Atherosclerosis- Hema Negi

8/6/2019 Atherosclerosis- Hema Negi

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ATHEROSCLEROSIS

INTRODUCTION:-

Atherosclerosis is a condition in which fatty material collects along the walls of arteries. Thisfatty material thickens, hardens (forms calcium deposits), and may eventually block the arteries.

Atherosclerosis is characterized but the formation of plaque thats builds up inside the arteries.

Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over

time, plaque hardens and narrows the arteries, limiting the flow of oxygen-rich blood to the

different parts of the body. This can lead to serious problems, including heart attack, stroke, or

even death.

ATHEROSCLEROSIS RELATED DISEASE :-

Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms,

legs, and pelvis. As a result, different diseases may develop based on which arteries are affected.

1) Coronary Heart Disease :-

CHD occurs if plaque builds up in the coronary arteries. These arteries supply oxygen-

rich blood to the heart.

Plaque narrows the coronary arteries and reduces blood flow to the heart muscle. It also

makes it more likely that blood clots will form in the arteries. Blood clots can partially or

completely block blood flow.

When blood flow to the heart muscle is reduced or blocked, it can lead to angina S(chest

pain) and a heart attack. CHD also is called coronary artery disease or heart disease. It's

the leading cause of death for both men and women in the United States.

2) Carotid Artery Disease

It occurs if plaque builds up in the arteries on each side of the neck. These arteries supply

oxygen-rich blood to the brain. When blood flow to brain is reduced or blocked, it canlead to a stroke.

3) Peripheral Arterial Disease

It occurs if plaque builds up in the major arteries that supply oxygen-rich blood to legs,

arms, and pelvis.
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When blood flow to these parts of the body is reduced or blocked, it can lead to

numbness, pain, and, sometimes, dangerous infections.

DESIRABLE LEVEL OF CHOLESTEROL :-

200mg/dl is the desirable level.

200mg/dl 239mg/dl is the manageable level.

High- above 240mg/dl.

RISK FACTORS FOR ATHEROSCLEROSIS INVOLVED :-

a) Diabetes

b) Heavy alcohol use

c) High blood pressure
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d) High blood cholesterol levels

e) High-fat diet

f) Increasing age

g) Obesity

h) Personal or family history ofheart disease

i) Smoking

MECHANISM OF ATHEROGENESIS:-

The "response-to-injury" theory is most widely accepted. Endothelial injury causes vascular

inflammation and a fibroproliferative response ensues. Probable causes of endothelial injury

include oxidized low-density lipoprotein (LDL) cholesterol; infectious agents; toxins, including

the by-products of cigarette smoking; hyperglycemia; and hyperhomocystinemia. Circulating

monocytes enters the intima of the vessel wall, and these tissue macrophages act as scavenger

cells, taking up LDL cholesterol and forming the characteristic foam cell of early

atherosclerosis. These activated macrophages produce numerous factors that are injurious to the

endothelium.

Elevated serum levels of LDL cholesterol overwhelm the antioxidant properties of the healthy

endothelium and result in abnormal endothelial metabolism of the lipid moiety. Oxidized LDL is

capable of a wide range of toxic effects and cell/vessel wall dysfunctions (dilation) that are

characteristically and consistently associated with the development of atherosclerosis. These

dysfunctions are the result of direct inactivation of nitric oxide by the excess production of free

radicals, reduced transcription of nitric oxide synthase messenger RNA (mRNA), and

posttranscriptional destabilization of mRNA.

The decrease in the availability of nitric oxide also is associated with increased platelet

adhesion, increased plasminogen activator inhibitor, decreased plasminogen activator, decreased

thrombomodulin, and alterations in heparin sulfate proteoglycans.

The consequences include a procoagulant and enhanced platelet thrombus formation. The

oxidized LDL activates inflammatory processes at the level of gene transcription by up-

regulation of nuclear factor kappa-B, expression of adhesion molecules, and recruitment of

monocytes/macrophages.
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Atherosclerotic plaques characteristically occur in regions of branching and marked curvature at

areas of geometric irregularity and where blood undergoes sudden changes in velocity and

direction of flow. Decreased shear stress and turbulence may promote atherogenesis at these

important sites within the coronary arteries, the major branches of the thoracic and abdominal

aorta, and the large conduit vessels of the lower extremities.

