Essential fatty acids are fatty acids that humans must obtain through their diet as the body cannot synthesize them on its own. There are two essential fatty acids - alpha-linolenic acid and linoleic acid. These fatty acids serve important functions in the body and are precursors to molecules like prostaglandins and leukotrienes. Essential fatty acids are obtained through foods like fish and some plant-based foods. Deficiencies in these fatty acids are rare.

1. Essential Fatty acids
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.
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). These are supplied to the body both, as the free fatty
acid or more commonly as some glyceride derivative. deficiency in these fatty acids is rare. These
fatty acids are essential because they are precursors to vitamins, cofactors. These derivatives
include prostaglandins, leukotrienes, thromboxanes, lipoxins, and others.
The term essential fatty acids (efa) refers to those polyunsaturated fatty acids (pufa) that must be
provided by foods because these cannot be synthesized in the body yet are necessary for health.
There are two families of EFA, omega-3 (ω-3) Linoleic Acid (LA) and Alha Linoleic Acid (ALA)
omega-6 (ω-6).
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.
Functions
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)
Essential nutrients are defined as those that cannot be synthesized de novo in sufficient quantities
for normal physiological function. This definition is met for Linoleic Acid (LA) and Alha Linoleic
Acid (ALA) but not the longer chain derivatives in adults
Food Sources
Essential fatty acids play a part in many metabolic processes, low levels of essential fatty acids, or
the wrong balance of types among the essential fatty acids, may be a factor in a number of illnesses,
including osteoporosis.
Fish is the main source of the longer omega-3 fats; eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA),
Some plant-based foods contain omega-3 in the form of alpha-linolenic acid (ALA), which appears
to have a modest benefit for cardiovascular health.The human body can convert ALA to EPA and
subsequently DHA. This elongation of ALA is inefficient. Conversion to DHA is higher in women than
in men; this is thought to reflect the need to provide DHA to the fetus and infant during pregnancy
and breast feeding.

2. Lipoprotein
Cholesterol and triglycerides are insoluble in water and therefore these lipids must be transported
in association with proteins. Lipoproteins are complex particles with a central core containing
cholesterol esters and triglycerides surrounded by free cholesterol, phospholipids, and
apolipoproteins, which facilitate lipoprotein formation and function. Plasma lipoproteins can be
divided into seven classes based on size, lipid composition, and apolipoproteins (chylomicrons,
chylomicron remnants, VLDL, IDL, LDL, and HDL).
Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids,
primarily cholesterol esters and triglycerides. This hydrophobic core is surrounded by a
hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins (Figure
1). Plasma lipoproteins are divided into seven classes based on size, lipid composition, and
apolipoproteins
 Very Low-Density Lipoproteins (VLDL)
These particles are produced by the liver and are triglyceride rich.
VLDL particles can vary depending on the quantity of triglyceride carried in the particle. When
triglyceride production in the liver is increased, the secreted VLDL particles are large. However,
VLDL particles are smaller than chylomicrons
 Intermediate-Density Lipoproteins (IDL; VLDL Remnants)
The removal of triglycerides from VLDL by muscle and adipose tissue results in the formation of
IDL particles which are enriched in cholesterol. These particles contain apolipoprotein B-100 and E.
These IDL particles are pro-atherogenic.
 Low Density Lipoproteins
LDL consists of a spectrum of particles varying in size and density. An abundance of small dense
LDL particles are seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2
diabetes (i.e. patients with the metabolic syndrome) and infectious and inflammatory states. These
small dense LDL particles are considered to be more pro-atherogenic than large
 High-Density Lipoproteins (HDL)
These particles play an important role in reverse cholesterol transport from peripheral tissues to
the liver, which is one potential mechanism by which HDL may be anti-atherogenic. In addition,
HDL particles have anti-oxidant, anti-inflammatory, anti-thrombotic, and anti-apoptotic properties,
which may also contribute to their ability to inhibit atherosclerosis. HDL particles are enriched in
cholesterol and phospholipids.

