[Discussion]Just how essential are "essential fatty acids".
I’m sure everyone in this community is aware of how debated the topic of polyunsaturated vs saturated fat is. The medical journals always yield us contradictory and confusing messages. This is not simply a topic where citing research shows a clear answer. I figured taking a step back and looking at what happens to the organism as a whole could yield us better answers.
So the pro-polyunsaturated argument generally states that these fats are essential to consume because we can’t make them ourselves. To someone with no biochemical background, this would sound like a pretty straightforward assumption. This dates all the way back to 1929 when the Burrs published a study showing that unsaturated fats, especially linoleic acid, are essential to prevent a particular disease involving dermatitis, slowed growth, sterility, and fatal kidney diseases.
But wait, is the whole idea that these fats are “essential” reside on the shoulders of a study done in the late 1920s. Further more, in the 1920s most of the B vitamins hadn’t even been discovered yet. The fact these rats were possibly lacking other essential nutrients is something most of the pro PUFA crowd hasn’t even taken into consideration. Also worth noting that in 1927, two years before the Burr study, Bernstine and Elias showed evidence that suggested a fat free diet prevented the growth of cancer.
So as you can see, this idea of EFAs is becoming more and more shaky as we keep getting deeper. The Burrs didn’t account for other nutritional deficiencies, and there’s studies contradicting their message of fatty acid essentially. Also in humans, an extremely low fat diet (0.03 grams of fat per kilogram of body weight) doesn’t seem to yield any negative results over a 6 month period, actually a few positive results. But okay, what about the heart health implications of replacing saturated fats with polyunsaturated fats? Surely this is settled science by now, right? Not exactly, firstly the immune suppression mechanism by which PUFA reduce LDL concentrations isn’t exactly a net positive. There’s many reasons why LDL can be temporarily elevated, one of them being a bacterial/viral infection. PUFAs immune suppression qualities have long been known by the medical community as well. It use to be used in a emulsion given to patients who received an organ transplant. It suppresses then immune system giving a greater chance the organ won’t be rejected.
Dr. William Lands, one of the world’s most prominent researchers in EFAs, has also been on record stating their essentially is greatly exaggerated, and as little as 1% of caloric intake from PUFA is all that’s needed to meet the average person’s daily requirement. 1% is exceedingly low, and on a standard 2,000 calorie diet would be roughly 2 grams of polyunsaturated fat a day. You could practically meet this recommendation by eating 1 egg fried in a ½ tbsp of butter.
So far we’ve established PUFAs and their “essential” role in our health is severely questionable, and just for arguments sake if they are essential the amount we need to meet the daily requirement is so low that we don’t even need to prioritize this issue. Because short of eating a laboratory made diet, we’re going to meet that 1% daily intake, likely much more than 1% for many of us. But is their any evidence to suggest dietary intake of PUFA can be actively harmful? Well, yeah their is. Lipid peroxidation is a central issue in regards to PUFA 1 2. There’s also some evidence to suggest replacing omega 6 fatty acids react unfavorably with inflammation, because they’re precursors to certain inflammatory prostaglandins. Replacing them with omega 3 fatty acids is thought to be less inflammatory 1. PUFAs, when incorporated into cell membranes, make cells more fluid, which makes them chaotropic, disorderly and reduces their function 1. The increase in fluidity will allow more water, sodium, chloride, and calcium into the cell (edema), and lower intracellular potassium and magnesium which will also destabilize the cell, and reduce cellular function. Metabolic processes cannot occur optimally in such an environment. This increase in fluidity increases excitation, and proliferation (tumor growth) or cell death. But probably one of the most pronounced toxic effects of PUFA is their ability to inhibit the crucial thyroid enzyme thyroid peroxidase 1.
So, just to recap the entire analysis of PUFA and their role in human health and metabolism. The main pro PUFA research dates all the way back to the late 20s, there’s circumstantial reasoning to suggest they didn’t account for B vitamin deficiencies in that study, and there’s some contradictory studies around the same time to suggest rats were not only able to live on an entirely fat free diet, but they were more resistant to cancer as well. Also there’s the fact that 1% of our caloric intake seems sufficient enough to not get the symptoms of EFA deficiency. Or maybe, another way of looking at it, 1% PUFA intake is simply inhibiting our metabolisms enough to prevent a hypermetabolic rate, which would make our daily nutritional requirements impractical. The one bad side to high metabolisms is we generate a lot of heat and burn through nutrient stores much quicker. So maybe a slight metabolism inhibition could be seen as a good thing. PUFAs may be able to lower our LDLs, but it comes at the cost of suppressing our immune systems. They also contribute to lipid peroxidation, inflammatory prostaglandin synthesis, and inhibit thyroid function. At this point, I’ve heard all I need to hear, and choose to not only limit PUFA intake, but proactively avoid it to the best of my ability. Because even the consumption of coconut oil and butter, which is around 2 and 3 percent linoleic acid, is enough to meet that 1% threshold.