The earliest pathologic lesion of atherosclerosis is the fatty streak. The fatty streak is observed in

the aorta and coronary arteries of most individuals by age 20 years. The fatty streak is the result

of focal accumulation of serum lipoproteins within the intima of the vessel wall. The fatty streak

may progress to form a fibrous plaque, the result of progressive lipid accumulation and the

migration and proliferation of smooth muscle cells.

Atherosclerosis is more common among men than women. The higher prevalence ofatherosclerosis in men is thought to be due to the protective effects of the female sex hormones.

This sex effect is absent after menopause in women.

FACTS:-

a) Triglycerides comprise 90% of the fats and oils in the diet. They are also produced

endogenously in the liver and transported in the blood with very low density lipoprotein

particles.

b) Obesity results in elevated insulin levels, which increase production of very low density

lipoprotein particles which contain 80% triglycerides and 20% cholesterol. The obesity-

induced overproduction of VLDL from the liver results in increased levels of VLDL

remains and LDL particles which are atherogenic.

c) Saturated fat and cholesterol reduce hepatic uptake of LDL particles further increasing

the levels of circulating LDL cholesterol.

d) Among the saturated fats, coconut oil is the most atherogenic. Vegetable oils such as

corn oil, safflower oil, and soybean oil contain large amounts of linoleic acid. While

polyunsaturated fats lower cholesterol by comparison to saturated fats when calories are

held constant.


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e) The cellular basis of atherosclerosis involves the action of monocytes expressing a CD-

36 receptor which binds oxidized cholesterol. Linoleic acid increases oxidation of

cholesterol and provides a stimulus to increased synthesis of the CD-36 receptors.

Endogenous antioxidants such as vitamin E are often removed during processing of

vegetable fats and oils so that the polyunsaturated fats in the diet can contribute to

oxidation processes including oxidation of cholesterol.

f) Phytosterols are plant protein constituents which compete with cholesterol for intestinal

uptake and thus lower the amount of cholesterol in the circulating pool.

g) Long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs) lowers the risk of

coronary heart disease (CHD) and protects against sudden cardiac death.

OMEGA- 3 FATTY ACID AND HUMAN NUTRITION :-

Omega-3 fatty acids are being increasingly promoted as important dietary components for

health and disease prevention. These fatty acids are naturally enriched in fatty fish like

salmon and tuna and in fish-oil supplements. Foods high in omega-3 fatty acids include

salmon, halibut, sardines, albacore, trout, herring, walnut, flaxseed oil, and canola oil. Other

foods that contain omega-3 fatty acids include shrimp, clams, light chunk tuna, catfish, cod,

and spinach. An increasing number of foods that are not traditional sources of omega-3 fatty

acids, such as dairy and bakery products are now being fortified with small amounts of these

fatty acids. This recent promotion of omega-3 fatty acids has likely been driven by

recommendations for omega-3 fatty acid consumption made by scientific groups such as the

American Heart Association. The search for the molecular and cellular mechanisms by

which omega-3 fatty acids affect health and disease has led to a large body of evidence

which suggests that these dietary lipids modulate numerous processes, including brain and

visual development, inflammatory reactions, thrombosis and carcinogenesis. An obvious

question that someone unfamiliar with omega-3 fatty acids might ask is: How can these

nutrients affect so many seemingly unrelated processes in different cell types and tissues?

The goal of this review is not to comment on the extent to which dietary omega-3 fatty acids


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affect health and disease, but rather it is to give an overview of the nature of these dietary

components and to present the multiple benefits of these.

PUFAs are important fatty acids in human nutrition and can be divided into two

subcategories: omega-3 (n-3) and omega-6 (n-6), depending on the location of their first

double bond: the n-3 PUFAs having their first double bond located at the third carbon

molecule, and the n-6 PUFAs at the sixth.

Linoleic acid (LA, 18:2n-6) is the predominant n-6 PUFA in humans, and they can be

elongated and desaturated to arachidonic acid, whereas alpha-linolenic acid (-LNA; 18:3n-

3) is elongated and desaturated into longer chain PUFA EPA.

Omega-3 and omega-6 PUFAs are not inter-convertible in the human bodythey are

essential fatty acids that are important components of practically all cell membranes.

