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What is extremely interesting to note is, that all one hears nowadays is stay away from the “bad fats”, you don’t want “trans-fats”; you do want the good cholesterol and so forth.  But when you study disease, or what interest’s students, absent is much in the way of interest, understanding and discussion of the fat terrorists or hyperlipidemia.  Thus a review of the top physicians and surgeons on this topic.

The reality is that what you hear is a siphoning of the evidence from somewhat multifaceted subjects which by the end of the day, are disorders of lipid metabolism intimately associated with diabetes mellitus, obesity, hypertension, and cardiovascular disease.  These disorders in conjunction with the prevalence of high-fat diets, obesity, the invention and utility of trans-fatty acids, and physical inactivity, have resulted in an epidemic of atherosclerotic disease in the United States and other developed countries. The interaction of common genetic and acquired disorders of lipoproteins with these adverse environmental factors leads to the premature development of atherosclerosis as a global epidemic which is getting worse evidenced by increasing world obesity and hypertension.   Thus, this is a basic introduction into a much deeper science involving Dyslipidemias, hyperlipidemia and even hypoliposis especially relative to hyperlipidemia, hypertension, obesity, diabetes mellitus and cardiovascular disease.

In the United States, mortality from coronary artery disease (CAD), particularly in persons younger than 60 years, has been declining since 1970; however, atherosclerotic cardiovascular disease remains the most common cause of death among both men and women. Globally, the World Health Organization reports that high cholesterol contributes to 56% of cases of coronary heart disease worldwide and causes about 4.4 million deaths each year.   The year 2000 was the first in recorded history in which the percentage of people worldwide who are obese exceeded the percentage of people who are starving or malnourished.  Internationally, hypertension is an epidemic where estimates run as high as 50% of the population older than 60 years in many countries.  Further, approximately 20% of the world's adults are estimated to have hypertension.  Thus, it is interesting to correlate that Dyslipidemias are clinically important, principally because of their contribution to atherogenesis.  Coronary heart disease, atherosclerosis, Diabetes Mellitus, Obesity, Pancreatitis and fatty liver disease are known manifestations of lipid disorders. Finally, Dyslipidemia's are related to both abnormally high and low lipoprotein levels, as well as disorders in the composition of these particles

Lipid Physiology:

The major plasma lipids, including cholesterol (or total cholesterol [TC]) and the triglycerides, do not circulate freely, but are bound to proteins and transported as macromolecular complexes called lipoproteins. The major lipoprotein classes are chylomicrons, very low density (pre-beta) lipoproteins (VLDL), low density (beta-) lipoproteins (LDL), and high density (alpha-) lipoproteins (HDL).  And although these are closely interrelated, they are usually classified in terms of physiochemical properties (e.g., electrophoretic mobility and density after separation in the ultracentrifuge). The major lipids transported in the blood are triglycerides; between 70 and 150 g enter and leave the plasma daily compared with 1 to 2 g of cholesterol or phospholipids.

Chylomicrons, the largest lipoproteins, carry exogenous triglyceride from the intestine via the thoracic duct to the venous system. In the capillaries of adipose and muscle tissue, 90% of chylomicron triglyceride is removed by a specific group of lipases.

Fatty acids and glycerol, derived from hydrolysis of chylomicrons, enter the adipocytes and muscle cells for energy use or storage. The liver then removes the remnant chylomicron particles.

VLDL carries endogenous triglyceride primarily from the liver to the same peripheral sites (adipocytes and muscle cells) for storage or use. The same lipases that act on chylomicrons quickly degrade endogenous triglyceride in VLDL, giving rise to intermediate density lipoproteins (IDL) that are short of much of their triglyceride and surface apoproteins.  Within 2 to 6 h, this IDL is degraded further by removal of more triglyceride, giving rise to LDL, which in turn has a plasma half-life of 2 to 3 days. VLDL is, therefore, the main source of plasma LDL.

