Hello Swillis,
My first thought after reading your question was ?Did he have his
blood drawn and tested at a reputable laboratory, preferably a
hospital lab, or was it done on a hand held meter at a health fair, or
in a doctor?s office. Doctor?s office testing ?can? be useful as a
screening test, provided the office uses proper testing methods, and
implements adequate QC and standards. However, for the most accurate
testing, ask that you be retested, after fasting overnight, at a
hospital laboratory. You may be surprised at the results.
You also did not mention your triglyceride level, which is generally
included in a lipid panel:
?? Association with hypertriglyceridemia needs attention. "When a low
HDL cholesterol is associated with high triglycerides (200-499 mg/dl),
secondary priority goes to achieving the non-HDL cholesterol goal. For
example, 1. In the patients with established CHD, or CHD risk
equivalent (10-year risk for CHD >20%), the 'LDL' goal is <100 mg/dl;
or the 'non-HDL cholesterol' goal is <130 mg/dl. 2. In persons with
multiple (2+) risk factors and 10-year risk of equal to or less than
20%, the 'LDL' goal is <130 mg/dl; while the 'non-HDL' goal is <160
mg/dl. 3. In persons with 0-1 risk factor, the 'LDL' goal is <160
mg/dl; and that for the 'non-HDL' is <190 mg/dl."
? Managing isolated low HDL cholesterol: "If the triglycerides are
<200 mg/dl (isolated low-HDL cholesterol), drugs for raising HDL
(fibrates or nicotinic acid) can be considered. Statins have only
modest effect. Treatment for isolated low HDL cholesterol is mostly
reserved for persons with CHD and CHD risk equivalents."
?Always consider secondary causes of low HDL levels, especially
medications, smoking habits, dietary patterns, and physical activity.
Patients with elevated TG levels (>500 mg/dL) commonly have low HDL-C
levels; address hypertriglyceridemia first in such patients. Patients
with moderately reduced HDL levels (20-35 mg/dL) usually have
secondary causes that should be addressed. Individuals with severely
reduced HDL levels (<20 mg/dL) may have a specific genetic etiology,
such as LCAT deficiency, Tangier disease, or mutations in apo A-I.
Ironically, these disorders are not commonly associated with an
increased risk of atherosclerosis.?
http://www.emedicine.com/med/topic3368.htm
A low LDL is desirable for everyone, not just people with a high
total cholesterol. You also didn?t state whether you smoke or not. If
you don?t smoke, I apologize for the ?No smoking? messages found in my
resources. But if you DO smoke, it?s time to quit!
Every reliable site I found (and Wikipedia is not always reliable)
stated the same thing: In order to lower LDL and raise HDL, increase
aerobic exercise, lose weight, increase carbohydrate intake, quit
smoking, replace saturated fats with unsaturated fats, and have your
doctor prescribe niacin and fibrates. Malabsorption syndromes and
inflammatory diseases can alter blood lipids too.
Be aware too, that some medications can cause your lipid results,
particularly the following class of drugs:
o Androgens
o Progestins
o Probucol
o High-dose thiazides
o High-dose beta-blockers
http://www.emedicine.com/med/topic3368.htm
Genetics can play a role in your low HDL. Are your tonsils orange?
Are you from Japanese ancestry?
Fewer than 50 people worldwide have been reported with Tangier
Disease? I?m including for interest, and to point out how genetics can
cause cholesterol anomalies!
?Tangier disease (TD) is a genetic disorder of cholesterol
transport named for the secluded island of Tangier, located off the
coast of Virginia. TD was first identified in a five-year-old
inhabitant of the island who had characteristic orange tonsils, very
low levels of high density lipoprotein (HDL) or 'good cholesterol',
and an enlarged liver and spleen.
TD is caused by mutations in the ABC1 (ATP-binding cassette) gene on
chromosome 9q31. ABC1 codes for a protein that helps rid cells of
excess cholesterol. This cholesterol is then picked up by HDL
particles in the blood and carried to the liver, which processes the
cholesterol to be reused in cells throughout the body. Individuals
with TD are unable to eliminate cholesterol from cells, leading to its
buildup in the tonsils and other organs.?
Fish eye disease is mentioned further down in the answer.
