Why is your HDL higher than your LDL?

Really low cholesterol levels, HDL and LDL.

• I've read a lot lately about good (HDL) and bad (LDL) cholesterol. I recently went to my doctor and had my blood tested. My total cholesterol is 119, 32 HDL, and 87 LDL. He noted that my total cholesterol level was great, my LDL level was good, but my HDL was low. The ration of my HDL/total cholesterol is 3.72. According to this page: http://www.all-about-lowering-cholesterol.com/cholesterol-level-scale.html The ideal total cholesterol level is less than 200. The ideal HDL is above 50. The ideal LDL level is less than 130. And the ideal ratio of HDL/TOTAL is less than 4.2. My total cholesterol and LDL cholesterol levels are great, but my HDL level is in the red zone (too low). According to this page: http://www.cbsnews.com/stories/2004/03/15/earlyshow/health/main606481.shtml "The American Heart Association says total cholesterol should be less than 200. Levels of good cholesterol should be above 40. Levels of bad cholesterol should be less than 130, or less than 100 if you already have heart disease or diabetes." Again, it looks like I'm great in the total and LDL levels, but not great in the HDL level. From what I can understand researching this subject is that in the past, people would just check their total cholesterol level not knowing about LDL and HDL. This could mislead them if say they had a total level around say 170 and HDL level around 15, they might think they were okay with the low total cholesterol but really they might be in danger. But what about having really, really low cholesterol like I do, but also really low HDL, can this be a problem? Or is it mostly people with high cholesterol that need to make sure they have low LDL? In case it helps, I am 24. I weigh 220lbs with a height of 5'10" and BMI of 31.6, which apparently counts as obese :-(. But I've been exercising more and eating better for the past several months, and really don't feel like the BMI scale is necessarily accurate for me. I don't have high blood pressure, sugar levels in my blood were good, and everything else measured during my physical checked out. The low HDL is just worrying me. (I've already done pretty good google/wikipedia searching, and all i've found are articles which boil down to "High cholesterol isn't necessarily bad as long as a good portion is HDL." I'm looking for information specifically addressing really low LDL cholesteral along with low HDL cholesterol)

• Answer:

  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 Search Terms ============ Raising + serum HDL genetics + low HDL cause + low HDL Blood lipids very low HDL