The fate of LDL is unclear: The liver removes about 70%, and active receptor sites have been found on the surfaces of hepatocytes and other cells that specifically bind to apolipoprotein B (apo B, the ligand associated with LDL that binds with LDL receptors) and remove most LDL from the circulation. A small but important amount of LDL appears to be removed from the circulation by non-LDL receptor pathways, including uptake by scavenger receptors on macrophages that may migrate into arterial walls, where they may become the foam cells of atherosclerotic plaques.

Hypercholesterolemia can result either from overproduction or defective clearance of VLDL or from increased conversion of VLDL to LDL. Overproduction of VLDL by the liver may be caused by obesity, diabetes mellitus, alcohol excess, nephrotic syndrome, or genetic disorders; each condition can result in increased LDL and TC levels and often is associated with hypertriglyceridemia. Defective LDL clearance may be due to genetically determined structural defects in apo B (the ligand) that diminish the binding of apo B to otherwise normal LDL receptors. Alternatively, reduced clearance may be due to diminished numbers or abnormal function (low activity) of the LDL receptors, which may result from genetic or dietary causes. Genetically mediated abnormal LDL receptor function usually results from molecular defects in the protein structure of the receptors--the usual mechanism of the genetic disorders described below.

When dietary cholesterol (as a constituent of chylomicron remnants) reaches the liver, the resulting elevated levels of intracellular cholesterol (or a metabolite of cholesterol in the hepatocyte) suppress LDL-receptor synthesis; this suppression occurs at the level of transcription of the LDL gene. A reduced number of receptors results in higher levels of plasma LDL and therefore of TC. Saturated fatty acids also increase plasma LDL and TC levels; the mechanism of action is related to a reduced activity of LDL receptors.  In the USA, dietary cholesterol and saturated fatty acid intake is high and is thought to account for an average increase of up to 25 to 40 mg/dL (0.65 to 1.03 mmol/L) of LDL blood levels--enough to increase significantly the risk of coronary artery disease (CAD). 

The Exogenous Pathway:

After a meal, intestinal cells absorb fatty acids and cholesterol, esterify them into triglyceride and cholesteryl ester, and incorporate them into the core of chylomicrons.  Triglyceride greatly predominates over cholesterol ester in the chylomicron core.  The chylomicrons are secreted into plasma, where apo C-II on the chylomicron surface activates endothelial-bound lipoprotein lipase (LPL). LPL in turn hydrolyzes the chylomicron's core triglyceride and releases free fatty acids, which are taken up by adipose tissue for storage and by muscle for energy.  During lipolysis, the chylomicron decreases in size, and some surface components are transferred to HDL; the remaining particle is the chylomicron remnant particle. This chylomicron remnant next acquires apo E from HDL and is subsequently taken up by the liver after binding to sites that recognize apo E.  It is then degraded, thereby delivering dietary cholesterol to the liver. 


The Endogenous Pathway:

The liver secretes triglyceride-rich VLDL into plasma, where they too acquire apo C-II from HDL. As with chylomicrons, VLDL interacts with LPL on the capillary endothelium, and the core triglyceride is hydrolyzed to provide fatty acids to adipose and muscle tissues.  About half of the catabolized VLDL remnants (IDL density) are taken up by hepatic receptors that bind to apo E for degradation; the other half—apo B-100 particles, depleted of triglyceride relative to cholesteryl ester—are converted by the liver to cholesteryl ester-rich LDL.  As IDL is converted to LDL, apo E becomes detached, leaving only one apolipoprotein, apo B-100. Each particle in this cascade from VLDL to LDL contains one molecule of apo B-100.

In the metabolism of both chylomicrons and VLDL, apo C-II permits the hydrolysis of triglyceride by lipoprotein lipase, and apo E prompts hepatic uptake of remnants. A major difference in the metabolism of these particles is that chylomicrons contain a truncated form of apo B (i.e., apo B-48), whereas VLDL contains the complete form (i.e., apo B-100).  Another difference is that chylomicron remnants are degraded after they are absorbed by the liver, whereas many of the VLDL remnants are most likely processed in the hepatic sinusoids to become LDL.

The National Cholesterol Education Program (NCEP) recommends checking the total cholesterol and HDL cholesterol levels as well as a full lipid profile (i.e., total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides) may be in order.  Since triglyceride and LDL levels are affected by eating, it is necessary to fast for 12 hours before testing.