The ratio between LA and -LNA, rather than the absolute amounts of -LNA in the diet,

may be critical for disease prevention, due to the competition between the two essential

PUFAs for their entry into the elongation and desaturation pathways, leading to the synthesis

of their respective eicosanoids.

The current recommendation of optimal dietary intake of -LNA should be about 2 g/day or

0.61% of total energy intake. Canola oil, nuts, mustard oil, leeks and green leafy vegetablesare the main sources of -LNA. Since, -LNA is highly sensitive to oxidation (due to its

three double bonds), a high intake of -LNA should be balanced with a high intake of

antioxidants (for example, in vegetables and fruits), to protect it from oxidation. On the other

hand, fish or fish oil supplements rich in EPA and DHA are the main source of long chain n-

3 PUFAs. The long-chain n-3 PUFAs are major structural components of membrane

phospholipids of tissues throughout the body and in addition, they influence membrane

fluidity and ion transports.

n-3 PUFAs increase high-density lipoprotein-cholesterol (HDL-C) and have a potent

triglyceride-lowering effect. The n-3 PUFAs may prevent CHD death by their effects on

haemostasis (by inhibiting platelet aggregations) and serum lipids (by lowering triglycerides

and/or increase HDL-C). However, the major effect of n-3 PUFA may be anti-arrhythmic

rather than anti-atherothrombotic.


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Diseases that may be prevented or ameliorated with omega-3 fatty acids, in

descending order of the strength of the available evidence :-

s.no Name of the Disease

1 Coronary heart disease and stroke2 Essential fatty-acid deficiency in infancy (retinal and brain development)

3 Autoimmune disorders (e.g. lupus, nephropathy)

4 Crohns disease

5 Cancers of the breast, colon, and prostate

6 Mild hypertension

7 Rheumatoid arthritis


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Fig : Desaturation and elongation pathway of the omega-3 and -6 PUFAs. PUFAs, poly

-unsaturated fatty acid, EPA,eicosapentaenoic acid; DHA, docosahexaenoic acid. The two

metabolic pathways, although largely using the same enzymes, are entirely inconvertible in

both animals and humans. Stable isotope studies have shown that humans can desaturate and

elongate -linolenicacid to EPA and DHA in plasma and blood cells. However,

conversion ofdietary -linolenic acid to EPA is limited, and to DHA is probably marginal at

best, even in well-nourished individuals.

EFFECTS OF SATURATED LIPIDS ON PLASMA MEMBRANE AND

LIPOPROTIEN:-

In humans, saturated fat intake increases LDL cholesterol in comparison with all nutrients

except trans fats (2010,Siri-Tarino PW, Sun Q, Hu FB, Krauss RM). Because saturated fat also

increases high-density lipoprotein (HDL) cholesterol, the total cholesterol (TC) to HDL

cholesterol ratio (a risk marker for CVD) is not altered. LDL particles are heterogeneous in size,

density, and composition. Smaller and denser LDL particles in particular have been strongly

associated with atherosclerotic CVD (2010, Krauss RM).

Changes in dietary saturated fat have been associated with changes in concentrations of larger,

more buoyant particles (1998, Dreon DM, Fernstrom HA, Campos H, Blanche P, Williams

PT,Krauss RM). In the context of a lower-carbohydrate diet (26% of total energy), highsaturated fat content (15% of energy) provided from dairy products was associated with

increased concentrations of large and medium LDL particles, but not small LDL particles,

compared with a diet lower in saturated fat (8% of energy) (2006, Krauss RM, Blanche

PJ, Rawlings RS, Fernstrom HS,Williams P).
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dreon%20DM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Fernstrom%20HA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Campos%20H%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rawlings%20RS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Fernstrom%20HS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dreon%20DM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Fernstrom%20HA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Campos%20H%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Blanche%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rawlings%20RS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Fernstrom%20HS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Williams%20PT%22[Author]


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Studies in animals have shown that saturated fats increase LDL cholesterol by inhibiting LDL

receptor activity and enhancing apolipoprotein (apo)B-containing lipoprotein production (1998,

Dietschy JM). This LDL cholesterolraising effect of saturated fatty acids has been shown to

depend on the level of dietary cholesterol, such that the greatest increases in plasma LDL

concentrations were observed at the highest levels of dietary cholesterol (1998, Dietschy JM). In

the absence of dietary cholesterol, and when polyunsaturated fatty acid intake is adequate (5%

