies WE, et al. "High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age." Archives of internal medicine 163.13 (2003): 1549-1554.
• Tuikkala, Päivi, et al. "Serum total cholesterol levels and all-cause mortality in a home-dwelling elderly population: a six-year follow-up." Scandinavian journal of primary health care 28.2 (2010): 121-127.
• Brescianini, Sonia, et al. "Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging." Journal of the American geriatrics society 51.7 (2003): 991-996.
• Schupf, Nicole, et al. "Relationship Between Plasma Lipids and All‐Cause Mortality in Nondemented Elderly." Journal of the American Geriatrics Society 53.2 (2005): 219-226.
• Rauchhaus, Mathias, Andrew JS Coats, and Stefan D. Anker. "The endotoxin-lipoprotein hypothesis." The Lancet 356.9233 (2000): 930-933.
• Forette, Bernard, Danièle Tortrat, and Yves Wolmark. "Cholesterol as risk factor for mortality in elderly women." The Lancet 333.8643 (1989): 868-870.
• Yam, Daniel, Abraham Eliraz, and Elliot M. Berry. "Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet." Israel journal of medical sciences 32.11 (1996): 1134-1143.
• Okuyama, Harumi, et al. "Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes." Pharmacology 98.3-4 (2016): 134-170.
• Yam, D., et al. "Subcutaneous, omentum and tumor fatty acid composition, and serum insulin status in patients with benign or cancerous ovarian or endometrial tumors. Do tumors preferentially utilize polyunsaturated fatty acids?." Cancer letters 111.1 (1997): 179-185.
• Hou, Jason K., Bincy Abraham, and Hashem El-Serag. "Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature." The American journal of gastroenterology 106.4 (2011): 563-573.
• Guyenet, Stephan J., and Susan E. Carlson. "Increase in adipose tissue linoleic acid of US adults in the last half century." Advances in Nutrition: An International Review Journal 6.6 (2015): 660-664.
• Ribeiro Barros Cardoso, Cristina, et al. "Influence of topical administration of n‐3 and n‐6 essential and n‐9 nonessential fatty acids on the healing of cutaneous wounds." Wound Repair and Regeneration 12.2 (2004): 235-243.
• Reed, M. J., et al. "Free fatty acids: a possible regulator of the available oestradiol fractions in plasma." Journal of steroid biochemistry 24.2 (1986): 657-659.
• Bruning, P. F., and J. M. G. Bonfrer. "Possible relevance of steroid availability and breast cancer." Annals of the New York Academy of Sciences 538.1 (1988): 257-268.
• Reed, M. J., et al. "The role of free fatty acids in regulating the tissue availability and synthesis of sex steroids." Prostaglandins, leukotrienes and essential fatty acids 48.1 (1993): 111-116.
• Benassayag, C., et al. "Does high polyunsaturated free fatty acid level at the feto-maternal interface alter steroid hormone message during pregnancy?." Prostaglandins, leukotrienes and essential fatty acids 60.5 (1999): 393-399.
• Giltay, Erik J., et al. "Docosahexaenoic acid concentrations are higher in women than in men because of estrogenic effects." The American Journal of Clinical Nutrition 80.5 (2004): 1167-1174.
• McNamara, Robert K., et al. "Gender differences in rat erythrocyte and brain docosahexaenoic acid composition: role of ovarian hormones and dietary omega-3 fatty acid composition." Psychoneuroendocrinology 34.4 (2009): 532-539.
• Sweeney, B., P. Puri, and D. J. Reen. "Polyunsaturated fatty acids influence neonatal monocyte survival." Pediatric surgery international 17.4 (2001): 254-258.
• Ferrante, Antonio, et al. "Neutrophil migration inhibitory properties of polyunsaturated fatty acids. The role of fatty acid structure, metabolism, and possible second messenger systems." Journal of Clinical Investigation 93.3 (1994): 1063.
• Church, M. W., et al. "Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring." Neurotoxicology and teratology 32.2 (2010): 171-181.
• Dirix, Chantal EH, Arnold D. Kester, and Gerard Hornstra. "Associations between term birth dimensions and prenatal exposure to essential and trans fatty acids." Early human development 85.8 (2009): 525-530.
• Liu, Y. L., and R. F. Borgman. "Influence in rats of dietary fats during the perinatal period: effects upon development and behavior of dams and offspring." American journal of veterinary research 38.10 (1977): 1657-1659.
• Borgman, R. F., R. G. Bursey, and B. C. Caffrey. "Influence of dietary fat upon rats during gestation and lactation." American journal of veterinary research 36.6 (1975): 795-798.
• Jones, Karen L., et al. "Maternal diet rich in omega-6 polyunsaturated fatty acids during gestation and lactation produces autistic-like sociability deficits in adult offspring." Behavioural brain research 238 (2013): 193-199.
• Jones, Karen L., et al. "Maternal diet rich in omega-6 polyunsaturated fatty acids during gestation and lactation produces autistic-like sociability deficits in adult offspring." Behavioural brain research 238 (2013): 193-199.