NCEP recommendations are based on the LDL cholesterol level which correlates with risk for heart attack and death.  Several drugs (progestins, anabolic steroids, and glucocorticoids) and disease states adversely affect low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) values associated with hypercholesterolemia.  Finally, today’s in vogue health habits such as high-fat diets alone or concomitant with susceptible inherited genetic traits are thought to be the cause of hypercholesterolemia.

For patients without clinical evidence of coronary or other atherosclerotic vascular disease, the NCEP recommends health screening, including measurement of TC and HDL cholesterol, at least once every 5 yr. Further evaluation is performed for those patients with a high TC, for those with low HDL cholesterol (< 35 mg/dL [< 0.91 mmol/L]), or for those with borderline TC who have at least two CAD risk factors (age > 45 for men or > 55 for women [or postmenopausal state without estrogen replacement], high BP, smoking, diabetes, HDL < 35 mg/dL, or a family history of CAD before age 55 in a male first-degree relative or before age 65 in a female first-degree relative). This evaluation should include fasting levels of TC, triglyceride, and HDL. LDL is then calculated by applying the following formula: LDL cholesterol = TC - HDL cholesterol - triglyceride/5. (This formula is valid only when triglyceride is < 400 mg/dL [< 4.52 mmol/L]).  A high HDL level (> 60 mg/dL [> 1.55 mmol/L]) is considered a negative risk factor and reduces the number of risk factors by one.

The NCEP recommends that treatment decisions be based on the calculated level of LDL.  For patients with an elevated LDL (>= 160 mg/dL [>= 4.14 mmol/L]) who have fewer than two risk factors in addition to elevated LDL and who do not have clinical evidence of atherosclerotic disease, the goal of treatment is an LDL level < 160 mg/dL.  For those who have at least two other risk factors, the goal of treatment is an LDL level < 130 mg/dL (< 3.37 mmol/L). When LDL levels remain > 160 mg/dL despite dietary measures and the patient has two or more risk factors (in addition to high LDL), or when LDL levels remain > 190 mg/dL (> 4.92 mmol/L) even without added risk factors, the addition of drug treatment should be considered.

For those with CAD, peripheral vascular disease, or cerebrovascular disease, the goal of treatment is an LDL < 100 mg/dL (< 2.59 mmol/L).   For that matter however, all patients with clinical evidence of coronary or other atherosclerotic disease should be evaluated with a fasting blood sample for measurement of TC, triglyceride, and HDL. LDL is again calculated, as described above.

In contrast to plasma TC, it is unclear whether plasma triglycerides are independent risk variables; like TC, they vary with age.  A triglyceride level of < 200 mg/dL (< 2.26 mmol/L) is considered normal, 200 to 400 mg/dL (2.26 to 4.52 mmol/L) is borderline high, and > 400 mg/dL (> 4.52 mmol/L) is high.  Hypertriglyceridemia has been associated with diabetes, hyperuricemia, and pancreatitis (when levels are > 600 mg/dL [> 6.78 mmol/L]).

As indicated below, even more information can be obtained about CAD risk by considering plasma TC as only one of several units of lipid transport--the lipoproteins.  Sixty to 75% of plasma TC is transported on LDL, the levels of which are directly related to cardiovascular risk.  HDL, which normally accounts for 20 to 25% of the plasma TC, is inversely associated with cardiovascular risk. HDL levels are positively correlated with exercise, moderate alcohol intake, and estrogen replacement therapy and are inversely correlated with smoking, obesity, and the use of most progestin-containing contraceptives.  Studies show that CAD prevalence at HDL levels of 30 mg/dL (0.78 mmol/L) is more than double that at 60 mg/dL, and high levels of LDL or low levels of HDL are independently associated with increased CAD risk.  One must determine, therefore, whether elevated TC levels are due to increased LDL or HDL.  In countries or in groups (e.g., lactovegetarians, Seventh-Day Adventists) where TC and LDL cholesterol are low because of nutritional habits (marked reduction in ingestion of total saturated fats and cholesterol), HDL levels are often relatively low and the risk for CAD is low.  In the U.S.-based Framingham Study, however, men and women (eating the typical high-fat American diet) with relatively normal LDL levels (120 to 160 mg/dL [3.11 to 4.14 mmol/L]) with HDL < 30 mg/dL were at increased risk for CAD.