10% of energy), saturated fat has been observed to have a negligible effect on LDL clearance in

nonhuman primates, and the lipoprotein profile remains relatively normal (LDL < 90 mg/dL)

(1997, Hayes KC, Khosla P, Hajri T, Pronczuk A). When individuals or animals are fed

excessive calories and dietary cholesterol, specific saturated fatty acids (particularly palmitic

acid) can contribute to decreased LDL receptor activity. Nonetheless, LDL receptor

downregulation by dietary cholesterol greatly exceeds that by saturated fatty acids (1997, HayesKC, Khosla P, Hajri T, Pronczuk A).

Feeding of dietary monounsaturated fat to nonhuman primates reduced LDL without lowering

HDL, and in comparison to saturated and polyunsaturated fat, provided the lowest LDL to HDL

ratio (2009, Degirolamo C, Shelness GS,Rudel LL.). On the other hand, replacement of some of

the saturated fat with monounsaturated fat was associated with an even greater enrichment of

LDL particles with cholesteryl oleate, a change in LDL particle composition that has been

shown to confer atherogenicity (2009, Degirolamo C, Shelness GS, Rudel LL.).
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dietschy%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dietschy%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosla%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hajri%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pronczuk%20A%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosla%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hajri%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pronczuk%20A%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dietschy%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dietschy%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosla%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hajri%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pronczuk%20A%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosla%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hajri%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pronczuk%20A%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]


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Different saturated fatty acids have varying effects on LDL cholesterol, HDL cholesterol, and

the TC:HDL cholesterol ratio when they replace carbohydrate. The longer chain stearic acid

(18:0) has been shown to have no effect on LDL or HDL cholesterol or the TC:HDL cholesterol

ratio, and saturated fatty acids of shorter length have been shown to have a greater LDL

cholesterolraising effect, such that lauric acid (12:0) raised LDL cholesterol the most, followed

by myristic (14:0) and palmitic (16:0) acids.

Lauric acid also increased HDL cholesterol most significantly, and it did this disproportionately

to TC, so that its replacement of carbohydrate actually led to a significant decrease in the

TC:HDL cholesterol ratio (2003, Mensink RP, Zock PL, Kester AD, Katan MB.).

It has been demonstrated that the expected increases in LDL cholesterol with high saturated fat

intake can be attenuated by reductions in levels of small, dense LDL particles resulting from

reduced dietary carbohydrate content and/or weight loss.
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]


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There exists considerable inter-individual variation in the response to dietary saturated fat. The

ability of saturated fats to raise LDL cholesterol is enhanced by increased intake of dietary

cholesterol as well as baseline LDL cholesterol concentration. Intrinsic differences in the

regulation of lipid metabolism may partly explain the heterogeneity of responses to dietary

saturated fat. In fact, an association of the apoE4 allele with a greater LDL response to saturated

fat has been reported in a number of studies, although this effect is confounded by the

relationship of apoE4 to baseline LDL levels. Studies have also shown that other factors,

including obesity, insulin resistance, hypertriglyceridemia, and female gender, may lead to

weaker LDL cholesterolraising effects of dietary saturated fat (2010, Siri-Tarino PW, Sun

Q, Hu FB,Krauss RM).

Finally, the effects of saturated fat can be modulated by the foods in which they are contained.

Cheeses may have smaller effects on LDL cholesterol concentrations than butter, and fermented

dairy foods, such as yogurt, have been associated with LDL reductions (2009, German

JB, Gibson RA,Krauss RM, Nestel P, Lamarche B,van Staveren WA, Steijns JM, de Groot

LC, Lock AL, Destaillats F). Recently, adipose tissue conjugated linoleic acid (CLA) was found

to be inversely associated with risk of myocardial infarction in a case-control study and

appeared to offset the strong risk observed with saturated fat. CLA can be found in meaningful

concentrations in the milk of pasture-fed cows (2010, Smit LA, Baylin A, Campos H). However,

the potential cardiovascular benefits of CLA need confirmation from prospective cohort studies

and intervention trials.

