“Getting Around Statins” – Part 2

DRILLING DOWN ON LDL

Friends:

The title of the topic, “Getting around statins.”, begs the question, are there concerns, aside from bestowing numerous studies supporting its well-documented benefits in controlling high cholesterol and reducing the risk of heart disease?

Cholesterol, the building block of all steroid hormones, is made by our bodies and is crucial for our health and survival–a precursor of Vitamin D, which is very much a steroid hormone.

Cholesterol is essential for membrane fluidity and its optimal functioning.

It supports our immune system–especially the bigger, more fluffy LDL particles, which transport cholesterol to tissues but also are barriers to certain bacterial pathogens.

Then what is the key issue and danger of high cholesterol–how and why does cholesterol become a toxic risk factor?

Is LDL a major risk factor for heart disease if it’s high?

Is all LDL dangerous? It gets a lot of negative publicity for being the “bad guy.”

One would think so when getting a blood test.

However, when you get a blood lipid panel test, it is almost always just total cholesterol, LDL, HDL, and Triglycerides.

From this test, it is possible that your physician may prescribe statins if the test, your age, and other health factors suggest an indication based on conventional medical protocol.

However, even if not indicated in your lipid profile test, which gives a total LDL number, it’s really only a great big net capturing everything called LDL.

Sometimes it will include VLDL ( very low-density LDL).

Still, it has nothing really to do with the size and formation of an LDL particle.

One may think, so what?

However, a very specific form in the cholesterol carrier system that is not typically measured separately unless requested is called “small dense” LDL(sdLDL).

This form is far more atherogenic and dangerous than the larger, fluffy buoyant forms of LDL!

To emphasize, a cholesterol test without the context and qualification of the LDL particle, its percentages, and ratios is inadequate and imprecise to create a reliable diagnosis and treatment strategy if needed!

Why You Need to Know More Than Your Basic Cholesterol …https://www.mdvip.com ›

 

“But if your LDL is large and fluffy, it’s much less “bad” than if your LDL is very small and dense. Smaller, denser LDL particles are considered more dangerous because they are much more numerous in the bloodstream, making it easier for plaque to accumulate and cardiovascular disease to develop..”. Feb 1, 2022.”

The sdLDL particles are greatly more susceptible to oxidation. Why important? Because the small dense LDL (sdLDL) easily penetrate into the endothelium tissue walls within arteries and vessels, and once “oxidized,” the body treats them like a foreign invader with inflammation and eroding of the arterial wall.

These are called “foam cells”–a precursor to atherosclerosis–mass of white blood cells, inflammatory cytokines, and immune system activation to attack these aberrant particles continually.

Secondarily, after clotting and inflammation, calcification eventually ensues as an adaptive, compensatory consequence in trying to quell the damage but ultimately becomes a source of pathological changes in itself, creating greater stiffness and rigidity of the blood vessel walls and less durability.

These changes aggravate blood vessels’ ability for flexibility and contribute to high blood pressure problems and risks, often creating more blood turburluene and spontaneous clotting, which could be a progenitor of clots, strokes, aneurysms, and vessel blockages.

Oxid Med Cell Longev. 2017; 2017: 1273042.

Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic DiseasesEkaterina A. Ivanova, 1 Veronika A. Myasoedova,

“Low-density lipoprotein (LDL) plays a key role in the development and progression of atherosclerosis and cardiovascular disease. LDL consists of several subclasses of particles with different sizes and densities, including large buoyant (lb) and intermediate and small dense (sd) LDLs. It has been well documented that sdLDL has a greater atherogenic potential than other LDL subfractions, and sdLDL cholesterol (sdLDL-C) proportion is a better marker for predicting cardiovascular disease than that of total LDL-C. Circulating sdLDL readily undergoes multiple atherogenic modifications in blood plasma, such as desialylation, glycation, and oxidation, further increasing its atherogenicity. Modified sdLDL is a potent inductor of inflammatory processes associated with cardiovascular disease.”

 

But hey, to the rescue would be statins. If we take the statins, that will take care of the situation, correct? Well, not necessarily so at all!

 

Statins may have little effect on the amount of sdLDL, but it appears, what does, in a different pathway, niacin (Vitamin B3) in pharmaceutical amounts.

Statins do not decrease small, dense low-density lipoproteinCheol Ung Choi 1, Hong Seog Seo, Eun Mi Lee,

 

PMID: 20844614

Abstract
“In an observational study, we examined the effect of statins on low-density lipoprotein (LDL) subfractions… Total cholesterol, LDL cholesterol, apolipoprotein B, and the LDL cholesterol/apolipoprotein B ratio were significantly lower in the statin group. However, the proportion of small, dense LDL was higher in the statin group (42.9% ± 9.5% vs. 41.3% ± 8.5%; P=0.046), and the proportion of large, buoyant LDL was lower (23.6% ± 7.5% vs. 25.4% ± 7.9%; P=0.011). In the statin group, persons without coronary artery disease had higher proportions of small, dense LDL, and persons with coronary artery disease tended to have higher proportions of small, dense LDL. Our study suggests that statin therapy–whether or not recipients have coronary artery disease–does not decrease the proportion of small, dense LDL among total LDL particles but, in fact, increases it while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL.”

