LIPIDS

They may be regarded as organic substance relatively insoluble in water and soluble in inorganic
solvents (alcohol, ether etc.) and utilized by living cells.

BIOMEDICAL IMPORTANCE

 They are important dietary constituents and act as fuel- 9 cal/g.

 They are stored in the adipose tissue of the body.

 They act as insulating material in the subcutaneous tissue.

 They supply essential fatty acids for normal human health and growth.

 They serve as the source of fat soluble vitamins- A, D, E and K.

 They are present as the important constituents of cell membrane (phospholipids) and cell organelles,
especially mitochondria.

 Fat content of nerve tissue is particularly high and is essential for their proper functioning.

CLASSIFICATION OF LIPIDS

Based on chemical composition, lipids are classified as:

1. Simple lipids

 They are esters of fatty acids with alcohol.

 They are of two types: Triglycerides (Fats and oils) and Waxes.

a. Triglycerides

 They are esters of fatty acids with glycerol.

 Oil is a liquid and fat is a solid at room temperature.

b. Waxes

 They are esters of fatty acids with alcohol other than glycerol.

 Eg: Lanoline and Beeswax

2. Complex/ Compound lipids

  They are esters of fatty acids with alcohol containing additional groups such as phosphate,
nitrogenous base, carbohydrates, proteins etc. Based on the prosthetic group present they are
classified as:

a. Phospholipids

 They contain phosphoric acid and frequently a nitrogenous base, in addition to fatty acids and
alcohol. Eg: Lecithin and cephalin.

b. Glycolipids

 They contain fatty acids, carbohydrates and nitrogenous base. They alcohol present is sphingosine,
hence they are also called glycosphingolipids. Eg: cerebrosides and gangliosides.

c. Lipoproteins

 They are macromolecular complex of lipids with proteins. Eg: HDL and LDL

d. Sulpholipids

 They are esters of fatty acids and alcohol with sulphate group.

3. Derived lipids

 They are derivatives obtained by hydrolysis of simple and complex lipids. Eg: glycerol, steroid
hormones, fat soluble vitamins etc.

4. Miscellaneous lipids

 They include a large number of compound possessing the characteristics of lipids. Eg: carotenoids
and terpenes.

5. Neutral lipids

 Those lipids which are soluble only in solvents of very low polarity are referred to as neutral lipids.
Eg: cholesterol

FATTY ACIDS

 They are the simplest forms of lipids.

 They are long chain or short chain (4-30 C) monocarboxylic organic acids.

 Their general formula is R-COOH, where R refers to the hydrocarbon tail.

 They are obtained from hydrolysis of fat.

  Fatty acids occur either as free fatty acids or in esterified form as major constituents of various lipids.

CLASSIFICATION OF FATTY ACIDS

Fatty acids are classified into three: 1. Even and odd carbon fatty acids 2. Saturated and
unsaturated fatty acids and 3. Essential and non-essential fatty acids, and

1. Even and odd carbon fatty acids

 Most of the fatty acids that occur in natural lipids are of even carbon.

 Even carbon fatty acids contain even number of carbon atoms. Eg: palmitic acid (16C) and stearic
acid (18C)

 Odd carbon fatty acids contain odd number of carbon atoms. Eg: propionic acid (3C) and valeric acid
(5C)

2. Saturated and unsaturated fatty acids

i. Saturated fatty acids- these are fatty acids with no double bond between their carbon in their
molecular chain. They can be:

a. Lower saturated fatty acids- having 10 or less carbon atoms. Eg: acetic acid and butyric acid

b. Higher saturated fatty acids- having more than 10 carbon atoms. Eg: palimtic acid and stearic acid.

ii. Unsaturated fatty acids- these are fatty acids with double bonds between carbon chains. They can be:

a. Mono-unsaturated fatty acids (MUFA)- fatty acids with one double bond. Eg: oleic acid

b. Poly-unsaturated fatty acids (PUFA)- fatty acids with two or more double bonds. Eg: linoleic acid,
linolenic acid and arachidonic acid.

3. Essential and non- essential fatty acids

i. Essential fatty acids- these fatty acids have to be provided through diet and cannot be synthesized by
the body. Linoleic acid, linolenic acid and arachidonic acid collectively contribute as essential fatty
acids.

Functions

 Required for membrane structure and function.

 Transport of cholesterol, formation of lipoproteins etc.

 Help to lower cholesterol level.

  Prolong clotting time and increase fibrinolytic activity.

