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What is Essential fatty acid and explain in detail?
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.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.

Functions
The biological effects of the ω-3 and ω-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 ω-3 and ω-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 ω-6 EFAs and resolvins from ω-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-κB, which is linked to pro-inflammatory cytokine production)

Fatty acids comprise an aliphatic hydrocarbon chain plus a carboxyl group (–COOH) group at one end, and terminated by a methyl group (–CH3) at the other end. They are almost always straight-chained. The carbon next to the carboxylate is known as α, the next carbon β, and so forth. Since biological fatty acids can be of diverse lengths, the last position is often labelled as a "ω", the last letter in the Greek alphabet. Thus, the ω-3 indicates that the first unsaturated carbon-carbon bond from the terminal end (ω) of then chain is the third one. Typically, the number of carbons and the number of double bonds are also listed in short descriptions of unsaturated fatty acids. For instance, ω-3 18:4, or 18:4 ω-3, or 18:4 n−3 indicates stearidonic acid, an 18-carbon chain with 4 double bonds, and with a double bond between the third and fourth carbon atoms from the CH3 end. Double bonds are cis and separated by a single methylene (CH2) group unless otherwise noted. In free fatty acid form, the chemical structure of stearidonic acid is:

Examples
Polyunsaturated fatty acids with 16- and 18-carbon chains are sometimes classified as short chain polyunsaturated fatty acids (SC-PUFA), as opposed to long-chain polyunsaturated fatty acids (LC-PUFA), which have more than 18 carbon atoms.Both the essential fatty acids are SC-PUFA with an 18-carbon chain:

ω-3 fatty acid:
α-linolenic acid or ALA (18:3n-3)
ω-6 fatty acid:
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 more desaturated fatty acids, most of which also have a longer carbon chain:

ω-3 fatty acids:
eicosapentaenoic acid or EPA (20:5n-3)
docosahexaenoic acid or DHA (22:6n-3)
ω-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)Except for GLA, which has a short 18-carbon chain, these fatty acids have more than 18 carbon atoms and are typically classified as LC-PUFA.ω-9 fatty acids are not essential in humans because they can be synthesized from carbohydrates or other fatty acids.

Essentiality in human diet
Mammals lack the ability to introduce double bonds in fatty acids beyond carbon 9 and 10, hence the omega-6 linoleic acid (18:2n-6; LA) and the omega-3 Alpha-linolenic acid (18:3n-3; ALA) are essential for humans in the diet. However, humans can convert both LA and ALA to fatty acids with longer carbon chains and a larger number of double bonds, by alternative desaturation and chain elongation.
In humans, arachidonic acid (20:4n-6; AA) can be synthesized from LA. In turn, AA can be converted to an even longer fatty acid, the docosapentaenoic acid (22:5n-6; DPA). Similarly, ALA can be converted to docosahexaenoic acid (22:6n-3; DHA), although the latter conversion 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 DPA from LA rather than DHA 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.
In preterm infants, the capacity to convert LA to AA and ALA to DHA 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. In the 1950s Arild Hansen showed that in humans: infants fed skimmed milk developed the 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 to four treatments: modified cows milk formula, skimmed milk formula, skimmed milk formula with coconut oil, or cows 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 ω-3 fatty acids or by arachidonic acid.
The main physiological requirement for ω-6 fatty acids is attributed to arachidonic acid