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5 + 4 about Good Cholesterol.

Cholesterol, the fat-like substance is the word that most people especially the middle-age group and above hate to hear.

It is a constant advice that we should all cut down or avoid red meats, seafood and products from animal fats because they are high in cholesterol or are high saturated fatty acids which will raise the triglycerides (a form of fat made in the body) and cholesterol levels in the body. However, for most people, without the wonderful delicious pork, beef, mutton, liver, skin of poultry, ham, bacon; drunken prawns, chilly/pepper “Sri Lanka” crabs, “hum/tua tao/lala” (clam), “sotong” (squid, cuttlefish), lobsters; butter, lard, egg yolk, etc., life will be meaningless.

That is just negative which we remembers. The flipped side is that our body needs cholesterol for functions such as making hormones. Besides being found in those products above, it is also produced in our body.

There are good and bad cholesterols. They can’t dissolve in the blood and have to be transported through the bloodstream in different carriers called lipoproteins. Low-density lipoproteins (LDL or “bad” cholesterol) deliver cholesterol to the body, while high-density lipoproteins (HDL or “good” cholesterol) take cholesterol out of the bloodstream to the liver which will then passes them out of the body.

We are told the higher your HDL cholesterol, the better it is. Now, I learned that biological reality is more complex as genes direct the body’s production of HDL and that many of us might not be lucky enough to inherit genes that result in a lot of HDL. Luckily, genes are only part of the story because lifestyle factors and, to a smaller extent, medications can strongly influence HDL levels.

The National Cholesterol Education Program (NCEP) and the American Diabetes Association advise people to aim for HDL levels of at least 40 mg/dL. An even more protective goal, according to the NCEP, is 60 mg/dL or higher.

Why is having high HDL cholesterol is important?

At first, scientists believed that HDL was simply a garbage collector that picked up cholesterol from an artery’s walls and delivered it to the liver for disposal. That’s still considered the main role of HDL, but research is starting to suggest that HDL can help protect the heart in many ways:

  • Reverse cholesterol transport. HDL latches onto LDL embedded in an artery wall, lugs it back into the bloodstream, and carries it to the liver. The liver collects cholesterol from the HDL particles, packages it into bile salts and bile acids, and dumps it into the intestines for excretion.
  • Antioxidant activity. LDL cholesterol in the artery wall is bombarded by oxygen free radicals, which turns it into oxidized LDL cholesterol. Oxidized cholesterol is the stuff that’s actually responsible for arterial damage — and research shows that HDL can help protect LDL cholesterol from free radicals.
  • Anti-inflammatory action. HDL helps to quiet the inflammation of an atherosclerotic plaque. Elevated levels of C-reactive protein (CRP) reflect the inflammation of such a plaque and HDL may neutralize CRP’s tendency to perpetuate the inflammatory cycle.
  • Antithrombotic activity. Plaque rupture triggers the formation of an artery-blocking blood clot. By halting the flow of oxygen-rich blood, the clot kills heart muscle cells (heart attack) or brain cells (stroke). HDL reduces clot formation and accelerates the healing process that dissolves clots.
  • Endothelial function. Blood vessels plagued with atherosclerosis sustain other damage. In particular, the endothelial cells lining the arteries fail to produce normal amounts of nitric oxide, the chemical that allows arteries to dilate (widen) when tissues need more oxygen. HDL helps preserve nitric oxide production and protect endothelial function.

How much does HDL help?

The Framingham Heart Study was responsible for many landmark discoveries about HDL cholesterol, and the Physicians’ Health Study helped confirm that HDL was protective, reporting that various HDL subtypes are all helpful. Data continue to show that the good cholesterol is very good indeed.

  • Heart disease. Low HDL levels are associated with an increased risk of heart attacks, while high levels are protective. According to the Framingham Heart Study, cardiac risk rises sharply as HDL cholesterol levels fall below 40 milligrams per deciliter (mg/dL). In general, each 1 mg/dL rise in an HDL cholesterol level can be expected to cut cardiac risk by 2% to 3%.
  • Stroke. Strokes come in many forms, but the most common type, ischemic stroke, shares many risk factors with heart attack. High HDL cholesterol levels reduce the risk of stroke; in several studies, HDL cholesterol is a much better predictor of risk than LDL cholesterol, particularly in people older than 75.
  • Erectile dysfunction. Normal erections depend on many things, including healthy arteries that produce good amounts of nitric oxide. It’s no surprise, then, that the Massachusetts Male Aging Study found that 16% of men with low levels of HDL cholesterol had erectile dysfunction, but none of the men with the highest levels did.
  • Longevity. Several investigations suggest that high HDL levels are linked to longevity, particularly exceptional longevity. Other research links high levels of HDL cholesterol to preserved cognitive function in old age. More research is needed to learn if HDL deserves the credit or if other genetic factors are responsible.