 Linoleic acid is necessary in diet for optimal vision.

 Deficiency of essential fatty acid produces fatty liver.

 Structural element of gonads, and thus plays a major reproductive function.

 Structural element of mitochondrial membrane. Deficiency of essential fatty acid causes swelling of
membrane reduces the efficiency of oxidative phosphorylation and may cause increased heat
production.

ii. Non-essential fatty acids- they are synthesized by the body and not supplied through diet. Eg:
palmitic acid.

Trans fatty acids

Trans-fatty acids are manufactured fats created during a process called

hydrogenation, which is aimed at stabilizing polyunsaturated oils to prevent them from becoming rancid and
to keep them solid at room temperature. Hydrogenated fats are used in stick margarine, fast foods,
commercial baked goods (donuts, cookies, crackers), and fried foods. Trans-fats raise your LDL (bad)
cholesterol. They also lower your HDL (good) cholesterol. High LDL along with low HDL levels can cause
cholesterol to build up in your arteries (blood vessels). This increases your risk for heart disease and stroke.
They may also pose a risk for certain cancers.

DIGESTION AND ABSORPTION OF LIPIDS

Digestion of lipids

Lipids and fats are digested by lipolytic enzymes (lipases). The major dietary lipids include are
triacylglycerol, cholesterol / cholesteryl esters and phospholipids.

Mouth: No digestion occurs in mouth, but lingual lipase is produced from the glands at the back of the
tongue and transported to stomach along with food. It has an optimum pH of 2.5-5. Therefore it continues to
be very active in stomach.

Stomach: Initial digestion of lipids takes place in the stomach, catalysed by the enzyme lingual lipase. The
stomach contains a separate gastric lipase, which can degrade fat containing short chain fatty acids or
triglycerides at neutral pH.

Emulsification in small intestine: Fat enters the intestine to stimulate intestinal glands, releasing the
hormone cholecystokinin. Cholecystokinin causes contraction of gall bladder and result in secretion of bile.
Within bile, emulsification takes place. Emulsification is the process of disposing lipids into smaller droplets
to increase their surface area. Now the enzyme can act easily on the lipid droplets. The process of
emulsification is favoured by (i) bile salts (detergent action) (ii) peristalsis (mechanical mixing) and (iii)
phospholipids (surfactants). Bile salts present in bile lower the surface tension. They emulsify the fat
droplets. Phospholipids increases the surface area of the particles for enhanced activity of enzymes.
Peristalsis movement help in emulsification by mixing the lipid molecules.

Pancreas: The pancreatic enzymes are responsible for the degradation of triglycerides, cholesterol ester and
phospholipids.

i. Degradation of triglycerides or fat by pancreatic lipase- pancreatic lipase is the major enzyme that
digests dietary fat. The final hydrolytic products are free fatty acids and glycerol.

ii. Degradation of cholesteryl ester by cholesteryl esterase- pancreatic cholesteryl esterase cleaves
cholesteryl esters to produce free cholesterol and free fatty acids.

iii. Degradation of phospholipids by phospholipase- phospholipases hydrolyses phospholipids. The

products are free fatty acids and lysophospholipids.

Absorption of lipids

 It occurs in the intestinal mucosal cells.

 The products of digestion, namely monoglycerides, long chain fatty acids, cholesterol, phospholipids
and lysophospholipids are incorporated into molecular aggregates to form mixed micelle (tiny
emulsified fat packets).

 Micelles are spherical particles with a hydrophobic interior and hydrophilic exterior core.

 They are then transported to the intestinal epithelial cells by simple diffusion.

 Inside the epithelial cells, digestive products are taken up by smooth endoplasmic reticulum, re-
synthesised into triglycerides and then packaged as chylomicrons (triglycerides + cholesterol +
phospholipids + protein carriers).

 Chylomicrons enter the lymphatic system and circulate to finally enter the bloodstream.