General Signs and Symptoms:

Early on in patient with elevated cholesterol blood levels symptoms are absent.  However, in time as hypercholesterolemia becomes chronic, specific physical manifestations such as a thickening of the tendons due to accumulation of cholesterol called xantomas, yellowish patches around the eyelids called xanthelasma palpabrum or more commonly a white discoloration of the peripheral cornea known as arcus senilis.

The chronic elevation or chronic hypercholesterolemia will lead to accelerated atherosclerosis in Peripheral vascular disease, Angina pectoris, Myocardial infarction, Transient ischemic attacks and of course,  Cerebrovascular accidents.



A useful clinical appraisal of lipids can usually be made by determining plasma TC, HDL-cholesterol, and triglyceride levels after the patient has fasted for >= 12 h. The specimen should also be observed for a milky chylomicron layer after it stands overnight in a refrigerator at 4° C (39.2° F). Plasma TC may be determined by colorimetric, gas-liquid chromatographic, enzymatic, or other automated "direct" methods. Enzymatic methods are usually most accurate and are standard in virtually all clinical laboratories. Plasma triglyceride is usually measured as glycerol by either colorimetric, enzymatic, or fluorometric methods after alkaline or enzymatic hydrolysis to glycerol and formaldehyde. HDL levels are measured enzymatically after precipitation of VLDL, IDL, and LDL from plasma. (For LDL estimation, see above.) Lipoprotein electrophoresis is useful only in Dyslipidemia and has generally been supplanted by analysis of the apolipoproteins.

Most elevations of TC and/or triglyceride are modest and are due primarily to dietary excess. More severe hyperlipidemia is due to a heterogeneous group of disorders differing in clinical features, prognosis, and therapeutic response. A high plasma level of any lipoprotein can result in hypercholesterolemia. Similarly, hypertriglyceridemia may result from increased levels of chylomicrons, VLDL, or both. Thus, defining the precise lipoprotein pattern is important, especially in selecting appropriate diet and drug therapy.   Since each lipoprotein class has a relatively fixed composition with respect to TC and triglyceride and since the two largest particle types (chylomicrons and VLDL) refract light and cause plasma turbidity, the specific type of hyperlipoproteinemia can often be determined by observing a standing plasma sample, after 24 h storage at 4° C (39.2° F), followed by a more precise TC and triglyceride assay. A turbid or cloudy plasma must be caused by increased VLDL; if the plasma is clear, an elevated TC must be caused by elevated LDL or HDL. If a layer of cream has formed, it must be the result of increased chylomicrons. Analysis of apolipoproteins or electrophoresis is not usually required.

Determining the lipoprotein pattern does not conclude the diagnostic process. Hyperlipoproteinemia may be secondary to other disorders that must be ruled out (e.g., hypothyroidism, alcoholism, kidney disease) or may be primary (usually familial), in which case screening should be performed to identify other family members (often asymptomatic) with hyperlipoproteinemia.

In evaluating lipid or lipoprotein measurements, one must be aware of the following: (1) Lipid and lipoprotein levels increase with age. A value acceptable for a middle-aged adult might be alarmingly high in a 10-yr-old child. (2) Because chylomicrons normally appear in the blood 2 to 10 h after a meal, a fasting specimen (12 to 16 h) should be used. (3) Lipoprotein levels are under dynamic metabolic control and are readily affected by diet, illness, drugs, and weight change. Lipid analysis should be performed during a steady state. If results are abnormal, at least two more samples should be tested before selecting therapy. (4) When hyperlipoproteinemia is secondary to another disorder, treatment of the latter usually will correct the hyperlipoproteinemia.