Ways to raise your HDL

  • Exercise. Exercise is an important way to boost HDL levels. On average, sedentary people who start to exercise regularly can expect their HDL levels to rise by 3% to 20%. The benefit can occur with as little as one mile of walking or jogging a day, but the more you do, the better your result. Brisk walking for 40 minutes a day is a good target, but if you need more help, aim higher.
  • Watch your dietary fats. Saturated fat won’t affect your HDL cholesterol, but it will raise your LDL cholesterol. The latest American Heart Association (AHA) guidelines call for limiting saturated fat to less than 7% of your total daily calories. Reduce your intake of trans fats to less than 1% of your total daily calories. Trans fat lowers HDL cholesterol and raises LDL cholesterol, a double whammy to health. But unsaturated fats like virgin olive oil may boost HDL levels, and the omega 3 fats in fish, nuts, and canola oil may promote cardiac health even if they don’t affect your HDL reading.
  • Watch your carbs! Or at least the types of carbs you’re eating. Diets that provide large amounts of rapidly absorbed carbohydrates are clearly linked to low levels of HDL cholesterol. Avoid highly refined carbohydrates in favor of coarsely ground, whole grain, unrefined carbs like whole grain bread, oatmeal, and beans.
  • Alcohol. Moderate drinking will raise HDL levels by about 4 mg/dL, which should cut cardiac risk by about 10%. This translates to one to two drinks a day for men, and one drink a day for women. For this “prescription,” count 5 ounces of wine, 1½ ounces of liquor, or 12 ounces of beer as one drink.
  • Weight control. Obesity is linked to low HDL levels, but weight loss can help. Exercise and diet are the dynamic duo for weight loss, but shedding excess pounds will boost HDL levels over and above the independent effects of regular exercise and a healthful diet.
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Coffee Drinking Increases Cholesterol

Cafestol, a compound found in coffee, elevates cholesterol by hijacking a receptor in an intestinal pathway critical to its regulation, said researchers from Baylor College of Medicine in a report that appears in the July issue of the journal Molecular Endocrinology. 

In fact, cafestol is the most potent dietary cholesterol-elevating agent known, said Dr. David Moore, professor of molecular and cellular biology at BCM, and Dr. Marie-Louise Ricketts, a postdoctoral student and first author of the report. Cafetiere, or French press coffee, boiled Scandinavian brew and espresso contain the highest levels of the compound, which is removed by paper filters used in most other brewing processes. Removing caffeine does not remove cafestol, however.

Studies by a co-author – Dr. Martijn B. Katan of Vriye Univeriteit Amsterdam, Institute for Health Sciences, The Netherlands – indicate that consuming five cups of French press coffee per day (30 milligrams of cafestol) for four weeks raises cholesterol in the blood 6 to 8 percent.  

However, while the cholesterol increase associated with cafestol had been identified previously, mainly through the work of Katan and his colleagues, the mechanism by which it acted remained a mystery. It was a mystery that Moore and Ricketts decided to address in the laboratory.

For a long time, Ricketts said she was stymied because of paradoxical effects of cafestol in the liver.

However, the discovery of a gene called fibroblast growth factor 15 or FGF 15 opened the door to understanding how cafestol affects farsenoid receptor X or FXR in the intestine. FXR was first identified as a bile acid receptor in studies in several laboratories, including Moore’s.  

“It is part of the body’s own way of regulating levels of cholesterol,” said Ricketts.

Through research in the test tube and in mice, she and Moore found that in the intestine, cafestol activates FXR and induces FGF15, which reduces the effects of three liver genes that regulate cholesterol levels.

While it is still unclear whether cafestol itself reaches the liver, the finding does confirm that the effect of the compound is in the intestine, which is directly involved in the transport of bile acids. 

Moore’s interest in cafestol began several years ago when his wife read an article on coffee’s effect on cholesterol. She suggested that he might change his brewing method, which involved a permanent coffee filter. The paper filters, the article suggested, removed the coffee oils, which contain cafestol.

Moore researched the problem, and found papers by co-author Katan. He was already working on FXR, and began to think about whether cafestol might be affecting that signal in the cholesterol pathway.  

Others who took part in the work include: Mark V. Boekschoten, Guido J.E.J. Hooiveld and Michael Müller of Wageningen University, Division of Human Nutrition, The Netherlands; Arja J. Kreeft, Corina J.A. Moen, Rune R. Frants of Center for Human and Clinical Genetics, LUMC, Leiden, The Netherlands; Soemini Kasanmoentalib of the Department of Medical Statistics, LUMC, Leiden, The Netherlands; Sabine M. Post and Hans MG Princen of TNO Pharma in Leiden, The Netherlands; J. Gordon Porter of Incyte Corporation, Palo Alto, CA.; and Marten H. Hofker of the Department of Pathology and Laboratory Medicine, University Medical Center in Groningen, The Netherlands.

Funding for this study came from the U.S. Department of Agriculture, National Institutes of Health, Wageningen Centre for Food Sciences, the Dutch Organization for Scientific Research and the Netherlands Heart Foundation.

Note: This story was extracted from Science Daily and  adapted from a news release issued by Baylor College of Medicine.