 The absorption of lipids from the micelle leaves the bile salt in the medium itself. The bile salts are
reabsorbed in the intestine and returned to the liver by the portal vein for re-secretion into the bile.
This process is called entero-hepatic circulation of bile salts.
 METABOLISM OF LIPIDS

BIOSYNTHESIS OF FATS/ TRIGLYCERIDES

 Triglycerides are formed by esterification of fatty acid (acyl CoA) with glycerol.
 It occurs mostly in liver and adipose tissue.
 Most of the enzymes are located in the endoplasmic reticulum of the cell, but mitochondria contain
some enzymes like glycerol-3-phosphate acyl transferase.
 Biosynthesis of triglycerides involves the following step:
1. Activation of fatty acids to Acyl CoA

2. Synthesis of triglycerides

LIPOLYSIS

 Triglycerides are split into glycerol and fatty acids during their metabolism. This process is
called as lipolysis, and occurs in the adipose tissue.
 The hormones including epinephrine, nor-epinephrine, cortisol, thyroid hormones and insulin
induces lipolysis by activating the enzyme lipases.
  The glycerol and fatty acids that result from lipolysis are catabolized via different pathways.
 Glycerol is converted to glyceraldehyde-3-phosphate and utilized for gluconeogenesis.
 Fatty acids are catabolized by β-oxidation.

Β-OXIDATION

 Β- oxidation is the major pathway for fatty acid oxidation. It involves oxidation of β-carbon to form
a β-keto acid.
 It occurs in the mitochondrial matrix.
 Tissues such as liver, heart, kidney, muscle, brain, lungs, adipose tissue and testes oxidize fatty acids
to yield energy.
 It involves 3 stages: i) Activation of fatty acids occurring in the cytosol ii) Transport of fatty acids
into mitochondria and iii) β-oxidation proper in the mitochondrial matrix.
i. Fatty acid activation in cytosol

ii. Transport of Acyl CoA into the mitochondria

 The inner mitochondrial membrane is impermeable to fatty acids a specialized carnitine carrier
system operates to transport activated fatty acids from cytosol to mitochondria.
 Acyl group of Acyl CoA is transferred to carnitine catalyzed by carnitine acyl transferase I.
 The acyl carnitine is transported across to mitochondrial matrix by a specific carrier protein.
 Carnitine acyl transferase II converts acyl carnitine to Acyl CoA.
 The carnitine released returns to cytosol for reuse.
iii. β-Oxidation proper in the mitochondrial matrix
 Each cycle of β oxidation, liberating a 2 carbon unit-Acyl CoA, occurs in a sequence of 4 reactions.
a) Oxidation- Acyl CoA undergoes dehydrogenation by an FAD dependent flavor enzyme Acyl CoA
dehydrogenase to form Trans enoyl CoA. A double bond is formed between α and β carbons.
b) Hydration- enoyl CoA hydratase brings about the hydration of double bond to form β hydroxyacyl CoA
c) Oxidation- β hydroxyacyl CoA dehydrogenase act on β hydroxyacyl CoA and catalyses the second
oxidation and generates NADH. The formed product is β ketoacyl CoA
d) Cleavage- β ketoacyl CoA undergoes thiolytic cleavage to form acetyl CoA and acylCoA. The newly
formed acyl CoA will undergo repeated cycles of β oxidation proper i.e steps a,b,c and d until the fatty
acid is completely converted to acetyl CoA.
Energetics of β-oxidation- Palmitic acid oxidation

Mechanism ATP yield

i. Β-oxidation 7 cycles
7 FADH2 7x2=14
7NADH 7x3=21
ii. From 8 acetyl CoA
Each acetyl CoA upon oxidation by TCA cycle gives 12 ATP 12x8=96

 Total energy from 1 mole of palmitoyl CoA 131

 Energy utilized for fatty acid activation -2
 Net yield 129 ATP

FATTY LIVER

 The normal concentration of lipids in liver is around 5%.

 Lipids especially triglycerides accumulate excessively in liver leading to fatty liver.

 It may occur due to three main reasons:

a. Increased synthesis of triglycerides

Increased mobilisation (from adipose tissues) and decreased utilisation of free fatty acids leads
to overproduction of triglyceride and its accumulation in liver. Diabetes mellitus, starvation, alcoholism and
high fat diet are associated with mobilisation of fatty acids, resulting in increased formation and
accumulation of triglycerides in liver.
 b. Impairment of lipoproteins

The lipoprotein VLDL helps to deliver triglycerides to body cells. The reduced synthesis of
VLDL can therefore alter this function. The synthesis of VLDL takes place in liver and requires
phospholipids and apoproteins. However, impairment in VLDL formation may be due to i) defect in
phospholipid synthesis, or ii) defect in apoprotein formation. VLDL synthesis is also affected in case of
toxic injury to liver. Eg: poisoning by compounds like carbon tetrachloride, arsenic, lead etc.

c. Deficiency of lipotropic factors

Lipotropic factors are the substances which prevent the accumulation of fat in liver. Important
lipotropic factors are choline, methionine, inositol, folic acid, vitamin B12, glycine, serine etc. The
deficiency of lipotropic factors causes accumulation of fat in liver.