• Campoy, Cristina, et al. "Effects of prenatal fish-oil and 5-methyltetrahydrofolate supplementation on cognitive development of children at 6.5 y of age." The American journal of clinical nutrition 94.6 Suppl (2011): 1880S-1888S.
• Stoney, R. M., et al. "Maternal breast milk long‐chain n‐3 fatty acids are associated with increased risk of atopy in breastfed infants." Clinical & Experimental Allergy 34.2 (2004): 194-200.
• Lowe, A. J., et al. "Associations between fatty acids in colostrum and breast milk and risk of allergic disease." Clinical & Experimental Allergy 38.11 (2008): 1745-1751.
• Oddy, Wendy H., et al. "Atopy, eczema and breast milk fatty acids in a high‐risk cohort of children followed from birth to 5 yr." Pediatric allergy and immunology 17.1 (2006): 4-10.
• Yu, G., N‐IM Kjellman, and B. Björkstén. "Phospholipid fatty acids in cord blood: family history and development of allergy." Acta Paediatrica 85.6 (1996): 679-683.
• Butterfield, D. Allan, et al. "Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairment." Neuroscience letters 397.3 (2006): 170-173.
• Roberts, L. Jackson, et al. "Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid." Journal of Biological Chemistry 273.22 (1998): 13605-13612.
• Bassett, C. N., and T. J. Montine. "Lipoproteins and lipid peroxidation in Alzheimer's disease." The Journal of nutrition, health & aging 7.1 (2002): 24-29.
• Butterfield, D. Allan, et al. "Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer’s disease brain contribute to neuronal death." Neurobiology of aging 23.5 (2002): 655-664.
• Pocernich, Chava B., and D. Allan Butterfield. "Acrolein inhibits NADH-linked mitochondrial enzyme activity: implications for Alzheimer's disease." Neurotoxicity research 5.7 (2003): 515-519.
• Lovell, Mark A., Chengsong Xie, and William R. Markesbery. "Acrolein, a product of lipid peroxidation, inhibits glucose and glutamate uptake in primary neuronal cultures." Free Radical Biology and Medicine 29.8 (2000): 714-720.
• Lovell, Mark A., Chengsong Xie, and William R. Markesbery. "Acrolein is increased in Alzheimer’s disease brain and is toxic to primary hippocampal cultures." Neurobiology of aging 22.2 (2001): 187-194.
• Williams, Taufika Islam, et al. "Increased levels of 4-hydroxynonenal and acrolein, neurotoxic markers of lipid peroxidation, in the brain in Mild Cognitive Impairment and early Alzheimer's disease." Neurobiology of aging 27.8 (2006): 1094-1099.
• Reed, Tanea T., et al. "Proteomic identification of HNE-bound proteins in early Alzheimer disease: insights into the role of lipid peroxidation in the progression of AD." Brain research 1274 (2009): 66-76.
• Reed, Tanea, et al. "Redox proteomic identification of 4-hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer's disease." Neurobiology of disease 30.1 (2008): 107-120.
• Cenini, Giovanna, et al. "Elevated levels of pro‐apoptotic p53 and its oxidative modification by the lipid peroxidation product, HNE, in brain from subjects with amnestic mild cognitive impairment and Alzheimer's disease." Journal of cellular and molecular medicine 12.3 (2008): 987-994.
• Markesbery, William R., and John M. Carney. "Oxidative alterations in Alzheimer's disease." Brain Pathology 9.1 (1999): 133-146.
• Sultana, Rukhsana, and D. Allan Butterfield. "Oxidatively modified GST and MRP1 in Alzheimer’s disease brain: implications for accumulation of reactive lipid peroxidation products." Neurochemical research 29.12 (2004): 2215-2220.
• Montine, Thomas J., et al. "Peripheral F2‐isoprostanes and F4‐neuroprostanes are not increased in Alzheimer's disease." Annals of neurology 52.2 (2002): 175-179.
• Montine, T. J., et al. "Cerebrospinal fluid F2‐isoprostane levels are increased in Alzheimer's disease." Annals of neurology 44.3 (1998): 410-413.
• Evans, Angela R., et al. "Isoprostanes, novel eicosanoids that produce nociception and sensitize rat sensory neurons." Journal of Pharmacology and Experimental Therapeutics 293.3 (2000): 912-920.
• Laurin, Danielle, et al. "Omega-3 fatty acids and risk of cognitive impairment and dementia." Journal of Alzheimer's Disease 5.4 (2003): 315-322.
• Picó-Santiago, Guillermo. "La enfermedad de Alzheimer: la historia que no se ha contado." PR health sci. j 12.2 (1993): 85-7.
• Bowling, Allen C., and M. Flint Beal. "Bioenergetic and oxidative stress in neurodegenerative diseases." Life sciences 56.14 (1995): 1151-1171.