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowSection&rid=gnd.section.237
http://www-personal.umd.umich.edu/~jcthomas/JCTHOMAS/1997%20Case%20Studies/J.%20Newman1.html
?Although population studies indicate that a high level of HDL-C in
general protects against CHD,2 3 a high HDL-C concentration in any
given individual may not necessarily confer cardioprotection. The
atherogenicity of low HDL-C seems to be influenced by an array of
genetic and environmental factors.
Tangier disease, a disorder caused by mutations in the ATP-binding
cassette transporter 1 (ABC1) gene,4 is characterized by the absence
of normal HDL, with only a very small quantity of abnormal HDL
present. However, early atherosclerosis (before 40 years) is not a
consistent feature of this disorder.5
In men of Japanese ancestry in Hawaii, mutations in the gene for
plasma cholesteryl ester transfer protein (CETP), which transfers
cholesteryl ester from HDL to TG-rich lipoproteins, have been shown to
result in elevated HDL-C levels.6 However, subjects carrying
heterozygous CETP gene mutations had a moderately increased CHD risk,
despite higher HDL-C levels. Elevated HDL-C caused by a common
mutation in the CETP gene also increases the risk of ischemic heart
disease in Danish women.7 This and other evidence indicates that both
genetic and environmental factors influence the atherogenicity of low
HDL-C and that an increase in HDL-C due to impaired CETP activity may
be atherogenic.?
http://circ.ahajournals.org/cgi/content/full/circulationaha;103/17/2213
?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.?
To raise your HDL:
1. Exercise
2. Cessation of smoking
3. Weight reduction
To decrease your LDL:
1. Decrease saturated fat intake
2. Maintain good body composition
3. Increase dietary fiber
4. 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.?
http://www.exrx.net/Testing/LDL&HDL.html
"Most of the drugs that lower LDL also tend to raise HDL so until
our study, when a person's health improved, you couldn't tell if that
was due to lowering of the LDL or raising the HDL level," says study
senior author William Tierney, M.D., IU Chancellor's Professor of
Medicine and a Regenstrief Institute, Inc. research scientist. "We now
know that more good cholesterol is more important than less bad
cholesterol.
"Having a high total cholesterol reading may not be bad, in fact it
may be good if it's the HDL component which is high. Conversely, a low
total cholesterol reading, is not necessarily good because it can hide
a low HDL level," said Dr. Tierney.
This study was repeated with stroke as the outcome rather than heart
disease, and the same results were the same: HDL cholesterol was a
strong predictor of stroke, and the LDL cholesterol was not.?
If you want to get really technical: ?HDL is a protein-enriched lipoprotein that
plays a pivotal role in reverse cholesterol transport, or the transfer
of cholesterol from extrahepatic sites, including vascular
macrophages, to the liver for biliary excretion.5 Although ?HDL? and
?HDL-C? are often used interchangeably, ?HDL? refers to the
lipoprotein particle and its properties, whereas ?HDL-C? refers to its
measured levels.?
?The good news is that weight loss ultimately improves the lipoprotein
profile, although there may be transient reductions in HDL-C levels
during active dieting. Specifically, for each kilogram (2.2 pounds) of
weight lost during active dieting, HDL-C levels fall by 8%. However,
once weight is stabilized there is a surge in the HDL-C level of about
1 mg/dL for every 7 pounds lost.8 There are no magic dietary bullets
that selectively raise HDL-C levels. However, replacing fat with
carbohydrates (which may stimulate production of very-low-density
lipoprotein) without reducing caloric intake may cause HDL-C levels to
fall by as much as 20%.? Please reference the web site for complete
information.
http://www.eurekalert.org/pub_releases/2006-04/iu-hgc040306.php
?Physical exercise, weight reduction, smoking cessation, diabetes
mellitus control, and specific drugs, including niacin, fibrates, and
estrogens, are effective methods to increase HDL levels. Niacin is the
oldest and most powerful clinical agent for raising HDL levels.