Cholesterol levels should be measured in children who have a parent with hyperlipidemia or coronary artery disease before age 55.  Routine screening of other children is not indicated.  Every adult should have a total serum cholesterol and HDL-cholesterol determined during his or her third decade.  A total cholesterol value less than 200 mg/dl at any time of the day does not require retesting for 5 years.  A level greater than 200 mg/ dl should lead to measurement of total cholesterol TB, and HDL-cholesterol after a 14-hour fast.  Similar testing is indicated in adults who have first degree relative with vascular disease or lipid disorders.  An HDL-cholesterol level below 35 mg/dl in men and below 45 mg/dl in women signifies clearly increased risk for disease.  If TG levels are over 500 mg/dl, then specific treatment of hypertriglyceridemia must be undertaken.  The highest total cholesterol commonly encounter (600 to 2000 mg/dl) is usually due to increases in chylomicrons and VLD. Elevated cholesterols, therefore, cannot be interpreted absent knowledge of TB levels. 

Thus, if TB levels are less than 400 mg/dl, then the LDL-cholesterol (LDLc) I calculated a follows: 

LDLc=Total C-(HDLc + VLDLc)

                     =Total C-(HDLc +TB/5) 

Elevated HDL levels are thought to confer protection against coronary heart disease and do not require treatment.  Even mild LDL elevations justify aggressive modification of other factors.


Initial Evaluation:

Diabetes Mellitus and metabolic syndromes, Kidney disease, Hypothyroidism, Anorexia nervosa, Zieve’s syndrome, family history of premature atherosclerosis, Family history of premature atherosclerosis, Diet history for saturated fat and record of cholesterol intake, Weight record, and Physical activity level must be noted on the initial evaluation. 

The evaluation generally begins with a risk-factor analysis. Patients are then categorized according to CHD or CHD risk equivalent (particularly diabetes), i.e., those with multiple risk factors and those at low risk (<2 risk factors). Patients with CHD or CHD equivalent risk have a greater than 20% 10-year risk for CHD events. Low-risk patients generally have a 10-year CHD risk of less than 10%. Patients with multiple risk factors may or may not be at high risk.

Risk factors include but are not limited to Age (males > 45 years, females > 55 years or menopause < age 40?), Family history of premature coronary artery disease; definite myocardial infarction (MI) or sudden death before age 55 in father or other male first-degree relative, or before age 65 in mother or other female first-degree relative, Current cigarette smoker, Hypertension (systolic blood pressure > 140 mmHg or diastolic blood pressure > 90 mmHg confirmed on more than one occasion, or current therapy with antihypertensive medications), Diabetes mellitus (DM), High-density lipoprotein (HDL)-cholesterol < 40 mg/dL. 

Initial Laboratory Evaluation:

Lab values:

Total Cholesterol                  100-199 mg/dL

Triglycerides                         0-149 mg/dL

HDL cholesterol                   40-59 mg/dL

VLDL cholesterol Cal                      5-40 mg/dL

LDL cholesterol Calc                       0-99 mg/dL 


  1. All men aged 35 years and older and all women aged 45 and older should be screened for lipids disorders.
  2. Younger adults – men aged 20-35 and women aged 20-45 – should be screened if they have other risk factors for heart disease (including tobacco use, diabetes, a family history of heart disease or high cholesterol, or high blood pressure).
  3. Clinicians should measure HDL in addition to measuring total cholesterol, or LDL.

Relative to continuous monitoring if HDL > 40 mg/dL, screen all patients via a fasting lipid profile every 5 years beginning at age 20 years. Patients with CHD should undergo a lipid profile determination at least yearly. Patients with multiple risk factors should have their lipid profiles determined at least every other year.  In 3 months, recheck the lipid profiles of patients treated with therapeutic lifestyle intervention. In 6-12 weeks, recheck the lipid profiles of patients treated with drugs.  Liver function testing is indicated periodically for patients taking statins or fibrates, although the risk for hepatotoxicity is very low. Liver function abnormalities are more common at the highest doses of each of the approved statins. Checking liver test results 6-12 weeks after an increase in the dose is reasonable, particularly in patients on high-dose statins. Periodic EKG and echocardiogram to monitor for ischemic and valvular heart disease are also in place.