• Simonian, Nancy A., and Bradley T. Hyman. "Functional alterations in Alzheimer's disease: selective loss of mitochondrial-encoded cytochrome oxidase mRNA in the hippocampal formation." Journal of Neuropathology & Experimental Neurology 53.5 (1994): 508-512.
• Picklo, Matthew J., et al. "4‐Hydroxy‐2 (E)‐nonenal inhibits CNS mitochondrial respiration at multiple sites." Journal of neurochemistry 72.4 (1999): 1617-1624.
• Picklo, Matthew J., and Thomas J. Montine. "Acrolein inhibits respiration in isolated brain mitochondria." Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease 1535.2 (2001): 145-152.
• Humphries, Kenneth M., Young Yoo, and Luke I. Szweda. "Inhibition of NADH-linked mitochondrial respiration by 4-hydroxy-2-nonenal." Biochemistry 37.2 (1998): 552-557.
• Katoh, Kazuo, et al. "Saturated fatty acids suppress adrenocorticotropic hormone (ACTH) release from rat anterior pituitary cells in vitro." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 137.2 (2004): 357-364.
• Bruder, Eric D., et al. "An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284.6 (2003): R1631-R1635.
• Beynen, A. C., R. J. Hermus, and J. G. Hautvast. "A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man." The American journal of clinical nutrition 33.1 (1980): 81-85.
• Rafael, Johannes, et al. "The effect of essential fatty acid deficiency on basal respiration and function of liver mitochondria in rats." The Journal of nutrition 114.2 (1984): 255-262.
• Burr, George O., and Mildred M. Burr. "A new deficiency disease produced by the rigid exclusion of fat from the diet." Journal of Biological Chemistry 82.2 (1929): 345-367.
• Burr, George O., and Mildred M. Burr. "On the nature and role of the fatty acids essential in nutrition." Journal of Biological Chemistry 86.2 (1930): 587-621.
• György, Paul, C. E. Poling, and Y. Subbarow. "Experiments on the Antidermatitis Component of the Filtrate Factor in Rats." Experimental Biology and Medicine 42.3 (1939): 738-740.
• Schneider, H., H. Steenbock, and Blanche R. Platz. "Essential fatty acids, vitamin B6 and other factors in the cure of rat acrodynia." Journal of Biological Chemistry 132 (1940): 539-551.
• Quackenbush, F. W., et al. "Linoleic acid, pyridoxine and pantothenic acid in rat dermatitis." Journal of Nutrition 24 (1942): 225-234.
• U.S. Department of Agriculture. Agricultural Research Administration. Office of Experiment Stations. Experiment Station Record, Volume 87, July-December, 1942. Washington. UNT Digital Library. http://digital.library.unt.edu/ark:/67531/metadc5069/. Accessed August 15, 2016.
• Williams, Mary Ann, and Inese Hincenbergs. "Methyl arachidonate supplementation of vitamin B6-deficient rats." Archives of biochemistry and biophysics 83.2 (1959): 564-565.
• Burr, George O., and ANDA J. BEBER. "Metabolism studies with rats suffering from fat deficiency." Journal of Nutrition 14 (1937): 553-566.
• Wesson, Laurence G., and George O. Burr. "The metabolic rate and respiratory quotients of rats on a fat-deficient diet." Journal of Biological Chemistry 91 (1931): 525-539.
• Goubern, M., et al. "Non-shivering thermogenesis and brown adipose tissue activity in essential fatty acid deficient rats." Archives internationales de physiologie et de biochimie 98.2 (1990): 193-199.
• Rafael, Johannes, Joachim Patzelt, and Ibrahim Elmadfa. "Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat." J Nutr 118.5 (1988): 627-632.
• Yazbeck, J., et al. "The effects of essential fatty acid deficiency on brown adipose tissue activity in rats maintained at thermal neutrality." Comparative Biochemistry and Physiology Part A: Physiology 94.2 (1989): 273-276.
• Cleland, Leslie G., et al. "Effect of dietary n-9 eicosatrienoic acid on the fatty acid composition of plasma lipid fractions and tissue phospholipids." Lipids 31.8 (1996): 829-837.
• Cleland, Leslie G. "Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits leukotriene B4 synthesis in rats and the effect is modified by dietary linoleic acid." The Journal of nutrition 126.6 (1996): 1534.
• Dirix, Chantal EH, Gerard Hornstra, and Jan G. Nijhuis. "Fetal learning and memory: Weak associations with the early essential polyunsaturated fatty acid status." Prostaglandins, Leukotrienes and Essential Fatty Acids 80.4 (2009): 207-212.
• Lefkowith, JAMES B., et al. "Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation." The Journal of Immunology 145.5 (1990): 1523-1529.
• James, Michael J., et al. "Effect of dietary supplementation with n-9 eicosatrienoic acid on leukotriene B4 synthesis in rats: a novel approach to inhibition of eicosanoid synthesis." The Journal of experimental medicine 178.6 (1993): 2261-2265.