OBESITY

 Abnormal increase in body weight due to excessive fat deposition is called obesity.

 Men and women are considered as obese if their weight due to fat exceeds more than 20% and 25%
of body weight respectively.

 Excess caloric intake or overeating coupled with lack of physical exercise contributes to obesity.

 Child born to two obese individuals have about 75% chance of being obese.

 'Ob gene' present in adipocytes of white adipose tissue, produces a protein called leptin. Leptin
secretion is stimulated when there is enough fat deposit, and is therefore, a direct indicator of
obesity.

CHOLESTEROL

 Cholesterol is widely distributed in the body. It is exclusively found in animals, hence often called as
animal sterol.

 It is present in tissues like brain and nervous tissue, liver, skin, intestinal mucosa, corpus leuteum etc.
They are also present in blood and bile and are major constituents of gall bladder stones.

 They occur either as free cholesterol or combined with long chain fatty acids as a cholesterol ester.

 It is synthesised in many tissues from acetyl CoA and ultimately eliminated from the body in the bile
as cholesterol or as bile salts.

 It occurs in food of animal origin such as egg yolk, meat, liver etc.
Chemistry

Cholesterol is a white waxy solid associated with fats but chemically different from them. It has
a parent nucleus which is said to be cyclo-pentano-perhydro-phenanthrin nucleus. It has hydroxyl group at
C3, an unsaturated bond at C5 and C6, a methyl group at C10 and C13 and eight carbon side chains attached
to C17.

Functions of cholesterol

 Structural component of cell membrane.

 It helps in permeability of cells.

 Control the RBC from being haemolysed.

 Transports fat to liver in the form of cholesterol ester for oxidation.

 It assists the formation of bile acids and bile salts.

 Act as precursor of all steroids in the body. Eg: vitamin D, bile acids, sex hormones etc.

 Insulating agent in myelin sheath of nerve fibres.

 Abnormality of cholesterol metabolism may lead to cardiovascular diseases and heart attacks.

 Normal cholesterol in blood= 150-250 mg/dl

Degradation of cholesterol

 Cholesterol is degraded to bile acids and excreted via feces.

 It also serves as precursor for synthesis of steroid hormones and Vitamin D
1. Synthesis of bile acids
 Cholesterol is converted to 7-hydroxy cholesterol by the enzyme 7-α-hydroxylase in liver.
 7-hydroxy cholesterol undergoe series of reactions to form cholic acid and chenodeoxycholic acid.
They are called as primary bile acids.
  The primary bile acids are conjugated with glycine or taurine to form conjugated bile acids-
glycocholic acid, glycochenodeoxy cholic acid, taurocholic acid and taurochenodeoxy cholic acid.
 In the bile, the conjugated bile acids exist as sodium or potassium salts, which are known as bile
salts- Na/K glycocholate, Na/K glycochenodeoxy cholate, Na/K taurocholate and Na/K
taurochenodeoxy cholate.
 In the intestine, primary bile acids undergo deconjugation by intestinal bacterial enzymes to form
deoxycholic acid and lithoxycholic acid. They are known as secondary bile acids.

2. Synthesis of steroid hormones

 Cholesterolact as precursor for the synthesis of 5 classes of steroid hormones. They are:
i. Glucocorticoids- Example, cortisol
ii. Mineralocorticoids- Example, Aldosterone
iii. Progestins- Example, Progesterone
iv. Androgens- Example, Testosterone
v. Estrogens- Example, Estradiol
3. Synthesis of Vitamin D

KETONE BODIES-FORMATION AND UTILIZATION

 The compounds namely acetone, acetoacetate and β-hydroxy butyrate are known as ketone bodies.

 Only the first two are true ketones while b-hydroxy butyrate does not possess a keto group (C=O).

 Ketone bodies are water soluble and energy yielding.

Ketone body formation-Ketogenesis

The synthesis of ketone bodies is called as ketogenesis. It occurs in the liver. The enzymes for
ketogenesis are located in the mitochondrial matrix. The reactions of ketogenesis include:

1. Formation of acetoacetyl CoA

 2 acetyl CoA molecules combine together in presence of enzyme thiolase to form acetoacetyl CoA.