Intervention studies have shown that cholesterol reduction using diet (MNT), drugs or surgery reduces the risk of development or progression of CHD.  In general, a 1 per cent fall in LDL-cholesterol has be associated with roughly a 2 per cent reduction in disease end points.  Arteriography studies have demonstrated that small but convincing regressions of arterial lesions.  General agreement exists that eating less saturated fat and cholesterol and adopting an MNT diet and exercise habits to reduce obesity will befit the health of all percipient folks. 


Medical Care:

Treatment of hypercholesterolemia involves lifestyle modification and pharmacologic therapy.

    • For patients with known atherosclerosis (clinical CHD, symptomatic carotid artery disease, peripheral arterial disease, or abdominal aortic aneurysm), the LDL-C goal is less than 100 mg/dL, although an LDL-C goal of less than 70 mg/dL is now considered a therapeutic option in patients considered to be at very high risk (acute coronary syndrome patients, diabetes mellitus, multiple risk factors with uncorrected risk factors such as continued smoking).
    • For patients with 2 or more risk factors, the LDL-C goal is less than 130 mg/dL, with recommendations for drug therapy that depend on the estimated 10-year risk of a CHD event based on the modified Framingham equation (see below).
    • For patients at low risk (0-1 risk factors), the LDL-C goal is less than 160 mg/dL.
    • The LDL-C goal for patients with CHD equivalent risk, including patients with diabetes mellitus, should also be less than 100 mg/dL. In patients considered to be very high risk, a goal of less than 70 mg/dL is an acceptable option

The new National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines recommend calculating a Framingham risk score in patients with multiple risk factors to quantify risk and set LDL-C goals. The Framingham score calculator is available through the NCEP and the US National Heart, Lung, and Blood Institute.

    • Patients with CHD or CHD equivalent are prescribed drug therapy simultaneously with therapeutic lifestyle changes if their LDL-C concentration is greater than or equal to 130 mg/dL. Drug therapy is optional for patients whose LDL-C value is 100-129 mg/dL.
    • For patients with multiple risk factors, the LDL-C level at which drug treatment is recommended depends on the Framingham score. The LDL-C goal is less than 130 mg/dL. For patients with multiple risk factors and a 10-year risk of greater than 20%, the treatment is similar to that of patients with CHD. For patients with a 10-year risk of 10-20%, drug treatment is considered if their LDL-C level is greater than or equal to 130 mg/dL. For patients with multiple risk factors and a 10-year risk of less than 10%, drug therapy is considered if their LDL-C levels are greater than or equal to 160 mg/dL.
    • For patients at low risk, the LDL-C goal is less than 160 mg/dL, with therapeutic lifestyle changes for patients with higher values and drug therapy considered at LDL-C levels of greater than or equal to 190 mg/dL.
    • Therapeutic lifestyle treatment (i.e., dietary changes and exercise) is recommended for patients whose LDL-C concentrations are greater than their goal LDL-C.

The new NCEP guidelines also recommend trying to identify patients with what has been called the metabolic syndrome. Such patients in particular should be targeted for therapeutic lifestyle changes. These patients meet at least 3 of the following criteria:

    • Abdominal obesity (waist >40 in for men, >35 in for women)
    • High triglyceride level (>150 mg/dL)
    • Low high-density lipoprotein cholesterol (HDL-C) value (<40 mg/dL for men, <50 mg/dL for women)
    • High blood pressure (>130/85 mm Hg)
    • Impaired fasting glucose (IFG) value (plasma glucose level >110 mg/dL, although the lower limit now generally used in the American Diabetes Association IFG cut point of 100 mg/dL or greater)

If the patient's serum triglyceride level remains greater than or equal to 200 mg/dL after the LDL-C goal is reached, a secondary non–HDL-C goal is set. The non–HDL-C goal is the LDL-C goal plus 30 mg/dL. This goal may be achieved with an increase in the statin dose, a more efficacious statin, or the addition of another agent (e.g., fibrate, niacin, fish oil). Fenofibrate has less of a propensity for drug interactions; therefore, it is preferred in most situations. If fish oil is used, the correct dose is at least 2-3 g of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) daily. Because most 1-g fish oil capsules contain only approximately 300 mg of DHA and EPA, a patient must consume 10 1-g fish oil capsules daily to reach the goal. More highly concentrated fish oil capsules or liquids can be used, but the patient usually cannot find these in local pharmacies.

