Essential fatty acids, or EFAs, are fatty acids that humans and other animals must ingest because the body requires them for good health but cannot synthesize them. Those not essential are non-essential fatty acids.
The term "essential fatty acid" refers to fatty acids required for biological processes but does not include the fats that only act as fuel. Essential fatty acids should not be confused with essential oils, which are "essential" in the sense of being a concentrated essence.
Only two fatty acids are known to be essential for humans: alpha-linolenic acid (an omega-3 fatty acid) and linoleic acid (an omega-6 fatty acid). Some other fatty acids are sometimes classified as "conditionally essential," meaning that they can become essential under some developmental or disease conditions; examples include docosahexaenoic acid (an omega-3 fatty acid) and gamma-linolenic acid (an omega-6 fatty acid).
When the two EFAs were discovered in 1923, they were designated "vitamin F", but in 1929, research on rats showed that the two EFAs are better classified as fats rather than vitamins.
Video Essential fatty acid
Functions
- The biological effects of the ?-3 and ?-6 fatty acids are mediated by their mutual interactions, see Essential fatty acid interactions for detail.
In the body, essential fatty acids serve multiple functions. In each of these, the balance between dietary ?-3 and ?-6 strongly affects function.
- They are modified to make
- the classic eicosanoids (affecting inflammation and many other cellular functions)
- the endocannabinoids (affecting mood, behavior and inflammation)
- the lipoxins which are a group of eicosanoid derivatives formed via the lipoxygenase pathway from ?-6 EFAs and resolvins from ?-3 (in the presence of acetylsalicylic acid, downregulating inflammation)
- the isofurans, neurofurans, isoprostanes, hepoxilins, epoxyeicosatrienoic acids (EETs) and Neuroprotectin D
- They form lipid rafts (affecting cellular signaling)
- They act on DNA (activating or inhibiting transcription factors such as NF-?B, which is linked to pro-inflammatory cytokine production)
Fatty acids are straight chain hydrocarbons possessing a carboxyl (COOH) group at one end. The carbon next to the carboxylate is known as ?, the next carbon ?, and so forth. Since biological fatty acids can be of different lengths, the last position is labelled as a "?", the last letter in the Greek alphabet. The physiological properties of unsaturated fatty acids largely depend on the position of the first unsaturation relative to the end position and not the carboxylate. For example, the term ?-3 signifies that the first double bond exists as the third carbon-carbon bond from the terminal CH3 end (?) of the carbon chain. The number of carbons and the number of double bonds are also listed.
?-3 18:4 (stearidonic acid) or 18:4 ?-3 or 18:4 n-3 indicates an 18-carbon chain with 4 double bonds, and with the first double bond in the third position from the CH3 end. Double bonds are cis and separated by a single methylene (CH2) group unless otherwise noted. So in free fatty acid form, the chemical structure of stearidonic acid is:
Examples
- For complete tables of ?-3 and ?-6 essential fatty acids, see Polyunsaturated fatty acids.
The essential fatty acids start with the short chain polyunsaturated fatty acids (SC-PUFA):
- ?-3 fatty acids:
- ?-Linolenic acid or ALA (18:3n-3)
- ?-6 fatty acids:
- Linoleic acid or LA (18:2n-6)
These two fatty acids cannot be synthesized by humans because humans lack the desaturase enzymes required for their production.
They form the starting point for the creation of longer and more desaturated fatty acids, which are also referred to as long-chain polyunsaturated fatty acids (LC-PUFA):
- ?-3 fatty acids:
- eicosapentaenoic acid or EPA (20:5n-3)
- docosahexaenoic acid or DHA (22:6n-3)
- ?-6 fatty acids:
- gamma-linolenic acid or GLA (18:3n-6)
- dihomo-gamma-linolenic acid or DGLA (20:3n-6)
- arachidonic acid or AA (20:4n-6)
?-9 fatty acids are not essential in humans because they can be synthesized from carbohydrates or other fatty acids.
Essential fatty acids
Mammals lack the ability to introduce double bonds in fatty acids beyond carbon 9 and 10, hence ?-6 linoleic acid (18:2,9,12), abbreviated LA (18:2n-6), and the ?-3 linolenic acid (18:3,9,12,15), abbreviated ALA (18:3n-3), are essential for humans in the diet. In humans, arachidonic acid (20:4,5,8,11,14, abbreviated 20:4n-6) can be synthesized from LA by alternative desaturation and chain elongation.
