DHA/EPA/ALA Disease & Horse Meat

By Atom Bergstrom

Atom’s Blog

According to “Horse carcasses with yellow fat disease,” The Catalan Slaughterhouse Support Network (SESC), Mar. 27, 2017 …

“Briefly, this disease consists in the fact that due to a lack of reducing power lipids are oxidized and what we observe in the microscope (which is what gives the yellowish-brown color to the fats) is the accumulation of pigments resulting from the degradation of these lipids, particularly within macrophages.”

According to the same source …

“Regarding public health, since it is a generalized inflammation of adipose tissue, we consider the carcasses unfit for consumption, but essentially no sanitary risk exists other than the organoleptic alteration of both color and probably taste (oxidized, rancid fat).”

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Ray Peat (“East West: The Science Behind the Dangers of Polyunsaturated Fats,” audio, Nov. 29, 2014) said …

“In the 1930s and 40s they found that they were killing their animals by feeding them too much of the seeds that were rich in polyunsaturated fats, or fish in some cases such as mink were the ones that were being killed by an excess of fish in the diet. But even horse meat was killing animals like mink, which were carnivorous, and so if the horses had eaten flax or linseed, their fat was toxic to the carnivorous animals. And in animals that ate too much of the unsaturated fats, they developed yellow fat disease, which, in mink, it developed paralysis fairly quickly at the hind quarters, and then it would kill them, and it would turn out that their fat tissue was inflamed and waterlogged, and eventually it would turn yellow or brown.”

According to the same source …

“And that’s the same pigment that appears in the uterus that has been overexposed to estrogen or in the skin of an old person that has been exposed to sunlight, and the brain. All the organs develop this pigment with aging, but it develops in proportion to the amount of unsaturated fats in the diet.”

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Docosahexaenoic acid (DHA), eicosapentanoic acid (EPA), and alpha-linolenic acid (ALA) have been doing their dirty deeds for many millions of years.

DHA is the General Zod of Superman Super-Villains.

EPA is Ursa.

ALA is Non.

Iron is Lex Luthor.

Estrogen is Doomsday.

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According to Dr. Jack Kruse (Apr. 1, 2016) …

“If you think Chris [Masterjohn] is wise riddle me this? Why did all complex life show up in the Cambrian explosion 580 million years ago 20 million years after DHA showed up in our oceans? Then the big problem for the academics … why has DHA never been replaced one time in 600 million years in the eukaryotic kingdom? When he answers that I will call him wise.”

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I have a less favorable outlook about DHA than Dr. Kruse.

Just because something has been around and never replaced for 600 millions years doesn’t mean it’s beneficial.

Cyanide has been around for millions of years longer — and has never been replaced either.

It has more in common with gas chambers than with health food stores.

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One very important fact — life didn’t begin in the sea.

Life began on land in moist mud.

Details are in Butterflies Need No Taxidermist, especially in Volume 3.

It’s also mentioned in Not Cancer…Cancel, in reference to biological hierarchy.

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You didn’t know life began on land?

Of course not. You went to school.

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Stephen R. Palumbi & Anthony R. Palumbi (The Extreme Life of the Sea, 2014) wrote …

“Normally, portals made of proteins in the membrane move nutrients and ions in and out, regulating the cell’s function, feeding it, removing wastes. But when membrane lipids are subjected to extreme pressure, they thicken and harden like bacon grease congealing in a mason jar. Cell membranes become congealed, and their gates shut down. The cell is unable to get what it needs, is unable to communicate with its fellows, and unable to function properly.

“In response, the deepest animals have re-engineered their membrane chemistry. A different lipid is used for membranes in the deep, one that remains fluid even under enormous pressure. One of the ways deep-sea animals accomplish this is by decreasing how much saturated fat they put in their cell membranes.”

According to the same source …

“Surface fish like salmon tip the scales at about 35% saturated fat. Three miles down, evolution under high hydrostatic pressure has fundamentally altered the same tissues: fish contain only 10% saturated fats. At depth, the loose lipids are compressed by pressure but retain the right fluidity for function. And of course, the process works in reverse. Deep-sea animals brought to the surface don’t behave normally, even if treated with care. Chaos ensues as their unsaturated lipids melt and proteins fail to function at low pressure.”

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Today’s framers are eager to transmute salmon into one of its deep-sea brethren.

According to Wikipedia …

“Work continues on substituting vegetable proteins for animal proteins in the salmon diet. This substitution results in lower levels of the highly valued omega-3 fatty acid content in the farmed product.”

Horses will opt for flax. Why not salmon?

Flax is cheap. That’s why it’s a “health” food.

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Spawning salmon burn off their fat stores, so folks who eat fish get less DHA and EPA.

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Nick Lane (Oxygen: The Molecule that Made the World, 2002) wrote …

“There is a price for fluidity, however: double bonds are easily oxidized. Some sort of compromise is necessary. The best compromise varies according to the type of performance required. For example, a high metabolic rate requires a fluid membrane, while a long life demands resistance to oxidation.

“With this in mind, Reinald Pamplona, Gustavo Barja, and their colleagues at the University of Lleida, in Spain, compared the fatty acid composition of mitochondria from different species, from rats to horses and pigeons to parakeets. They found a striking relationship. Animals with long lifespans had low levels of highly unsaturated fatty acids, such as docosahexaenoic acid (with six double bonds) and arachidonic acid (with four double bonds) but much higher levels of slightly unsaturated fatty acids with two or three double bonds, such as linoleic acid. In other words, the longer the lifespan, the lower the level of unsaturation.”

According to the same source …

“Animals get ‘more unsaturated’ as they age. Old rats double their content of highly unsaturated fatty acids, while the proportion of less-unsaturated fatty acids falls correspondingly. As a result, mitochondria become more vulnerable to oxidation with age, and lose their lubricant, cardiolpin.”

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Let’s count the double bonds …

Docosahexaenoic acid (DHA) has six double bonds.

Eicosapentanoic acid (EPA) has five double bonds.

Arachidonic acid (AA) has four double bonds.

Alpha-linolenic acid (ALA) has three double bonds.

Linoleic acid (LA) has two double bonds.

Oleic acid has one double bond.

Saturated fatty acids have no double bonds.

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Cardiolpin is “almost exclusively associated with membranes designed to produce ATP.”

It’s called “the signature phospholipid of mitochondria.”

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According to Dr. Jack Kruse …

“DHA allows our cells to power up electrons with photons.”

Don’t ask Dr. Kruse about DHA. (He’s obviously keen about it.)

Ask him about Yellow Fat Disease.
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