LIPID EFFECTS OF REDUCING SATURATED FATS:-

Replacement of Saturated Fat with Polyunsaturated Fat:-

Replacement of saturated fat with polyunsaturated fat has been shown to decrease TC and LDL

cholesterol by lowering LDL cholesterol production rates and/or increasing LDL clearance rates

(Siri-Tarino PW, Sun Q, Hu FB, Krauss RM). Although replacement of saturated fat with

polyunsaturated fat has been shown to decrease HDL cholesterol, it decreases LDL cholesterol

even more substantially; thus, the HDL:LDL ratio is increased (1992, Mensink RP, Katan MB.)
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22German%20JB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22German%20JB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gibson%20RA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Nestel%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lamarche%20B%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22van%20Staveren%20WA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Steijns%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22de%20Groot%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22de%20Groot%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lock%20AL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Destaillats%20F%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22German%20JB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22German%20JB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gibson%20RA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Nestel%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lamarche%20B%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22van%20Staveren%20WA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Steijns%20JM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22de%20Groot%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22de%20Groot%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lock%20AL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Destaillats%20F%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Siri-Tarino%20PW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sun%20Q%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Krauss%20RM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]


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and the TC:HDL cholesterol ratio is decreased (2003, Mensink RP, Zock PL, Kester AD, Katan

MB).

Some studies have suggested that saturated fat may increase LDL cholesterol only if the

polyunsaturated fat intake falls below a threshold level; specifically, the availability of linoleicacid may determine the cholesterolemic effects of other fatty acids (2004, Wijendran V, Hayes

KC). The ratio of polyunsaturated fat to saturated fat was recently shown to be inversely

associated with LDL cholesterol and TC but not with hemoglobin A1c, blood pressure, serum

triglycerides, and HDL cholesterol in 1004 Japanese men and women (2010, Guo Z, Miura K,

Turin TC, et al). Overall, through its effects on plasma lipoproteins (ie, lowering of LDL

cholesterol, minimal effect on HDL cholesterol, and lowering of the TC:HDL cholesterol ratio),

the replacement of saturated fat with polyunsaturated fat has been projected to modestly lower

coronary heart disease risk (by about 10% for each 5% energy substitution). However, these

benefits are likely to be underestimated because polyunsaturated fats can have other benefits

beyond cholesterol, including improving insulin sensitivity and reducing inflammation (2002,

Hu FB, Willett WC).

Replacement of Saturated Fat with Monounsaturated Fat:-

Replacement of saturated fat with monounsaturated fat has also been associated with decreased

total, LDL, and HDL cholesterol, although the magnitude of reduction for each of these lipids isslightly less than when polyunsaturated fats are the replacement nutrient (1992, Mensink

RP, Katan MB).

Replacement of Saturated Fat with Carbohydrate:-

Replacement of saturated fat with carbohydrate results in lower total, LDL, and HDL cholesterol

but also increases triglycerides. The magnitude of reduction of HDL cholesterol is comparableto the reduction in TC, so that the TC:HDL cholesterol ratio is, on average, not changed (2003,

Mensink RP, Zock PL, Kester AD, Katan MB.).

HIGH CARBOHYDRATES INTAKE CONTRIBUTES TO DYSLIPIDEMIA:-
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Wijendran%20V%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Willett%20WC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Wijendran%20V%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hayes%20KC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Willett%20WC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mensink%20RP%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zock%20PL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kester%20AD%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Katan%20MB%22[Author]


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Elevated triglycerides, reduced HDL cholesterol concentrations, and increased concentrations of

small, dense LDL particles characterize the dyslipidemia that is part of a metabolic profile

considered to be a major contributor to increased CVD risk. Both insulin resistance and high

carbohydrate intakes have been shown to contribute to this dyslipidemia, and refined

carbohydrates, in particular, can raise triglyceride and lower HDL cholesterol concentrations

(2009, Schaefer EJ, Gleason JA, Dansinger ML). Of interest, reductions in dietary carbohydrate,

even in the context of a diet high in saturated fat, have been associated with reduced

concentrations of small, dense LDL.

The type of carbohydrate consumed can affect blood lipid profiles. Using the glycemic index

(GI) as a classification system that rates dietary carbohydrates by their ability to increase

postprandial blood glucose levels, the consumption of lower-GI foods has been associated with

lower triglycerides and higher HDL cholesterol (2008, Barclay AW, Petocz P,McMillan-Price

J, Flood VM, Prvan T, Mitchell P,Brand-Miller JC). Substituting low-GI foods for high-GI

foods may lower triglyceride concentrations by 15% to 25% (2001, Pelkman CL). There is also

considerable evidence that high intake of added sugars and fructose in particular (2010,

Stanhope KL, Havel PJ), adversely affects all components of atherogenic dyslipidemia.

