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What do you know about cholesterol?

Dyslipidemia (or high cholesterol) means that an individual has an overabundance of lipids (fats) in their bloodstream. This is important because high cholesterol levels are linked to an increase in cardiovascular disease and obesity. Cardiovascular disease associated with high cholesterol are due to atherosclerosis or hardening of the arteries that takes place when cholesterol is deposited into the lumen of arteries and begins to limit blood flow to organs of the body. The arteries become more and more occluded over time until the artery can no longer supply an organ with the blood that it needs. This can lead to heart attacks (myocardial infarctions) or even stroke or death.

how-high-cholesterol-causes-atherosclerosis

Image shows as cholesterol plaque grows, it gets harder for blood to pass through.

 

It is important to contact your physician for regular visits to see if you are an at risk patient for high cholesterol. Patients that are in high risk groups should be screened regularly based on the American Heart Association and The American College of Cardiologists guidelines. Any person over the age of two years old who is in a at risk group should see their physician in order to make sure their cholesterol levels are within healthy levels.

Who is at risk? Major risk factors include:

  • Advancing age
  • High total cholesterol levels
  • High LDL
  • High triglyceride levels
  • Established coronary artery disease (CAD)
  • Family history of CAD
  • Presence of hypertension
  • Presence of diabetes mellitus
  • Smoking
  • Obesity
  • Family history
  • Elevated apo B
  • High C-reactive protein
  • Polycystic Ovarian Syndrome
  •  Hyperhomocysteinemia
  • hyperuricemia

Cholesterol is an essential fat that is used to make hormones and is integral in maintaining the integrity of cell membranes. The body makes cholesterol and it is also found in foods like:

  • Animal fats
  • Cheese
  • Egg yolks
  • Shell fish
  • Breast milk

Doctors use three different measures to determine lipid balance:

  1. LDL-Low Density Lipoprotein (bad cholesterol) the higher your LDL level, the higher your risk for cardiovascular disease and plaque formation.
  2. HDL-High Density Lipoprotein (good cholesterol) HDL removes bad cholesterol throughout your body and returns it to your liver so that it can be removed from your body. High HDL is protective and low HDL is linked to cardiovascular disease.
  3. Triglycerides-Fat in the blood. This is the fat that you eat mostly from plant oils and animal fats. Increased triglyceride levels increase the risk of cardiovascular disease by contributing to atherosclerotic plaque formation.

The American Heart Association and American College of Cardiology determine what healthy cholesterol levels are. The table demonstrates the general guidelines of the different types of cholesterols:

Cholesterol-Levels-Chart

Treatments:

While lifestyle and dietary changes like exercise and healthy eating are paramount, medical treatment has been found to be very effective in controlling high cholesterol. Avoid foods like the ones mentioned earlier and exercise regularly if deemed fit by your physician. Some medical treatments available are as follows. Remember, your physician is the only person that can prescribe the correct drug and correct dosage for you based on your own individual blood work: Refer to the pathway below for statin drugs that act by blocking HMG-CoA

