Blood Cholesterol (HDL, LDL, & Triglycerides)

http://www.exrx.net/Testing/LDL&HDL.html

Blood Cholesterol (HDL, LDL, & Triglycerides)

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Cholesterol will not mix with water, and therefore, needs some assistance to travel
throughout the blood stream. With the help of a form of cholesterol HDL (high
density lipoprotein), packets of cholesterol are formed to help move cholesterol
through the blood. HDL helps remove cholesterol from the body by transporting it
to the liver. Another form of cholesterol is LDL (low density lipoprotein). LDL does
not aid in the transportation of cholesterol out of the body, instead it deposits
cholesterol onto the vessel wall. LDL molecules contain much more cholesterol
than HDL molecules.
How to Increase HDL
(Good Guys)
1. Exercise
2. Cessation of smoking
3. Weight reduction

How to Decrease LDL

(Bad Guys)
1. Decrease saturated fat intake
2. Maintain good body composition
3. Increase dietary fiber
4. Increase aerobic exercise

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The total cholesterol/HDL ratio is more indicative of cardiovascular disease than

TC (total cholesterol). The amount of HDL and LDL in the blood are added
together, this number for all practical purposes, indicates the amount of total
cholesterol. Therefore, if your HDL count is low, the LDL count will account for the
remainder of the total. For men an acceptable ratio of TC/HDL is 4.5 or below, and
women is 4.0 or below.

Risk
Very low (1/2
average)
Low risk
Average risk
Moderate risk
(2x average)
High risk (3x
risk)

Risk
Very low (1/2
average)
Average risk
Moderate risk
(2x average)
High risk (3x
risk)

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Ratio of total Cholesterol to

HDL
Men
Women
<3.4

<3.3

4.0
5.0

3.8
4.5

9.5

7.0

>23

>11

Triglycerides
(mg/dl)
< 130 Desirable
< 150 Normal
150-199 Borderline
200-499 High
>= 500 Very High

Ratio of LDL to HDL

Men
Women
1

1.5

3.6

3.2

6.3

5.0

6.1

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Blood Cholesterol (HDL, LDL, & Triglycerides)

http://www.exrx.net/Testing/LDL&HDL.html

HDL levels have an inverse relationship with coronary heart disease. The ability of
HDL to predict the development of coronary atherosclerosis has been estimated
to be four times greater than LDL and eight times greater than TC. Treatment is
recommended for those with an HDL level below 40 mg/dL. An HDL of 60 mg/dL
is considered protection against heart disease.
New MNR imaging tests assess the size of LDL particles. Small LDL particles are
associated with a higher risk of cardiovascular disease.

Triglycerides
Elevated triglycerides in the blood increase the risk of heart disease. Triglycerides
do not come directly from dietary fats. Instead, they are produced in the liver from
any excess carbohydrates that have not been used for energy.

NCEP Blood Lipid Guidelines

Adults 20 years and older should undergo cholesterol screening (total cholesterol,
LDL cholesterol, HDL cholesterol, and triglycerides) every 5 years. Blood samples
should be obtained after fasting.
Triglycerides
HDL
Total Cholesterol
LDL Cholesterol
(mg/dl)
Cholesterol
(mg/dl)
(mg/dl)
(mg/dl)
<150 Normal
<200 Desirable
<100 Optimal
Low
Borderline
200-239 Borderline
Near
<40
150-199
100-129
(undesirable
High
Optimal
>=240 High risk
High
200-499 High
Borderline
>60
130-159
(desirable)
High
>500 Very High
160-189 High
> 190 Very High
The National Cholesterol Education Program (May 16, 2001), Journal of the
American Medical Association

Blood Lipid Transport

After consuming a meal containing fat, the blood
undergoes a transient increase in lipids, particularly
triacylglycerols, lasting several hours. This is known
as postprandial lipemia. Individuals consuming a
typical Western diet spend approximately 18 hours
per day in this state.
Exogenous fat transport begins in the intestine
where dietary fats are packaged into lipoprotein
particles called chylomicrons. Chylomicrons enter
the bloodstream and deliver their triglyceride to
adipose tissue and muscle. The remnant of
chylomicrons is removed from the circulation by the
liver.
Endogenous fat transportation begins when the liver secretes a Very Low Density
Lipoprotein particle (VLDL). When a VLDL particle reaches the capillary of muscle
or adipose tissue, its triglyceride is extracted, leaving an Intermediate Density
Lipoprotein (IDL). Half of the IDL particles are removed from circulation by the

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Blood Cholesterol (HDL, LDL, & Triglycerides)

http://www.exrx.net/Testing/LDL&HDL.html

liver within two to six hours of their formation. The remaining IDL transforms into
Low Density Lipoproteins (LDL) which circulate for approximately two and a half
days before binding to LDL receptors in the liver and other tissues.
Small dense low density lipoprotein (LDL) are more atherogenic that larger LDL
particles because they are
more easily enter the vessel wall
more prone to oxidative modification
bind more tightly to the arterial wall
cleared more slowly
The composition of triglyceride-rich lipoproteins (TRLs) are metabolically linked to
LDL. LDL particle size is primarily affected by the plasma TG levels. Postprandial
hyperlipidemia is associated with an increase in the proportion of small, dense
LDL. Furthermore, prolonged lipemia promotes the transfer of core lipids between
TRLs and high density lipoprotein (HDL) leading to a reduction in HDL cholesterol
levels. This combination is known as the lipid triad or atherogenic lipoprotein
profile:
high plasma TG concentrations
increased small dense LDL
low HD
Bravo E, Napolitano M, and Botham KM (2010). Postprandial Lipid Metabolism:
The Missing Link Between Life-Style Habits and the Increasing Incidence of
Metabolic Diseases in Western Countries? The Open Translational Medicine
Journal, 2010, 2, 1-13

Cholesterol Regulation
Elevated circulating cholesterol reduces the cells ability to make its own
cholesterol by turning off the production of HMG CoA reductase, which interrupts
a step in the biosynthetic pathway of cholesterol. Incoming LDL derived
cholesterol promotes the storage of cholesterol in the cell by activating ACAT
which reattaches a fatty acid to excess cholesterol molecules. This results in
cholesterol esters that are deposited in storage droplets. The accumulation of
cholesterol within the cell drives a feedback mechanism which stops the cells
synthesis of new LDL receptors. The cell adjusts its receptors, so only enough
cholesterol is brought in to supply its needs.
With Familial Hypercholesterolemia, an inherited mutant gene causes the
absence of LDL receptors. High circulating levels of LDL are found to be caused
by an increased production and a decrease in the removal of LDL. Consequently,
Familial Hypercholesterolemia leads to high blood cholesterol and heart attacks in
the young.

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