3. Cholesterol
Cholesterol travels through the blood on proteins called “lipoproteins.” Two types of lipoproteins
carry cholesterol throughout the body:
LDL (low-density lipoprotein) cholesterol, sometimes called “bad” cholesterol, makes up most of
your body’s cholesterol. High levels of LDL cholesterol raise your risk for heart disease and stroke.
HDL (high-density lipoprotein) cholesterol, sometimes called “good” cholesterol, absorbs
cholesterol in the blood and carries it back to the liver. The liver then flushes it from the body. High
levels of HDL cholesterol can lower your risk for heart disease and stroke.
When body has too much LDL cholesterol, the LDL cholesterol can build up on the walls of your
blood vessels. This buildup is called “plaque,” and it can cause health problems, such as heart
disease and stroke. Triglycerides are a type of fat in your blood that your body uses for energy.
The combination of high levels of triglycerides with low HDL and/or high LDL cholesterol levels can
increase risk for health problems, such as heart attack.
A complete cholesterol test, also called a lipid panel or lipid profile , is a blood test that can measure
the amount of cholesterol and triglycerides in your blood.
A cholesterol test can help determine your risk of the buildup of fatty deposits (plaques) in your
arteries that can lead to narrowed or blocked arteries throughout your body (atherosclerosis).
A cholesterol test is an important tool. High cholesterol levels often are a significant risk factor for
coronary artery disease.
A complete cholesterol test includes the calculation of four types of fats in your blood:
 Total cholesterol. This is a sum of your blood's cholesterol content.
 Low-density lipoprotein (LDL) cholesterol. This is called the "bad" cholesterol. Too much
of it in your blood causes the buildup of fatty deposits (plaques) in your arteries
(atherosclerosis), which reduces blood flow. These plaques sometimes rupture and can lead
to a heart attack or stroke.
 High-density lipoprotein (HDL) cholesterol. This is called the "good" cholesterol because
it helps carry away LDL cholesterol, thus keeping arteries open and your blood flowing
more freely.
 Triglycerides. Triglycerides are a type of fat in the blood. When we eat, our body converts
calories it doesn't need into triglycerides, which are stored in fat cells. High triglyceride
levels are associated with several factors, including being overweight, eating too many
sweets or drinking too much alcohol, smoking, being sedentary, or having diabetes with
elevated blood sugar levels.

4. Fatty acid oxidation
Fatty acid transport into mitochondria
Fatty acids are activated for degradation by conjugation with coenzyme A (CoA) in the cytosol. The long-
chain fatty-acyl-CoA is then modified by carnitine palmitoyltransferase 1 (CPT1) to acylcarnitine and
transported across the inner mitochondrial membrane by carnitine translocase (CAT). CPT2 then coverts the
long chain acylcarnitine back to long-chain acyl-CoA before beta-oxidation.
Beta-oxidation
Beta-oxidation consists of four steps:
1) Dehydrogenation catalyzed by acyl-CoA dehydrogenase, which removes two hydrogens between carbons 2
and 3.
2) Hydration catalyzed by enoyl-CoA hydratase, which adds water across the double bond.
3) Dehydrogenation catalyzed by 3-
hydroxyacyl-CoA dehydrogenase, which
generates NADH.
4) Thiolytic cleavage catalyzed beta-
ketothiolase, which cleaves the terminal acetyl-
CoA group and forms a new acyl-CoA which is
two carbons shorter than the previous one.
The shortened acyl-CoA then reenters the beta-
oxidation pathway.

5. Cholestrol synthesis
Cholesterol is synthesized via a cascade of enzymatic reactions known as the mevalonate
pathway. This series of reactions is primarily regulated by a rate-limiting step involving the
conversion of hydroxyl-methyl glutaryl-coenzyme A (HMG-CoA) into mevalonate.