cholesterolsynthesis

  • Statins– (atorvastatin, etc.): Statins act by competitively inhibiting HMG-CoA reductase, the first and key rate-limiting enzyme of the cholesterol biosynthetic pathway. Statins mimic the natural substrate molecule, HMG-CoA, and compete for binding to the HMGCR enzyme. This competition slows the rate of mevalonate production, the next molecule in the serial steps to produce cholesterol. Hence, in the presence of statins, the precursor HMG-CoA is not efficiently processed forward to produce mevalonate, blocking the pathway.
  • Fibrates-(Gemfibrozil): activators of the peroxisome proliferator-activated receptor-α (PPARα) in liver and muscle. In the liver this leads to increased β-oxidation of fatty acids (breakdown), thereby decreasing the liver’s secretion of triacylglycerol- and cholesterol-rich VLDLs, as well as increased clearance of chylomicron remnants, increased levels of HDLs and increased lipoprotein lipase activity which in turn promotes rapid VLDL turnover.
  • Niacin-Nicotinic acid:reduces the plasma levels of both VLDLs and LDLs by inhibiting liver VLDL secretion, as well as suppressing the flux of free fatty acid (FFA) release from adipose tissue by inhibiting lipolysis (fat breakdown). In addition, nicotinic administration strongly increases the circulating levels of HDLs. HOWEVER, do not use without contacting your physician first because niacin can cause flushing which can be extremely uncomfortable.
  • Resins-( Cholestyramine or colestipol):These compounds are non-absorbable resins that bind bile acids which are then not reabsorbed by the liver but excreted. The drop in hepatic reabsorption of bile acids releases a feedback inhibitory mechanism that had been inhibiting bile acid synthesis. As a result, a greater amount of cholesterol is converted to bile acids to maintain a steady level in circulation. Additionally, the synthesis of LDL receptors increases to allow increased cholesterol uptake for bile acid synthesis, and the overall effect is a reduction in plasma cholesterol. This treatment is ineffective in homozygous FH patients, since they are completely deficient in LDL receptors.
  • Ezetimibe: This drug is sold under the trade names Zetia® or Ezetrol® and is also combined with the statin drug simvastatin and sold as Vytorin® or Inegy®. Ezetimibe functions to reduce intestinal absorption of cholesterol, thus effecting a reduction in circulating cholesterol.

Latest Research from Up-To-Date:

Specific results from some of the trials of statins include:

●The Scandinavian Simvastatin Survival Study (4S) of patients with hyperlipidemia (baseline plasma total cholesterol levels between 212 and 309 mg/dL [5.5 and 8.0 mmol/L]) found that simvastatin therapy versus placebo for 5.4 years resulted in statistically significant reductions in total mortality (8 versus 12 percent), major coronary events (19 versus 28 percent), CHD deaths (42 percent reduction), revascularization procedures (CABG or coronary angioplasty, 37 percent reduction), and fatal plus nonfatal cerebrovascular events (2.7 versus 4.3 percent)

●The CARE trial treated patients with average cholesterol levels (mean serum total cholesterol concentration of 209 mg/dL [5.4 mmol/L]) with pravastatin (40 mg before sleep) or placebo [5]. At five years, benefits with pravastatin compared with placebo included significant reductions in the combined incidence of coronary death and nonfatal MI (10.2 versus 13.2 percent, p = 0.003), the need for revascularization (14.1 versus 18.8 percent, p<0.001), and the frequency of stroke (2.6 versus 3.8 percent, p = 0.03). The benefits were more apparent among women, older patients (above age 60), and pretreatment serum LDL-C above 125 mg/dL (3.2 mmol/L).

●More recently, the Heart Protection Study randomly assigned 20,536 subjects to simvastatin (40 mg/day) or placebo: 33 percent had baseline LDL-C <116 mg/dL (<3 mmol/L), 25 percent had a level of 116 to 135 mg/dL (3 to 3.5 mmol/L), and 42 percent had levels >135 mg/dL (>3.5 mmol/L) [13]. Entry criteria included a history of cardiovascular disease (coronary cerebrovascular or peripheral vascular disease), diabetes mellitus, or treated hypertension. Thus, most patients were treated for secondary prevention.

After an average follow-up of 5.5 years, there were significant reductions in all-cause mortality (12.9 versus 14.7 percent; relative risk reduction [RRR] 13 percent), deaths from heart disease or related blood vessel disease (7.6 versus 9.1 percent; RRR 17 percent), and major cardiovascular events (19.8 versus 25.2 percent; RRR 24 percent). The percent reduction in events was similar in the three tertiles of baseline LDL-C (the lowest being <116 mg/dL [<3 mmol/L]) and was also similar in those with a baseline LDL-C below 100 mg/dL (2.6 mmol/L).

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