Niaspan, an extended-release niacin formulation, is as potent as
immediate-release niacin in increasing levels of HDL cholesterol;
subfractions HDL2 and HDL3; apolipoprotein A-I, the major protein of
HDL, and its cardioprotective subfraction lipoprotein A-I. Recent
research from our laboratory suggests a novel mechanism by which
niacin inhibits hepatic removal of HDL-apoprotein A-I without
interfering with the removal of cholesterol carried by HDL, thus
augmenting reverse cholesterol transport.?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9915662&dopt=Citation
?The success of methods for raising HDL-C levels is often interrelated
with other variables,
including body mass index, triglyceride levels, and associated
metabolic abnormalities.?
?Low HDL-C is the most common lipoprotein abnormality in patients with
CHD and is predictive of subsequent CHD events, even when total
cholesterol is within the desirable range.2,3 The National Cholesterol
Education Program?s ATP III report clearly defines a serum HDL-C level
less than 40 mg/dL as an independent risk factor for CHD.?
http://www.ccjm.org/pdffiles/Miller603.pdf
??Diets high in carbohydrate and low in fat reduce both LDL and HDL
cholesterol, sometimes producing no improvement or a worsening in
TC:HDL ratio (3). The significance of low HDL levels in vegetarians
and in people consuming low-fat diets continues to be a subject of
debate. On the one hand, it has been suggested that low HDL does not
matter when total cholesterol is low (4). However, some research
suggests that the TC:HDL ratio is predictive of heart disease risk at
all levels of total cholesterol.
?Some research shows that HDL cholesterol levels stay depressed for as
long as the low-fat diet is consumed and that it is not a transient
effect as has been suggested
?While replacing fat with carbohydrate reduces both LDL and HDL
cholesterol, replacing saturated fat with unsaturated fat lowers
mainly LDL cholesterol
?Monounsaturated fatty acids may inhibit the oxidation of lipoproteins
?Concerns have been raised over the ratio of essential fatty acids in
some vegetarian diets. Vegetarians, and in particular, vegans, consume
little if any of the long chain omega-3 fatty acid docosahexanoic acid
(DHA) which is found predominantly in fish oil and eggs. Although the
omega-3 fatty acid linolenic acid can be converted to DHA, linoleic
acid can interfere with the conversion process. Diets that are either
too high in linoleic acid or too low in all fats may not provide
optimal ratios of linoleic to linolenic acid to allow for optimal
conversion of linolenic acid to DHA
?Some high fat foods that are routinely discouraged in very low fat
diet patterns are associated with protective effects against coronary
heart disease. For example, the Adventist Health Study found that nut
consumption is associated with protection against both fatal and
nonfatal coronary heart disease and with decreased risk of death from
all causes
?Compared to a high carbohydrate diet, a diet high in monounsaturated
fats (45% fat from predominantly olive oil), was associated with a
significant reduction in triglyceride and VLDL cholesterol levels in
people with non-insulin dependent (Type 2) diabetes. It was also
associated with mild improvements in HDL cholesterol levels, glycated
hemoglobin levels, and fasting plasma glucose levels
http://www.andrews.edu/NUFS/challenge%20of%20defining%20optimal%20fat%20intake.html
?Exercising and losing weight, if you are overweight, are also
critical. They can increase your "good" HDL cholesterol and lower your
"bad" LDL cholesterol and triglycerides. Losing weight can also help
lower high blood pressure and help prevent diabetes and
osteoarthritis. Most health experts recommend that you exercise for a
minimum of 30 to 45 minutes most days of the week.
Another critical lifestyle change you can make is to stop smoking
cigarettes. Smoking decreases "good" HDL cholesterol and changes LDL
cholesterol so that it promotes the buildup of deposits on the walls
of your coronary arteries. It also increases the risk of heart
disease.?
http://www.bchealthguide.org/kbase/topic/special/hw115432/sec1.htm
?Therapeutic options for patients with low HDL-C include
treatment with statins, fibrates and nicotinic acid, either as
monotherapy or in combination. Of these options, nicotinic acid is not
only the most potent agent for raising HDL-C but is also effective in
reducing key atherogenic lipid components including triglyceride-rich
lipoproteins (mainly very low-density lipoproteins [VLDL] and VLDL
remnants), LDL-C, and lipoprotein(a). The principal features of the
atherogenic lipid profile in type 2 diabetes and the metabolic
syndrome make them logical targets for nicotinic acid therapy, either
alone or in combination with a statin. The lack of comprehensive
European data on the prevalence of low HDL-C levels highlights a
critical need for education on the importance of raising HDL-C in CHD
prevention and treatment. The development of a reliable and accurate
assay for HDL-C, as well as clarification of criteria for low and
optimal levels of HDL-C in both men and women, constitute critical
factors in the reliable identification and treatment of patients at
elevated risk of CHD due to low HDL-C. Based on the available
evidence, the European Consensus Panel recommends that the minimum
target for HDL-C should be 40 mg/dL (1.03 mmol/L) in patients with CHD
or with a high level of risk for CHD, including patients at high
global risk with type 2 diabetes or the metabolic syndrome.?