 

So if all this is true, what is going on?

 

There is little discrimination or motivation in conventional screening protocol to more precisely pinpoint or even understand the actual conspicuous, well-documented culprits, only because of ease, the standard of practice, and expense.

 

Presently medical decisions are made based on broad statistical population “generalizations” and trying to apply them to individuals–oftentimes, a big miss in precision diagnosis and treatment strategies unless you would work with a highly trained specialist even beyond most well-intended internists or cardiologists.

 

The present technique makes the “net” big enough to capture all those LDL variants, even with sdLDL grossly, then incidentally skews the statistics to look more favorable in the drug’s efficacy.

 

So does this mean statins should not be used in medicine?

 

Absolutely not–it’s powerful with purpose and benefits but needs to have far more precision in its use either alone, with other drugs, and ideally, as we will discuss later in a follow-up article, with natural synergistic compounds, as practiced far more in Complementary Medicine than Traditional Standard Medicine that is essentially and conveniently over protocol-oriented because of medical-legal fears.

 

But statins offer a double edge sword and cannot be taken for granted by just looking at one disease factor with “tunnel vision” to inhibit the de novo synthesis of cholesterol.

 

Now that we have a huge population of users, new findings have come to light. The interesting and meaningful relationship that needs much more research is that there appears to be an effect on bone. Low-dosage statins have some evidence to help bones, but higher amounts exacerbate bone loss.

 

The mechanism is logical and not really surprising if one considers health more holistically since cholesterol carries the structure for all steroid hormones. When low, less estrogen and androgen are synthesized de novo, so bingo, perhaps fewer sex hormones that affect muscle mass and bones?

 

The Annals of the Rheumatic Diseases study investigated nearly the whole population of Austria. Altogether, the researchers analyzed health data from the start of 2006 to the end of 2007 on 7.9 million people. They compared rates of osteoporosis diagnosis in statin users with those who had never used statins. They looked at the effect of different doses of lovastatin, pravastatin, rosuvastatin, and simvastatin.

The comparison revealed lower rates of osteoporosis diagnoses among low-dose statin users and higher rates among high-dose users.

The team defined low-dose statin use as up to 10 milligrams (mg) per day.“In the lower dose groups,” says Dr. Alexandra Kautzky-Willer, senior study author and head of the Gender Medicine Unit at the University of Vienna in Austria, “there were fewer osteoporosis cases than expected.” “With doses of 20 mg and more, however, the tide seems to turn,” she adds, explaining, “We found more osteoporosis cases in patients treated with simvastatin, atorvastatin, and rosuvastatin than expected.” The analysis also showed that the effect got stronger as the dose increased.

But let’s remember this subject, its complexities, nuances of manifestations, and even the advances in treating hyperlipidemia and hypolipidemia more rarely can become immensely complicated.

 

However, there are enough concerns with statins, with enough people, especially many kinds of intolerances, including muscle pain, perhaps engendering more susceptibility to diabetes, and cognitive effects, for the pharmaceutical industry to create alternatives–even now early on, specific monoclonal antibodies to help slow-down production and synthesis within the cholesterol-manufacturing gene sites.

 

Another upcoming example is NEXLIZET — a prescription medicine that contains two cholesterol-lowering medicines, bempedoic acid, and ezetimibe.

 

It is used, along with diet and other lipid-lowering medicines, in treating adults who need additional lowering of “bad” cholesterol (LDL-C) and have intolerances to statins.

 

However, even if less provocative in its range of symptoms than statins, it still has its own noted, important and very important side effects that must be carefully and absolutely considered before taking this drug!

 

It is unknown as of yet whether NEXLIZET can decrease problems related to high cholesterol, such as heart attacks or strokes.

 

It works further up in enzyme inhibtion of cholesterol LDL synthesis ( HMG-Coenzyme A) than statins with fewer side effects, but that does not mean any less intense or important side effects that can be very significant to your overall health.

 

Do you think this is the answer?

 

Can we use this with natural therapies, a smart diet, exercise, and fewer statins?

 

For sure, this makes for much more immediate sense, and all this is open for rich and much-needed exploration.

 

Ideally, and perhaps, very much up to us, it will be really motivating with more serious discussion, to use less expensive and remarkably efficacious natural compounds, diet, and lifestyle, with more minimal use of pharmaceuticals as or if needed, as the basis of a treatment strategy, not only for stubborn and challenging cholesterol issues but also for a whole host of health ailments.

 

My sequel’s next article will look at natural substances such as botanicals and some interesting facts about specific foods and how these may tie together.