EFFECTS OF SATURATED FATS ON CORONARY HEART DISEASES :-

ANIMAL STUDIES :-

Assessment of the effects of dietary saturated fat on atherosclerosis has been studied in various

animal models. Interestingly, in nonhuman cholesterol-fed primates, despite the favorable lipid

profiles conferred by monounsaturated fat feeding compared with saturated fat feeding, both

diets led to equivalent amounts of atherosclerosis, whereas similar intake of omega-6

polyunsaturated fat afforded atherosclerosis protection (2009, Degirolamo C, Shelness

GS, Rudel LL.). Similarly, more atherosclerosis was observed in LDL knockout mice fed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Schaefer%20EJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gleason%20JA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dansinger%20ML%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Barclay%20AW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Petocz%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22McMillan-Price%20J%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22McMillan-Price%20J%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Flood%20VM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Prvan%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mitchell%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Brand-Miller%20JC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pelkman%20CL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Stanhope%20KL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Havel%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Schaefer%20EJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gleason%20JA%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Dansinger%20ML%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Barclay%20AW%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Petocz%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22McMillan-Price%20J%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22McMillan-Price%20J%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Flood%20VM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Prvan%20T%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mitchell%20P%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Brand-Miller%20JC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pelkman%20CL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Stanhope%20KL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Havel%20PJ%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Degirolamo%20C%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shelness%20GS%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rudel%20LL%22[Author]


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monounsaturated fats compared with mice fed either polyunsaturated or saturated fat (2001,

Merkel M, Velez-Carrasco W, Hudgins LC, Breslow JL).

CLINICAL TRIALS :-

Clinical trials designed to evaluate dietary effects on CVD risk have reduced saturated fat by

increasing the consumption of a replacement nutrient. A recent meta-analysis of eight clinical

studies that replaced saturated fat with polyunsaturated fat (n = 13,614 participants with 1042

CHD events) estimated a coronary heart disease (CHD) risk reduction of about 10% for each 5%

energy replacement of saturated fat with polyunsaturated fat, an effect comparable to that

predicted from the effects of the intervention on TC:HDL cholesterol ratio (2010, Mozaffarian

D, Micha R, Wallace S).

In contrast, replacement of saturated fat with carbohydrate was not associated with

improvements in CHD risk in the Womens Health Initiative, a dietary intervention originally

designed to test the effects of a low-fat intervention on cancer and cardiovascular risk. The 8-

year study effectively lowered total fat as well as saturated fat intake, although not to the degree

that the investigators had intended. The type of carbohydrate consumed has been associated with

differences in CVD risk. A higher glycemic load, which ranks carbohydrates based on their GI

and portion size, was associated with increased risk of CHD in the Nurses Health Study (22006,

Halton TL, Willett WC,Liu S, Manson JE,Albert CM, Rexrode K, Hu FB).

More recently, a prospective cohort study in 53,644 women showed an increased risk of

myocardial infarction when high-GI foods replaced saturated fats (2010, akobsen MU,

Dethlefsen C, Joensen AM, et al.). Only when saturated fats were replaced with low-GI foods

was there an association with a lower risk of myocardial infarction.

TREATMENT

The goal of treatment is to reduce the risk ofatherosclerotic heart disease. Those who inherit

only one copy of the defective gene may respond well to diet changes combined with statin

drugs.

LIFESTYLE CHANGES
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Merkel%20M%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Velez-Carrasco%20W%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hudgins%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Breslow%20JL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mozaffarian%20D%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mozaffarian%20D%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Micha%20R%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Wallace%20S%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Halton%20TL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Willett%20WC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Liu%20S%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Manson%20JE%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Albert%20CM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rexrode%20K%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://health.nytimes.com/health/guides/disease/atherosclerosis/overview.htmlhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Merkel%20M%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Velez-Carrasco%20W%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hudgins%20LC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Breslow%20JL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mozaffarian%20D%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mozaffarian%20D%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Micha%20R%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Wallace%20S%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Halton%20TL%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Willett%20WC%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Liu%20S%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Manson%20JE%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Albert%20CM%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rexrode%20K%22[Author]http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hu%20FB%22[Author]http://health.nytimes.com/health/guides/disease/atherosclerosis/overview.html


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Diet changes include reducing total fat intake to less than 30% of the total calories you eat.

