Fats, or more precisely fatty acids, are composed of long (14+), medium (6-12), or short (<6), chains of carbon atoms that are bonded to hydrogen atoms with a carboxylic acid head group (this is where each of the three carbons forming a triglyceride attach to the glycerol backbone). Whether the carbon atoms are bonded to their maximum number of hydrogen atoms determines whether they are saturated, no double bonds, monounsaturated, one double bond, or polyunsaturated, containing two or more double bonds. The configuration of the hydrogens around the double bond, whether they are on the same side or opposite, determines whether the fat is a trans fat (opposite side) or a cis fat (same side). Saturated fats tend to be solid at room temperature, like butter, tallow, lard, and coconut oil, but because coconut oil is composed of lots of medium chain fatty acids, it has a lower melting point and may be liquid in a warmer environment. Monounsaturated fats, like olive, avocado, or macadamia nut oil, are going to be liquid at room temperature but will partially solidify if put in a refrigerated environment. The polyunsaturated fats, like canola, soy, grapeseed, corn, flax, etc. will be liquid at room temperature and remain liquid until well below freezing.
Polyunsaturated fats are most prevalent in temperate (areas of mild temperature) seeds, nuts, and their extracted oils. This means all grains, nuts, seeds, and non-ruminant animals (pigs and poultry) fed things like corn, soybeans, and/or flaxseeds will contain a large percentage of polyunsaturated fat. The most common vegetable PUFAs are linoleic acid (18:2) and linolenic acid (18:3). The first number is how many carbons are contained in the fatty acid and the second number is how many double bonds it contains. Linoleic acid (LA) is what you think of when someone says omega 6 fat. Its first double bond is six carbons from the last carbon in the chain. Linolenic acid (ALA) is the plant omega 3 which means its first double bond is three carbons from the last carbon in the chain. Both of these fats need chemical conversion in the body to the "active" biological forms like arachidonic acid (AA) a 20:4 fatty acid, made from LA, and EPA (20:5) and DHA (22:6), which are made from ALA. There is a lot to be said about the function of AA, EPA, and DHA in the body and the chemical reactions they undergo for prostaglandin and leukotriene synthesis(regulators of inflammation) but I want to focus more on the problems associated with the consumption of these fats in general rather than their supposed biologic function and role in inflammation (which is another article completely).
Like we discussed in the previous post, the polyunsaturated fats, oxidize quicker than Tyrion Lannister jumps into bed with a harlot, especially when exposed to heat and oxygen. The formation of the PUFA oxidation products, which are reactive aldehydes like malondialdehyde (MDA), 4-HNE, and acrolein, are the heavy hitters in producing many of the toxic effects of the polyunsaturated fatty acids. MDA and 4-HNE are especially toxic to the liver allowing for the formation of fatty liver disease and cirrhosis. It has been suggested that fatty liver and cirrhosis are impossible without the damage induced by PUFA free radicals. It should be mentioned that very low levels of 4-HNE are hormetic (a stressor/toxin that is paradoxically beneficial to the cell/organism) much like radiation, exercise, or alcohol mostly by increasing the antioxidant status of the cell. MDA and 4-HNE are also especially good at increasing the permeability of the intestinal epithelial cells making them leaky to both resident bacteria as well as proteins from food. Leakiness to bacteria is especially nasty, as certain strains (the gram negative) like E. coli, Salmonella, and Shigella contain a very toxic component in the outter porton of their cell membraine called lipopolysaccharide (LPS). LPS is responsible for the nasty symptoms of sepsis or sometimes called blood poisoning. High levels of LPS are very serious and a medical emergency but lower levels of plasma LPS are very damaging to the blood vessels and the liver due to the immune reaction they illicit once inside the blood. Strangely enough, cholesterol, which we are told is bad, is able to bind and inactivate LPS and its toxic effects. It is very possible that leaky gut, regardless the cause, is a significant contributor to heart and vascular disease. The leaky gut produced by exposure to toxic PUFA lipid peroxides also sets the stage for developing food sensitivities and food allergies. There are other things and substances that can cause and/or contribute to developing a leaky gut but considering the rise in PUFA consumption and their potent ability to increase intestinal permeability, they are likely the greatest single contributor to leaky gut in all but a few cases.
Next up will be a discussion of what foods to eat, what foods to avoid, how to protect yourself if you have to ingest some PUFA, and what to do about the PUFA you already have stored in your body.
Summary
- fats come in a variety of shapes (saturated, monounsaturated, and polyunsaturated) and sizes (4-24+ carbons long)
- fats with more double bonds (PUFAs) are more susceptible to oxidation and damage
- oxidized/damaged fats, called lipid peroxides, are responsible for a myriad of nasty effects in the body
- lipid peroxides damage the liver and the intestinal wall/lining (among other things)
- a damaged liver is less capable of processing nutrients and regulating metabolic processes like fatty acid transport, cholesterol synthesis, and detoxification
- a leaky gut allows bacteria and food proteins into the bloodstream (inappropriately) which can set the stage for more liver damage, blood vessel damage, inflammation, and food sensitivities/allergies
In good health,
CH
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