A Must-read PUFA Primer

[Amazoniac]

- Advanced Human Nutrition (9781284123067)

Spoiler: Figure 5.19: Eicosanoid Formation Pathways

 

[Jem Oz]

Great post @haidut.

 

[Amazoniac]

- Advanced Nutrition and Human Metabolism (978-1-337-11555-1)

"Two systems of notation have been developed to provide a shorthand way to indicate the chemical structure of a fatty acid."​

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"The delta (Δ) system of notation has been established to denote the chain length of the fatty acids and the number and position of any double bonds that may be present. For example, the notation 18:2 Δ9,12 describes linoleic acid. The first number, 18 in this case, represents the number of carbon atoms; the number following the colon refers to the total number of double bonds present; and the superscript numbers following the delta symbol designate the carbon atoms at which the double bonds begin, counting from the carboxyl end of the fatty acid."​

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"A second commonly used system of notation locates the position of double bonds on carbon atoms counted from the methyl, or omega (ω), end of the hydrocarbon chain. For instance, the notation for linoleic acid would be 18:2 ω-6. Substitution of the omega symbol with the letter n has been popularized. Using this designation, the notation for linoleic acid would be expressed as 18:2 n-6. In this system, the total number of carbon atoms in the chain is given by the first number, the number of double bonds is given by the number following the colon, and the location (carbon atom number) of the first double bond counting from the methyl end is given by the number following ω- or n-. This system of notation takes into account the fact that double bonds in a fatty acid are always positioned so that they are separated by three carbons. Thus, if you know the total number of double bonds and the location of the first relative to either the methyl or carboxylic end, you can determine the locations of the remaining double bonds."​

- Overview About Lipid Structure

- Fatty acid synthesis - Wikipedia

"The positions of the double bonds in a fatty acid chain can, therefore, be indicated in two ways, using the C-n or the ω-n notation. Thus, in an 18 carbon fatty acid, a double bond between C-12 (or ω-7) and C-13 (or ω-6) is reported either as Δ12 if counted from the –COOH end (indicating only the "beginning" of the double bond), or as ω-6 (or omega-6) if counting from the -CH3 end. The "Δ" is the Greek letter "delta", which translates into "D" (for Double bond) in the Roman alphabet. Omega (ω) is the last letter in the Greek alphabet, and is therefore used to indicate the "last" carbon atom in the fatty acid chain."​

If you want another association, ω (or n) looks like a flipped 'm', that can stand for nnethyl. For the delta system, counting begins from the Δcidic, carboxyl end. Knowing one suffices to remember the other.

Oxidation starts from carboxyl to methyl, synthesis from methyl to carboxyl?

 

[Amazoniac]

- Aldehyde toxicity and metabolism: The role of aldehyde dehydrogenases in detoxification, drug resistance and carcinogenesis (!)

Aldehydes are carbonyl compounds found ubiquitously in the environment, derived from both natural and anthropogenic sources. As the aldehydes are reactive species, therefore, they are generally toxic to the body. To reduce the toxicity and pathogenesis related to aldehydes, the human body contains several aldehyde metabolizing enzyme systems including aldehyde oxidases, cytochrome P450 enzymes, aldo-ketoreductases, alcohol dehydrogenases, short-chain dehydrogenases/reductases and aldehyde dehydrogenases (ALDHs). These enzyme systems maintain a low level of aldehydes in the body by catalytically converting them into less-harmful and easily excreted products. The human ALDH (hALDH) superfamily consists of 20 functional ALDH genes identified so far at distinct chromosomal locations, expressing 20 ALDH proteins, which belong to 11 different ALDH families. They are involved in the NAD(P)+-dependent oxidation of a wide range of exogenous and endogenous aldehydes to their corresponding carboxylic acids. The hALDHs are present in all sub-cellular locations and have a wide tissue distribution. This review gives an account of aldehydes; their source, toxicity and metabolism, different aldehyde metabolizing enzymes with special emphasis on ALDHs including their biochemical, physiological and pathophysiological roles in the body.

- Aldehyde Sources, Metabolism, Molecular Toxicity Mechanisms, and Possible Effects on Human Health (!)

Aldehydes are organic compounds that are widespread in nature. They can be formed endogenously by lipid peroxidation (LPO), carbohydrate or metabolism ascorbate autoxidation, amine oxidases, cytochrome P-450s, or myeloperoxidase-catalyzed metabolic activation. This review compares the reactivity of many aldehydes towards biomolecules particularly macromolecules. Furthermore, it includes not only aldehydes of environmental or occupational concerns but also dietary aldehydes and aldehydes formed endogenously by intermediary metabolism. Drugs that are aldehydes or form reactive aldehyde metabolites that cause side-effect toxicity are also included. The effects of these aldehydes on biological function, their contribution to human diseases, and the role of nucleic acid and protein carbonylation/oxidation in mutagenicity and cytotoxicity mechanisms, respectively, as well as carbonyl signal transduction and gene expression, are reviewed. Aldehyde metabolic activation and detoxication by metabolizing enzymes are also reviewed, as well as the toxicological and anticancer therapeutic effects of metabolizing enzyme inhibitors. The human health risks from clinical and animal research studies are reviewed, including aldehydes as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden; and the toxic effects of aldehydes in liver disease, embryo toxicity/teratogenicity, diabetes/ hypertension, sclerosing peritonitis, cerebral ischemia/neurodegenerative diseases, and other aging-associated diseases.

 

[PaRa]

“…Slagsvold observed that cod liver oil poisoned cattle, with stiffness and muscle lesions as symptoms. In another study the toxicity of cod liver oil in calves was manifested as a severe muscular dystrophy. The effect was traced to the unsaturated acids and not the non-saponifiables in which vitamins A and D occur. Thus the effect is not due to hypervitaminosis. Similar lesions were observed in a variety of herbivors fed cod liver oil.”

what's the interest of this haidut ? how feeding cow or herbivores with preformed EPA and DHA is significant ? it's the same lvl as the studies saying dietary cholesterol is bad because if you feed dietary cholesterol to rabbit they get sides, there is none in their normal diet, dha and epa are mostly part of omni/carnivore animals

rats studies on cod liver/dha and epa are irrelevant
and rats studies are mostly irrelevant for human nutrition too