Reduce saturated fat intake by:

Decreasing amounts of beef, chicken, pork, and lamb

Substituting low-fat dairy products for full-fat ones Eliminating coconut and palm oils

Dietary counseling is often recommended to help people make these adjustments to their eating

habits. Weight loss and regular exercise may also aid in lowering cholesterol levels.

MEDICATIONS

There are several types of drugs available to help lower blood cholesterol levels, and they work

in different ways. Some are better at lowering LDL cholesterol, some are good at loweringtriglycerides, while others help raise HDL cholesterol.

The most commonly used and effective drugs for treating high LDL cholesterol are called

statins. The include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor),

fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor).

Other cholesterol-lowering medicines include:

Bile acid-sequestering resins

Ezetimibe

Fibrates (such as gemfibrozil)

Nicotinic acid

Those with more severe forms of this disorder may need a treatment called extracorporealapheresis. This is the most effective treatment. Blood or plasma is removed from the body.

Special filters then remove the extra LDL-cholesterol, and the blood plasma is then returned.

CONCLUSION:-
http://health.nytimes.com/health/guides/nutrition/niacin/overview.htmlhttp://health.nytimes.com/health/guides/nutrition/niacin/overview.html


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Evaluation of the association of saturated fat with lipid profiles and CVD risk requires

consideration of the replacement nutrients. Studies in animals and humans support the concept

that replacement of saturated fats with polyunsaturated fats results in improved lipid profiles,

specifically, decreased TC and LDL cholesterol with minimal decreases in HDL cholesterol, as

well as with decreased CVD risk. Although replacement of saturated fats with monounsaturated

fats results in improved lipid profiles, the association of this substitution with CVD risk is less

clear. Finally, replacement of saturated fat with carbohydrates, particularly refined

carbohydrates and added sugars has been associated with dyslipidemia and either no

improvement in CVD risk or even increased CVD risk. Given the current epidemics of obesity

and insulin resistance, reductions in the consumption of refined carbohydrates and added sugars,

in addition to weight control and obesity prevention, should be the prioritized public health

dietary goals.


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ATHEROSCLEROSIS

SATURATED FATTY ACID AND RISK OF CORONARY HEART

DISEASE

SUBMITTED BY: SUBMITTED TO:

HEMA NEGI Dr. PANDA KUSUMA KUMARI

MSB/10/214

M.Sc. BIOTECHNOLOGY

SEMESTER II

AMITY INSTITUTE OF BIOTECHNOLOGY

CONTENT S

TOPIC PAGE NO.

Introduction 1

Atherosclerosis Related Disease 1

Level of Cholesterol 2

Risk Factor For Atherosclerosis 3

Mechanism Of Atherogenesis 3

Facts 4

Omega-3 Fatty Acid And Human 5


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Nutrition

Disease Prevented by Omega-3 Fatty

Acid

6

Effect of Saturated Fatty Acid On Plasma

Membrane And Lpoproteins

8

Lipid Effect Of Reducing Saturated Fats 11

High Carbohydrates Intake Contributes

to Dyslipidemia

12

Effect of Saturated Fatty Acid On CHD 13

Treatments 14

Conclusion 16

References 17

REFERENCES

David L. Nelson, Michael M. Cox: Lehninger Principles Of Biochemistry, fourthEdition. Page no.827-829. W.H.Freeman and Company,New York. 2008.

J.L.Jain, Sunjay Jain, Nitin Jain: Fundamentals of Biochemistry. Page no.621-629.S.Chand and Company Ltd,2007.

Jeremy.M.Berg, John L.Tymoczko,Lubert Stryer: Biochemistry fifth Edition. Pageno.1069-1075. W.H.Freeman and Company, New York, 2007.