The dosage and approximate LDL-C lowering of various statins is as follows:

    • For atorvastatin at 10-80 mg/d, the LDL-C level is lowered by 39-60%.
    • For fluvastatin at 20-80 mg every bedtime or 40 mg twice daily, the LDL-C level is lowered by 22-36%.
    • For lovastatin at 20-40 mg every evening or 40 mg twice daily, the LDL-C level is lowered by 24-42%.
    • For pravastatin at 10-80 mg every bedtime, the LDL-C level is lowered by 22-34%.
    • For rosuvastatin at 5-40 mg/d, the LDL-C level is lowered by 45-63%.
    • For simvastatin at 20-80 mg every bedtime, the LDL-C level is lowered by 38-47%.


The NCEP has created dietary guidelines for all people older than 2 years. The reduction of saturated fat intake is vitally related to reduced LDL-C levels. In general, replacing fat with complex carbohydrates is helpful. Because carbohydrates are less calorically dense than fat, this substitution may also help prevent obesity. Adopting an appropriate diet may help patients reduce their LDL-C value by approximately 10-15%. However, in real-world studies, a 5% reduction is more likely. Reduction in trans fat intake also helps reduce LDL-C levels and may help raise HDL-C levels.

  • NCEP dietary guidelines are as follows:
    • total fat - Less than 30% of energy intake (calories)
    • Saturated fat - Less than 7% of energy intake
    • Polyunsaturated fat - Less than or equal to 10% of energy intake
    • Monounsaturated fat - From 10-15% of energy intake
    • Cholesterol - Less than 200 mg/dL
    • Carbohydrates - From 50-60% of energy intake
  • Extreme fat and cholesterol restriction has been achieved with vegetarian diets, as demonstrated by the 1990 studies performed by Ornish and colleagues. This type of dietary restriction has resulted in a marked reduction in LDL-C levels and improvement in CHD symptoms. Whether these dietary restrictions are realistic for most Americans is debatable. Moreover, such a diet also reduces HDL-C levels and raises triglyceride levels.
  • Plant sterols and plant stanol esters can be included in the diet and may reduce LDL-C values by approximately 10-15%. Commercial preparations are available as margarine substitutes (eg, Benecol, Take Control).
  • Recently, after years of lay promotion, small, short-term (6 mo) studies have suggested that high-fat low-carbohydrate diets (eg, the Atkins diet) may facilitate weight loss without adversely affected serum lipid concentrations. However, the long-term effects of such diets remain to be determined.
  • MNT diets seem to have the most benefit.

Summary for MNT diet (NCEP dietary guideline) foods:

1. Two servings of Fish/week because of its high levels of omega-3 fatty acids, which can reduce your blood pressure and risk of developing blood clots. In people who have already had heart attacks, fish oil — or omega-3 fatty acids — reduces the risk of sudden death.

2. Foods with at least 2 grams of plant sterols or stanols can help reduce LDL cholesterol by more than 10 percent. The amount of daily plant sterols needed for results is at least 2 grams — which equals about two 8-ounce (237-milliliter) servings of plant sterol-fortified orange juice a day.

3. Oatmeal, oat bran and high-fiber foods reduces your low-density lipoprotein (LDL), the "bad," cholesterol. Soluble fiber is also found in such foods as kidney beans, apples, pears, barley and prunes. Soluble fiber can reduce the absorption of cholesterol into your bloodstream. Five to 10 grams or more of soluble fiber a day decreases your total and LDL cholesterol. If you add fruit, such as bananas, you'll add about 4 more grams of fiber.

4. 2 tablespoons of extra-virgin Olive oil/day contains a potent mix of antioxidants that can lower your "bad" (LDL) cholesterol but leave your "good" (HDL) cholesterol untouched.

5. Eat a handful of unsalted Walnuts, almonds, pistachio's and other nuts can reduce blood cholesterol. Rich in polyunsaturated fatty acids, walnuts also help keep blood vessels healthy.