2. Formation of acetoacetate

 Acetoacetyl CoA is converted to HMGCoA by the enzyme HMGCoA synthase .

 HMGCoA is then converted to acetoacetate by the enzyme HMGCoA lyase.

3. Formation of acetone and β-hydroxy butyrate.

 Acetoacetate is converted to β-hydroxy butyrate by the enzyme β-hydroxy butyrate dehydrogenase.

 Acetoacetate is converted to acetone by spontaneous decarboxylation.

Utilization of ketone bodies-Ketolysis

 Ketone bodies are water soluble and are easily transported from liver to various tissues.

 The two ketone bodies, acetoacetate and β-hydroxy butyrate serve as an important source of energy
for extrahepatic tissues such as muscle, kidney, brain, heart, adrenal gland etc.

 The production of ketone bodies and their utilization become more significant when glucose is in
short supply to the tissues- in diabetes mellitus and starvation.

 During prolonged starvation, ketone bodies are the main fuel source for the brain and other parts of
CNS. Ketone bodies are not utilized by the liver, due to the absence of the enzyme thiophorase.
  Ketone bodies play pivotal roles as signaling mediators, drivers of protein post-translational
modification (PTM), and modulators of inflammation and oxidative stress.

 The reatcions of ketolysis include:

1. Formation of acetoacetate

 β-hydroxybutyrate gets converted to acetoacetate by the enzyme β-hydroxybutyrate dehydrogenase.

2. Formation of acetoacetyl CoA

 Acetoacetate gets converted to acetoacetyl CoA by thiophorase.

3. Formation of acetyl CoA

 Acetoacetyl CoA gets converted to 2 molecules of acetyl CoA by the enzyme thiolase.

Fate of acetone- Acetone is difficult to be oxidised invivo. Excess of acetone is breathed out and also
excreted in urine. This gives a fruity smell in breath and urine.

Ketone bodies in starvation

 Starvation is accompanied by increased degradation of fatty acids (from fuel reserve triglycerides) to
meet energy needs of body.

 Breakdown of fat from adipose tissues result in overproduction of acetyl CoA and consequently
ketone bodies.

 Acetyl coA can enter TCA cycle to release energy.

Ketone bodies in diabetes mellitus

 Due to lack of insulin, carbohydrates are not utilized properly.

  Fat in adipose tissue is utilized for energy purposes.

 Breakdown of fat result in overproduction of acetyl CoA and consequently ketone bodies.

 Acetyl CoA cannot be utilized by the liver through TCA cycle due to lack of oxaloacetate (utilized
for gluconeogenesis). So it is converted to ketone bodies.

Diabetic ketoacidosis

 Both acetoactetae and β-hydroxybutyrate are strong acids.

 Increase in their concentration in blood would cause acidosis.

 Diabetic ketoacidosis is dangerous as it may result in coma and even death if not treated.

LIPOPROTEINS

Lipids are complexed with proteins to form lipoproteins. The protein part of lipoprotein is called
apolipoprotein or apoprotein. E.g., apo C, apo E, apo B-48 etc. The density of lipoproteins is inversely
proportional to their lipid content. Depending on density, lipoproteins aree classified into 5 major groups:

1. Chylomicrons

 They are synthesised in the smooth endoplasmic reticulum in epithelial cells present in small
intestine.

 They contain 1-2% proteins, 85% triglycerides, 7% phospholipids and 6-7% cholesterol.

 Their apoproteins consist of apo B-48, apo I and apoC-II.

 Chylomicrons are metabolised in adipose tissue and skeletal muscle. Their half life in blood is 1 hr.

 ApoC-II activates lipoprotein lipase, which break triglycerides into fatty acids and glycerol. This
makes the chylomicrons to shrink in size.

 Chylomicrons are thus stored in the adipose tissue and utilised by heart and skeletal muscle for ther
energy needs.

2. Very low density lipoproteins

 They are also called as pre-β lipoproteins.

 They are synthesized in liver form excess dietary carbohydrate and proteins, along with
chylomicrons remnants, and finally secreted into the bloodstream.

 They are rich triglycerides.

  Their function is to deliver triglycerides to body cells (from liver to peripheral tissues)

 Cholesterol, cholestryl esters and triglycerides are exported into the blood stream in the form of
VLDL.

 VLDL contains apoproteins apoB-100 (major apoprotein), apoC-II and apo E.

 Apo C-II activates lipoprotein lipase, which break triglycerides into fatty acids and glycerol.

