New cholesterol drugs could be more effective than statins

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A new class of cholesterol drugs is being developed. Preliminary research suggests that the drugs reduce levels of "bad" cholesterol more effectively than anything currently available, and significantly reduce the risk of heart attacks and stroke. The drugs have the potential to be more effective than statins, which are the currently the most common cholesterol-lowering drug. But it has not been proved that statins reduce the risk of heart disease in stroke. Furthermore, recent research has indicated that statins may increase the risk of type 2 diabetes. Heart diseases is one of the most common diabetic complications. One study concluded that statins increase the risk of type 2 diabetes by 46 per cent. The new drugs, known as evulocumab and alirocumab, reduce levels of low-density lipoprotein in the body, potentially by as much as 60 per cent. The drugs could be more effective than statins. Both drugs inhibit PCSK9, which is a protein responsible for the regulation of cholesterol.

11 Replies

  • Hi .

    Whenn do you think this drug would be avalaiblethanks ben

  • There are PCSK9 trials underway in the UK. So at least 1 year.

    If you have FH diagnosed by genetic testing (ie, one or more mistakes in your DNA), and are on maximum possible statin & other treatments, have a word with your lipidologist to see if you can get on the trial.

  • Thanks for the info. I dont think it helps here im from the uk .but live in lithuania with my lithuanian wife,and the medical departments here are wellbehind other countries but once again many thanks to you

  • Please check with your GP.

  • Thanks bala.

  • Or you could eat healthily by keeping your carbohydrate intake below what you use in a day, which lowers the harmful VLDL; aiding, not impairing your body functions.

  • "VLDL" ??? WTF (What the *uck )is that ???

    Please explain in plain English as most of us only understand that language

  • Very Low Density Lipoprotein. Usually when they give you test results, they only calculate LDL and don't break it down further. There are schools of thought that vLDL is the most harmful or even the only harmful component.

    Personally, varying my carbohydrate intake seemed to do nothing beyond slowly varying my weight, but I seem to have Familial Hypercholesterolaemia (inherited high cholesterol) so there may be something else at work.

    Please try not to swear. I know it can be frustrating reading some of the more... eh... enthusiastic promoters of some views.

  • Very Low Density Lipoprotein, as opposed to the harmless large-fluffy LDL that saturated fat can increase (along with the beneficial HDL).

  • And there is more

    Very-low-density lipoprotein (VLDL) cholesterol is a type of lipoprotein. Although you may hear about VLDL, your VLDL level usually isn't reported to you as a part of a routine cholesterol screen.

    There are several types of cholesterol, each made up of lipoproteins and fats. Each type of lipoprotein contains a mixture of cholesterol, protein and a type of fat (triglyceride), but in varying amounts.

    Of the lipoprotein types, VLDL contains the highest amount of triglyceride. Because it contains a high level of triglyceride, having a high VLDL level means you may have an increased risk of coronary artery disease, which can lead to a heart attack or stroke. Higher amounts and large VLDL particles are also associated with an increased risk of high blood pressure and stroke.

    There's no simple, direct way to measure VLDL cholesterol, which is why it's normally not mentioned during a routine cholesterol screening. VLDL cholesterol is usually estimated as a percentage of your triglyceride value. A normal VLDL cholesterol level is between 5 and 30 milligrams per deciliter.


  • And More:

    The chylomicrons are transported via the intestinal lymphatic system and enter the blood stream at the left subclavian vein. During circulation throughout the body, triacylglycerols are removed by the peripheral tissues, by endothelial-bound lipoprotein lipase with entry of fatty acids into muscle for energy production and adipocytes for storage. However, the apo B48 remains with the residual particle. The chylomicrons also contain some apo A1, which is only synthesised in the intestines, but this is transferred spontaneously to the HDL as soon as the chylomicrons reach the circulation. Transfer of apo E and apo C in the reverse direction from the HDL to the surface of the chylomicrons occurs at the same time. The depleted or ‘remnant’ chylomicrons, containing the dietary cholesterol, apo E and apo B48 mainly, eventually reach the liver where they are cleared from the circulation by a receptor-mediated process that requires the presence of apo E.

    Chylomicron and VLDL metabolism

    The triacylglycerols of the remnant chylomicrons, together with cholesterol and cholesterol esters, are secreted by the liver into the circulation in the form of VLDL, which contain one molecule of the full-length form of apo B, apo B100. In addition, an appreciable amount of triacylglycerol in VLDL is synthesised in the liver from free fatty acids reaching it from adipose tissue via the plasma in the post-absorptive and fasted states. In effect, VLDL serve to buffer the plasma free fatty acids released following lipolysis in adipose tissue in excess of the requirements of muscle and liver.

    Within the liver, the nascent VLDLs are synthesised in the endoplasmic reticulum and are transported to the Golgi in a complex multistep process, involving a specific VLDL transport vesicle. In the lumen of the cis-Golgi lumen, VLDLs undergo a number of essential modifications before they are transported to the plasma membrane and secreted in the circulatory system. The surface layer of the newly synthesised VLDL is enriched in phosphatidylethanolamine, which rapidly exchanges with the phosphatidylcholine of other lipoproteins. The newly synthesised VLDL contain a little apo C, but they rapidly take up more (10-20 molecules of apo C2) and apo E from HDL after a few minutes in the circulation. The small amount of apoA1 of intestinal origin is transferred to HDL.

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