?This Australian study has a very positive message for persons who
have to control or lower their LDL-C levels. It is possible to lower
"harmful" LDL-C levels in the blood, without lowering "protective"
HDL-C levels, by using a low-fat diet which is a great deal more
realistic in composition than the very-low-fat diet, provided the diet
is supplemented with monounsaturated fat. Olive oil and products, such
as margarine made from olive oil, can be a useful adjunct to
cholesterol-lowering diets. In Thailand, olive oil is readily NOT
available, AND tends to be rather expensive, while I have personally
not come across margarines made from olive oil.?
http://www.thai-otsuka.co.th/pxnews/0198nl06.htm
?RECENT FINDINGS: The primary genetic determinants associated with
relative HDL-C deficiency states are the ATP binding cassette protein,
ABCA1; apolipoprotein (APO) A1; and lecithin cholesteryl acyl
transferase. Other potentially important candidates invoked in low
HDL-C syndromes in humans include APOC3, lipoprotein lipase,
sphingomyelin phosphodiesterase 1, and glucocerebrosidase. Molecular
variation in ABCAI and APOAI and, in selected cases, lecithin
cholesteryl acyl transferase deficiency have been associated with
increased CHD, whereas two notable variants, APOAIMilano and
APOAIParis, are associated with reduced risk. SUMMARY: Low HDL-C
syndromes have generally been correlated with an increased risk of
CHD. However, single-gene abnormalities responsible for HDL-C
deficiency states may have variable effects on atherothrombotic risk.?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15218400&dopt=Abstract
?Hypoalphalipoproteinemia (HA) includes a variety of conditions,
ranging from mild to severe, in which concentrations of
alpha-lipoproteins or high-density lipoprotein (HDL) are reduced. The
etiology of HDL deficiencies ranges from secondary causes, such as
smoking, to specific genetic mutations, such as Tangier disease and
fish eye disease.
HA has no clearcut definition. An arbitrary cutoff is the 10th
percentile of HDL cholesterol (HDL-C) levels. A more practical
definition derives from the theoretical cardioprotective role of HDL.
The US National Cholesterol Education Program (NCEP) Adult Treatment
Panel III (ATP III) recently redefined the HDL-C level that
constitutes a formal coronary heart disease (CHD) risk factor. The
level was raised from 35 mg/dL to 40 mg/dL for both men and women. For
the metabolic syndrome in which multiple mild abnormalities in lipids,
waist size (abdominal circumference), blood pressure, and blood sugar
increase the risk of CHD, the designated HDL-C levels that contribute
to the syndrome are sex-specific. For men, a high-risk HDL-C level is
still less than 40 mg/dL, but for women, the high-risk HDL-C level is
less than 50 mg/dL.
A low HDL-C level is thought to accelerate the development of
atherosclerosis because of impaired reverse cholesterol transport and
possibly because of the absence of other protective effects of HDL,
such as decreased oxidation of other lipoproteins.
The common, mild forms of HA have no characteristic physical findings,
but patients may have premature coronary heart or peripheral vascular
disease and a family history of low HDL-C levels and premature CHD.
Therapy to raise the concentration of HDL-C includes weight loss,
smoking cessation, aerobic exercise, and pharmacological management
with niacin and fibrates.?
http://www.emedicine.com/med/topic3368.htm
Fish eye disease, an other orphan disease:
http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=650
I hope this has given you a broader knowledge of blood lipids! If not,
please request an Answer Clarification, and allow me to respond,
before rating. I will be happy to assist you further, before you rate.
Regards, Crabcakes
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