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Geoffrey M. Cooper, Robert E. Hausman; The Cell-A Molecular Apporach, fourthEdition:The LDL Receptor. Page no. 559-560. ASM Press, Washington, D.C.2009

N-3 Polyunsaturated Fatty Acids in Coronary Heart Disease: A Meta-analysis ofRandomized Controlled Trials-Heiner C. Bucher, MD, MPH, Peter Hengstler,MD,Christian Schindler, PhD,Gabriela Meier, MD.

http://ceb-institute.org/fileadmin/upload/refman/Am_J_Med_2002_112_298_304_Bucher.pdf

http://www.ncbi.nlm.nih.gov/pubmed/11893369 http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-

49KSCVB-GS&_user=10&_coverDate=06%2F11%2F1994&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0df8f5ad84703082b6868e27e27e5f3c&searchtype=a

TheAmericanJournalofCardiologyVolume 94, Issue 10, 15 November 2004, Pages 1260-1267

Encyclopedia of Human Nutrition, 2005, Pages 487-494K. Srinath Reddy

Lee KW, Lip GY. The role of omega-3 fatty acids in the secondary prevention ofcardiovascular Diseases QJM2003:96:465-80.

West J Nurs Res, February 2010; vol. 32, 1: pp. 64-80., first published on November14, 2009. Djousse L, Folsom AR, Province MA, Hunt SC, Ellison RC; National Heart,Lung,and Blood Institute. Family Heart Study. Dietary linolenic acid and carotidatherosclerosis: the National Heart, Lung, and Blood Institute Family Heart Study.Am JClin Nutr2003;77(4):819-25.39. Ascherio A, Rimm EB, Giovannucci EL, SpiegelmanD, Stampfer M, Willett WC.

European Journal of Clinical Nutrition (2010) 64, 410418; doi:10.1038/ejcn.2009.151;

published online 17 February 2010.

www.pubmed.gov

www.springerlink.com www.sciencedaily.com http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/ http://www.healthscout.com/ency/68/38/main.html http://www.sciencedirect.com/science/journal/00219150

CERTIFICATE
http://www.sciencedirect.com/science?_ob=PublicationURL&_tockey=#TOC%234876%232004%23999059989%23556072%23FLA%23&_cdi=4876&_pubType=J&view=c&_auth=y&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=144d77f3dae836afaa840313cb9941d3http://www.sciencedirect.com/science?_ob=PublicationURL&_tockey=#TOC%234876%232004%23999059989%23556072%23FLA%23&_cdi=4876&_pubType=J&view=c&_auth=y&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=144d77f3dae836afaa840313cb9941d3http://www.pubmed.gov/http://www.springerlink.com/http://www.sciencedaily.com/http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/http://www.healthscout.com/ency/68/38/main.htmlhttp://www.healthscout.com/ency/68/38/main.htmlhttp://www.sciencedirect.com/science/journal/00219150http://www.sciencedirect.com/science?_ob=PublicationURL&_tockey=#TOC%234876%232004%23999059989%23556072%23FLA%23&_cdi=4876&_pubType=J&view=c&_auth=y&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=144d77f3dae836afaa840313cb9941d3http://www.pubmed.gov/http://www.springerlink.com/http://www.sciencedaily.com/http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/http://www.healthscout.com/ency/68/38/main.htmlhttp://www.sciencedirect.com/science/journal/00219150


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This is to certify that Atherosclerosis- Saturated Fatty Acid and Risk of Coronary Heart

Disease is a record work doneby Hema Negi, M.Sc. Biotech (sem-II) at Amity Institute Of

Biotechnology, Amity University, in partial fulfillment for the degree ofM.Sc.Biotechnology

and submitted to Amity Institute of Biotechnology. I also certify that this work represents

independent effort on the part of the candidate.

Internal Faculty Examiner

Place:

Date: Signature of the Candidate.

ACKNOWLEDGEMENT


21/21

This work was carried out at the Amity Institute Of Biotechnology. I would like to

thank all those who have directly and indirectly contributed to this thesis.

I would like to thank:

My Faculty Dr. Panda Kusuma kumari for introducing me to the field of Medical Biotechnology

and providing research papers and her guidance for completing my term paper.

All the Faculty of Amity Institute Of Biotechnology for being available for help, for the patience

with me, and for constantly guiding me throughout my work and also for their never ending

encouragement.

My family and friends for their constant support and endless love.

Above all Lord almighty for everything.

Documents

Atherosclerosis- Hema Negi