Although exercise has little effect on LDL-C concentrations, aerobic exercise may improve insulin sensitivity, HDL-C concentrations, and triglyceride levels and, thus, may help reduce CHD risk. Patients who exercise and adhere to an appropriate diet appear to be more successful in long-term lifestyle modifications that improve their CHD risk profile.

Discussion of Medications:

  • HMG-CoA reductase inhibitors (statins) are the medications of choice for the treatment of LDLc elevations because they have the greatest efficacy and are easily tolerated and because multiple randomized, placebo-controlled trials have shown that lowering LDLc levels with statins reduces coronary morbidity and mortality and, in some cases, total mortality. The strongest statins, rosuvastatin and atorvastatin, at their maximum approved doses, can be expected to reduce LDLc levels 50-60%.  Even the maximum doses of the strongest statins are usually inadequate for patients with familial hypercholesterolemia, and the addition of one or more nonstatin cholesterol-lowering medications is necessary.
  • Bile acid sequestrants (eg, cholestyramine, colestipol, colesevelam) can be added with no risk of drug interaction, with the exception of affecting the absorption of the statin (and many other medications) if taken at the same time. Bile acid sequestrants modestly decrease LDLc levels and slightly increase HDLc and triglyceride levels. Other medication should be taken 1 hour before or 4 hours after a bile acid sequestrant.
  • Nicotinic acid (niacin) not only lowers LDLc levels but also has significant HDL-raising and triglyceride-lowering effects. There is little data to support the belief that niacin even slightly increases the risk of myopathy if combined with a statin.
  • Fibric acid derivatives include gemfibrozil (Lopid) and fenofibrate (Tricor). Outside of the United States, bezafibrate is also available. The fibrates lower triglyceride levels and raise HDLc levels, but they do not reliably lower LDLc levels. They increase the risk of statin-induced myositis more so than niacin.
  • The cholesterol absorption inhibitor, ezetimibe, reduces LDLc levels approximately 18% and has a small HDLc-raising and triglyceride-lowering effects. Because the mechanism by which it inhibits cholesterol absorption is quite specific, ezetimibe does not cause the side effects or drug interactions associated with bile acid sequestrants. When combined with a statin, substantially greater LDLc decreases have been observed and this medication has a major role in LDL-lowering when a statin alone is not sufficient.

Two statin formulations are now available in combination with either extended-release niacin (Advicor) or ezetimibe (Vytorin). These are particularly appropriate medications for patients with familial disease, most of whom require 2 or more drugs to reach their LDLc goals. In addition, significantly greater than expected decreases in the LDLc level (~16%) are frequently observed when ezetimibe is added to statin therapy.



It is now clear from the evidence that rapid advances in understanding the dynamics of cholesterols and lipids relative to hypertension, obesity, diabetes mellitus, arterial vascular disease, cardiac, liver and kidney disease proves chronic evaluation can not only prevent disease, can reduce disease and slow the course of disease.  Because of the importance to life and quality of life, once a condition of hypercholesterolemia, Dyslipidemia, or the genetic inheritance as noted above is proven, return visits for data recording and minor changes in diet, exercise, and medicinal therapy could prevent any of the disease in the early elevated yet clinically silent stages, to prevent or reduce chance of disease or progression of disease.  It is now perfectly clear that unless cured or corrected, the interrelationships of the disease and conditions mentioned demands upon prudent prophylactic actions on the part of not only the treating physician but the patient (Deemed Mandatory rather then permissive)

If the patient and their health care team can work strategically relative to chronic evaluation and surveillance, often orchestrated by the well educated patient, then a tremendous improvement in patient’s quality life around our world will continue and improve for a better place in which all of us can live and thrive.




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  • Kasper Dennis L et al, Harrison’s Principles of Internal Medicine, 16th edition, Mc Graw Hill, pages 250-251


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By Scott David Neff for Family Medicine October 8th, 2006

"The most acceptable service to God is doing good to man"   Ben Franklin

© & TM 1998 American Academy for Justice Through Science. All rights reserved.

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