Now there’s the saturated fat, and how they play a the role in human health. As an opening defense to saturated fat I think it’s important to take a step back and examine mammals as a whole. I don’t care where you look, every warm blooded mammal has a high degree of saturation in their adipose tissues. We store saturated fatty acids for a reason, they’re more stable to our warm blooded nature. If we were amphibious cold blooded organisms, then this would be a horse of a different color. Mammals also have a high degree of saturation in our mitochondria, and we expose ourselves to increasingly higher amounts of unsaturated fat, our cells become more fluid like, causing our metabolisms to slow down. Probably the most compelling case to recognize the importance of saturated fatty acids is realizing we will synthesize them on a very low fat diet. If you eat a low fat, high carb, diet we will use fatty acid synthesis which is an internal mechanism for converting glucose, to acetyl-CoA, into various saturated fatty acids. Primarily converted into palmitic and stearic acids. Stearic acid can further be desaturated into monounsaturated fats as well. So I think it’s important for people to realize the so called bad, unessential fats in the mainstream are the fats our bodies will go out of their way to make, even if we’re not consuming them directly. In a funny way, you could put a very good argument forward to suggest saturated fat is indeed the only essential fatty acid. I’m getting tired now, so for the closer in my rant about this topic I’ll address the common misconception that saturated fat is somehow related to heart disease. The glaring obvious fact I always notice in these debates that put saturated fat under the microscope is that none of the critics ever take into account the cholesterol turnover rate. Cholesterol’s main jobs in the body is to convert itself into bile acids and convert itself into pregnenolone for downstream steroid synthesis. To do both these jobs sufficiently the body needs adequate vitamin A and adequate thyroid hormone. When were lacking just one of these, the cholesterol turnover rate decrease and we start having a habitually higher serum cholesterol (LDL) value.
This has nothing to do with saturated fat, and more to do with either a micronutrient deficient diet, or a lack of active thyroid hormone due to either genetics, PUFAs, low carb diets, etc. When subjects with high cholesterol are supplemented with thyroid they see a sharp decline in their cholesterol 1. It’s glaringly obvious to me that an individual’s metabolic rate, or lack thereof, is responsible for people’s high cholesterol. It’s why one person can eat butter everyday of their life and die at 42 of a heart attack, and another person can eat butter everyday of their life and not die until 95. Walt Kempner also provided the scientific community with some very important findings when he put his patients on the rice diet and many of their chronic illnesses where reversed. His diet was much less important than the underlying mechanism he discovered, which was a reduction in serum free fatty acids tends to heal the organism. Well the main cause of excess serum FFAs is an excess amount of stress hormones, particularly adrenaline and cortisol. Which thyroid normally keeps in check, but when lacking the stress metabolism will elevate to compensate for the thyroid deficiency. So thyroid, and circulating free fatty acids, play a much bigger role in process that leads up to coronary heart disease than saturated fat. Broda Barnes was a medical doctor who had 1,500+ patients over a 20 year period, he didn’t control their diet, exercise, cholesterol ,or smoking but he was still able to prevent and reverse 94% of heart disease and 100% of diabetes just by giving his patients a desiccated thyroid supplement. Given the parameters of his study, and purposefully not adjusting for co-factors like diet and smoking, Barnes’s study is absolutely one of the most solid cases for determining cause and cure of heart disease.
Given all this, it should be noted that when you have chronically high LDL levels it’s likely a sign of poor thyroid function. And a safer, not to mention more efficient way, of lowering your LDL is to take desiccated thyroid not statin medication which is masking a symptom and not addressing the cause. Other notable ways to lower cholesterol is supplementing pregnenolone, activated charcoal, and niacin. Getting the PUFA, grains, and legumes out of the diet and focusing on lean meats, eggs, veggies, fruits, and starchy tubers is also a move in the right direction. Make sure you’re getting other coronary markers checked as well. Lp(a), CRP, LDH, homocysteine, and ferritin are perhaps just as important if not more important at judging cardiac risk factor than just LDL.
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