Humans can convert both LA and ALA to docosapentaenoic acid (22:5n-6) and docosahexaenoic acid (22:6n-3; DHA) respectively, although the conversion to DHA is limited, resulting in lower blood levels of DHA than through direct ingestion. This is illustrated by studies in vegans and vegetarians. If there is relatively more LA than ALA in the diet it favors the formation of docosapentaenoic acid (22:5n-6) from LA rather than docosahexaenoic acid (22:6n-3) from ALA. This effect can be altered by changing the relative ratio of LA:ALA, but is more effective when total intake of polyunsaturated fatty acids is low. However, the capacity to convert LA to AA and ALA to DHA in the preterm infant is limited, and preformed AA and DHA may be required to meet the needs of the developing brain. Both AA and DHA are present in breastmilk and contribute along with the parent fatty acids LA and ALA to meeting the requirements of the newborn infant. Many infant formulas have AA and DHA added to them with an aim to make them more equivalent to human milk.
Essential nutrients are defined as those that cannot be synthesized de novo in sufficient quantities for normal physiological function. This definition is met for LA and ALA but not the longer chain derivatives in adults. The longer chain derivatives particularly, however, have pharmacological properties that can modulate disease processes, but this should not be confused with dietary essentiality.
Between 1930 and 1950, arachidonic acid and linolenic acid were termed 'essential' because each was more or less able to meet the growth requirements of rats given fat-free diets. However, they were yet to be recognized as essential nutrients for humans. In the 1950s Arild Hansen showed that infants fed skimmed milk developed essential fatty acid deficiency. It was characterized by an increased food intake, poor growth, and a scaly dermatitis, and was cured by the administration of corn oil.
Later work by Hansen randomized 426 children, mainly black, to four treatments: modified cow's milk formula, skimmed milk formula, skimmed milk formula with coconut oil, or cow's milk formula with corn oil. The infants who received the skimmed milk formula or the formula with coconut oil developed essential fatty acid deficiency signs and symptoms. This could be cured by administration of ethyl linoleate (the ethyl ester of linoleic acid) with about 1% of the energy intake.
Collins et al. 1970 were the first to demonstrate linoleic acid deficiency in adults. They found that patients undergoing intravenous nutrition with glucose became isolated from their fat supplies and rapidly developed biochemical signs of essential fatty acid deficiency (an increase in 20:3n-9/20:4n-6 ratio in plasma) and skin symptoms. This could be treated by infusing lipids, and later studies showed that topical application of sunflower oil would also resolve the dermal symptoms. Linoleic acid has a specific role in maintaining the skin water-permeability barrier, probably as constituents of acylglycosylceramides. This role cannot be met by any ?-3 fatty acids or by arachidonic acid.
The main physiological requirement for ?-6 fatty acids is attributed to arachidonic acid. Arachidonic acid is the major precursor of prostaglandins, leukotrienes, and anandamides that play a vital role in cell signaling. Metabolites from the ?-3 pathway, mainly from eicosapentaenoic acid, are mostly inactive, and this explains why ?-3 fatty acids do not correct the reproductive failure in rats where arachidonic is needed to make active prostaglandins that cause uterine contraction. To some extent, any ?-3 or ?-6 can contribute to the growth-promoting effects of EFA deficiency, but only ?-6 fatty acids can restore reproductive performance and correct the dermatitis in rats. Particular fatty acids are still needed at critical life stages (e.g. lactation) and in some disease states.
In nonscientific writing, common usage is that the term essential fatty acid comprises all the ?-3 or -6 fatty acids. Conjugated fatty acids like calendic acid are not considered essential. Authoritative sources include the whole families, but generally only make dietary recommendations for LA and ALA with the exception of DHA for infants under the age of 6 months. Recent reviews by WHO/FAO in 2009 and the European Food Safety Authority have reviewed the evidence and made recommendations for minimal intakes of LA and ALA and have also recommended intakes of longer chain ?-3 fatty acids based on the association of oily fish consumption with a lower risk of cardiovascular disease. Some earlier review lumped all polyunsaturated fatty acids together without qualification whether they were short or long-chain PUFA or whether they were ?-3 and ?-6 PUFA.
Conditionally essential
Traditionally speaking, the LC-PUFAs are not essential. Because the LC-PUFA are sometimes required, they may be considered conditionally essential fatty acids, or not essential to healthy adults.
Source of the article : Wikipedia
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