 They are similar to chylomicrons, but made by different tissues.

3. Intermediate density lipoproteins

 They are also known as broad beta lipoproteins.

 They are smaller than VLDL and is formed from VLDL by its degradation.

 They help in triglyceride transport and are precursors of LDL.

 They contain the same apoproteins as that of VLDL (apoB-100, apoC-II and apo E).

4. Low density lipoproteins

 They are also called β-lipoproteins.

 Normal value=130 mg/dl

 They are synthesised in the liver and secreted into the blood.

 The loss of triglycerides converts VLDL to LDL.

 LDL is the major carrier of cholesterol in blood.

 The major apoprotein present is apoB-100.

 LDL transport cholesterol to peripheral tissues and regulate the cholesterol synthesis.

 LDL infiltrates through arterial walls and are taken up by macrophages or scavenger cells.

 This results in oxidation of LDL and release of toxins into the arterial wall.

 LDL, WBCs and toxins forms lipid foam. The foam expands on the arterial wall slowly growing into
a plaque deposit.

 Minerals like calcium gets attached to this plaque deposit to form plaque-calcium deposits. The
condition is called arthrosclerosis.
  Rupturing of these deposits block arteries finally affecting coronary artery, leading to myocardial
infarction.

 Since LDL is over deposited in tissues leading to sever arthrosclerosis and myocardial infarction, it is
called as bad cholesterol or lethally dangerous lipoprotein.

5. High density lipoproteins

 They are also called alpha lipoproteins. They are the smallest of all lipoproteins.

 Normal value= >60mg/dl

 The liver and intestinal cells synthesise the components of HDL and release them into bloodstream.

 HDL contains apoenzymes apoA-I, apoC-I, apoC-II and apo E.

 The free cholesterol derived from the peripheral tissues are taken up by HDL.

 Their major function is to pick up cholesterol from body cells and take it back to the liver. The
process is called reverse cholesterol transport.

 Due to this 'anti-arthrogenic' or protective property, they reduce the risk of arterial blockages
(arthrosclerosis) and heart attacks. Therefore they are considered as good cholesterol or highly
desirable lipoproteins.

LIPID PROFILE

 Lipid profile tests are done to detect the lipid levels in blood and to assess the risk of any
cardiovascular diseases.

 Samples should be taken after 12-14 hours fasting.

 Lipid profile is assessed by estimating the following fractions in plasma:

LDL cholesterol is calculated by the formula: LDL cholesterol= total cholesterol – HDL + VLDL

VLDL= TG / 5
ATHEROSCLEROSIS

 A complex disease characterised by thickening or hardening of arteries due to accumulation of lipids.

It narrows and ultimately blocks the arteries leading to stoppage of blood flow, resulting in death of
affected tissues.

 Coronary arteries which supply blood to the heart are mostly affected, leading to myocardial
infarction or heart attack.

 The disease starts when inner lining of the artery (endothelium) is damaged. The endothelium
becomes compromised, allowing large unstable LDL cholesterol molecules and other cellular waste
products to penetrate and accumulate the damaged area.

 Chemical reactions occurring within these accumulated products cause cholesterol molecules to
oxidize and form toxins. This initiates an inflammatory response and causes WBCs to gather at the
site of injury.

 Gradually these substances (including LDL, toxins and WBCs) form a lipid foam. The foam expands
on the arterial wall, slowly growing to form an arterial plaque deposit.

 As the plaque increases in size, the arterial wall thickens and hardens. At the same time, smooth
muscle cells within the arterial wall begin to multiply. Most of them move to the surface of the
plaque, and form a firm fibrous cap covering the plaque. They also attract minerals like calcium, to
form a hard shell over the plaque deposit.

 The plaque-calcium deposit can grow undetected for many years. Some deposits can even occlude
the artery with no effect. But, if the deposit ruptures, the fibrous cap breaks open and the plaque
inside comes into contact with your blood. This can trigger a blood clot to form. This blood clot
(known as a “thrombus”) blocks your blood flow and leads to a heart attack or stroke.

 Lack of oxygen rich blood supply would cause coronary artery disease (CAD), angina (chest pain),
fluctuation in pressure and discomfort, and an increased risk of heart attack.

 Arthrosclerosis can be caused due to obesity, high consumption of saturated fat, lack of exercise,
stress condition, hypertension, positive family history, diabetes mellitus, cigarette smoking etc.
Solving the above causes can reduce the incidence of atherosclerosis.