Arachidonic acid in foods and endogenous synthesis
Arachidonic acid is a polyunsaturated fatty acid with 20 carbon atoms [20: 4 (ω-6)].
Also known as 5-8-11-14 eicosatetraenoic acid, or more simply indicated by the acronym AA, arachidonic acid is widely distributed in nature and can be taken through food - especially animal ones (eggs, fish and meat) - or synthesized by the body from linoleic acid. Endogenous synthesis is minor, while the contribution of nutrition is rather high, especially in industrialized societies. For all these reasons arachidonic acid is considered a semi-essential fat, indispensable when insufficient quantities of linoleic acid (mainly contained in seed oils) are taken. In the human body, the highest concentrations of arachidonic acid are recorded in the muscle and brain tissues.
Arachidonic acid is also present in good quantities in breast milk (more than twice as much as cow's milk) and it is not by chance that it is considered an important nutrient for the good growth of the fetus and the newborn. In particular it has proved to be very important to promote the child's nervous and intellectual development (an action shared with omega-three fatty acids).
In our organism, arachidonic acid concentrates at the level of membrane phospholipids, ie in that phospholipid double layer which - by distributing itself on the outer surface of the cells - regulates the entry and exit of the various cellular metabolites (nutrients, hormones, substances waste etc.).
Arachidonic Acid, Leukotrienes and Inflammatory Waterfall
Arachidonic acid is the main precursor of eicosanoids, substances involved in the inflammatory response of the body. In the presence of tissue damage, enzymes belonging to the class of phospholipases A2 (PLA2) release arachidonic acid from membrane phospholipids (where it has been esterified), for example from phosphatidylethanolamine (PE), from phosphatidylcholine (PC), from phosphatidylinositol ( PI) and phosphatidylserine (PS). Two different molecular types can thus be obtained from arachidonic acid: the series 2 of PROSTAGLANDINE and TROMBOSSANI (from the cycloxygenase pathway) and the series of LEUCOTRIENES (from the lipoxygenase pathway). Like the starting fatty acid, all these substances are called eicosanoids because of the 20-carbon structure that characterizes them.
The synthesis of the series 2 of prostaglandins and thromboxanes starting from free arachidonic acid is mediated by the enzyme cyclooxygenase, which is present in the human body in the form of COX1 and COX2. Corticosteroid drugs perform their anti-inflammatory action by inhibiting the enzyme phospholipase A2 (PLA2), while non-steroidal anti-inflammatory drugs (such as aspirin or ibuprofen) inhibit the action of the COX1 and / or COX2 enzymes.
Prostaglandins produced from arachidonic acid perform a vasodilating action and increase capillary permeability, supporting the inflammatory state (fever, pain, edema). This action counteracts the anti-inflammatory action performed by the prostaglandins of series one (PEG-1) and three (PEG-3), which are instead produced from alpha linolenic acid (fish oil, hemp oil, linseed oil) and from linoleic acid (which as we have seen can be converted into arachidonic acid and thus also indirectly originate PEG-2). The speech, however, is not so simple, given that from the arachidonic acid not only prostaglandins with pro-inflammatory action originate, but also others with diametrically opposite effect. In physiological conditions, arachidonic acid and the ecosanoids that derive from it therefore perform a regulatory and control action on inflammatory processes. The prostaglandins produced in the cyclo-oxygenase pathway, in fact, act quickly on the cells in which they were synthesized and on neighboring tissues, after which they are inactivated and eliminated with urine; in this way they control the inflammation preventing the development of abnormal reactions.
The leukotrienes originating from the lipoxygenase pathway, due to the bronchoconstrictor effect, are implicated in the pathophysiology of asthma and anaphylactic shock.
Dietary intake and nutritional balance
Since inflammation is involved in the origin and maintenance of many morbid conditions (rheumatoid arthritis, chronic ulcerative colitis, lupus, pelvic inflammatory disease, atherosclerosis, etc.), dietary strategies able to reduce prostaglandin synthesis have been studied pro-inflammatory in favor of those with anti-inflammatory action. For this purpose it is advisable to reduce the consumption of vegetable oils and fatty meats, in favor of fish and some particular oils, such as flax and hemp. It is also advisable to prefer lean dairy products and to limit the consumption of eggs, especially of the yolk; at the same time these protein sources should be replaced on at least a couple of weekly occasions with legumes like lentils, chickpeas, beans and soy-based products. In this way it is plausible that greater amounts of eicosapentaenoic acid and docosahexaenoic acid (omega-three) are incorporated in the membrane phospholipids instead of arachidonic acid. In the presence of a phlogistic imput the inflammatory response would therefore be less violent.
Obesity is a condition heavily associated with a chronic inflammatory state of the body, so in these cases a low-calorie diet can be indirectly considered anti-inflammatory.
Recently the nutritional importance of arachidonic acid has been widely re-evaluated in the sports field, to the point that today it is marketed as a supplement designed to maximize muscle growth in bodybuilders.
