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 |
How to Decrease LDL |
|
(Good Guys) |
(Bad Guys) |
- Exercise
- Cessation of smoking
- Weight reduction
|
- Decrease saturated fat intake
- Maintain good body composition
- Increase dietary fiber
- Increase aerobic exercise
|
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.
|
|
Ratio of total Cholesterol to HDL |
|
Risk |
Men |
Women |
|
Very low (1/2 average) |
<3.4 |
<3.3 |
|
Low risk |
4.0 |
3.8 |
|
Average risk |
5.0 |
4.5 |
|
Moderate risk (2x average) |
9.5 |
7.0 |
|
High risk (3x risk) |
>23 |
>11 |
|
|
Triglycerides (mg/dl) |
|
< 130 |
Desirable |
|
< 150 |
Normal |
|
150-199 |
Borderline |
|
200-499 |
High |
|
>= 500 |
Very High |
|
|
|
Ratio of LDL to HDL |
|
Risk |
Men |
Women |
|
Very low (1/2 average) |
1 |
1.5 |
|
Average risk |
3.6 |
3.2 |
|
Moderate risk (2x average) |
6.3 |
5.0 |
|
High risk (3x risk) |
8 |
6.1 |
|
|
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 a 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.
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.
|
LDL Cholesterol (mg/dl) |
|
<100 |
Optimal |
|
100-129 |
Near Optimal |
|
130-159 |
Borderline High |
|
160-189 |
High |
|
> 190 |
Very High |
|
|
Total Cholesterol (mg/dl) |
|
<200 |
Desirable |
|
200-239 |
Borderline |
|
>=240 |
High risk |
|
|
HDL Cholesterol (mg/dl) |
|
<40 |
Low (undesirable |
|
>60 |
Hight (desirable) |
|
|
Triglycerides (mg/dl) |
|
<150 |
Normal |
|
150-199 |
Borderline High |
|
200-499 |
High |
|
>500 |
Very High |
|
The National Cholesterol Education Program (May 16, 2001),
Journal of the American Medical Association
Elevated circulating cholesterol reduces the cells ability
to make its own cholesterol by turning off the production of
HMG CoA reductace which interrupts a step in the biosynthic 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 synthesize of new LDL receptors.
The cell adjusts its receptors so only enough cholesterol is
brought in to supply its needs.
With Familial Hypercholesterolemia, an inhereted mutant gene
causes the absence of LDL receptors. High circulating levels
of LDL are found 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.
Exogenous fat transport begins in the intestine where dietary
fats are packaged into lipoprotien particles called chylomicrons.
Chylomicrons enter the bloodstream and deliver their triglyceride
to adipose tissue and muscle. The remnant of chylomicrons is
removed from the arculation by the liver.
Endogenous fat transportation begins when the liver secretes
a Very Low Density Lipoprotien particle (VLDL). When a VLDL particle
reaches the capillary of muscle or adipose tissue, its triglyceride
is extracted leaving a Intermediate Density Lipoprotien (IDL).
Half of the IDL particles are removed from circulation by the
liver within two to six hours of their formation. The remaining
IDL transform into Low Density Lipoprotiens (LDL) which circulate
for approximately two and a half days before binding to LDL receptors
in the liver and other tissues.
|