I am not a doctor, scientist, or expert in anything. This content should not be construed as advice or recommendation, but is intended for entertainment and informational purposes only.
High cholesterol causes plaques to build up in the arteries which can cause heart attacks. Cholesterol lowering medications lead to fewer plaques and fewer subsequent heart attacks.
Quite a simplistic explanation on the surface don’t you think? And it sounds like it makes sense.
This is the current hypothesis regarding the prevention and treatment of cholesterol driven heart disease. It’s very… reductionist.
The problem is that this hypothesis has never really been tested. Statins undoubtedly lower LDL, the “bad” cholesterol, but meta-analyses of statin users only show a slight reduction of cardiovascular events yet overall mortality does not change, and for some types of treatments overall mortality actually gets worse.
But the question of whether or not statins prevent or improve plaque development in the arteries has been lightly explored. Remember, the general rule of thumb in pharma world is if you’re afraid of what you might find, you don’t go looking for it.
Some newer data has emerged that calls into question this prevailing lipid hypothesis, and the conventional medical world, unsurprisingly, is not having any of it. Too many careers and egos have been built on, and too many dollars are wrapped up in the conventional hypothesis and corresponding treatments to seriously consider that they could be wrong.
All humans suffer from some degree of perspective myopia, and experts and specialist probably suffer more so as a result of their hyper-focused specializations. As the old saying goes, sometimes we miss the forest for the trees.
But we are a skeptical bunch, and in these digital pages we like to explore this contradictory information to broaden our perspectives. So, we will use our non-expert eyes and common senses to parse some of this information.
As always, I am not making any recommendations, but am only exposing data that the current system finds uncomfortable and would rather you not even consider. It’s why we’re now told to not be self-reliant and think for ourselves, but to blindly follow the almighty experts who are often wrong but never in doubt.
A review of numerous studies was published in 2015 in Clinical Pharmacology. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms explores the evidence that long-term statin use actually increases coronary heart disease (CHD) and heart failure (HF).
One of the interesting graphs early in the paper was related to the results of clinical trials on statins prior to 2004, and the results after 2004 when the EU implemented new penal regulations in regard to clinical trials.
Prior to 2004, clinical trials of statins showed incredibly positive results across the board for primary and secondary prevention of coronary artery events. Clinical trials performed after 2004 show a mixed bag, and overall, no significant benefit in terms of reducing coronary events.
Source: https://cardiacos.net/wp-content/uploads/2019/04/2015-Statins-stimulate-atherosclerosis-and-heart-failure-pharmacological-mechanisms.pdf
It’s important to remember that clinical trials are designed and bankrolled by the drug companies, and then are outsourced to hospitals and testing centers which enroll patients, administer the treatments, and collect the data. The data goes back to drug companies where number crunchers begin to torture the data ensuring that the results they are trying to achieve look as good as possible.
This data is then presented as a study in some journal, and unpaid peer reviewers, who do not get to examine the raw data and want to make sure they get funding for their studies, give it the thumbs up or down.
CoQ10 Deficiency
But back to the premise of the review and the assertions that long-term statin use actually causes CHD and HF. It’s well known that statins deplete CoQ10 which is critical to ATP production. Often times, a CoQ10 supplement is recommend when statins are being prescribed.
Heme A is another biomolecule critical in ATP production that is also depleted by statin use. ATP is the energy produced in the mitochondria of our cells, and is critical to the health and proper functioning of our cells, in particular our muscle and heart cells. Heart failure is a result of CoQ10 and heme A deficiency. A sign of the depletion of CoQ10 and heme A is muscle cramping, a common adverse effect of statins.
Essentially, statins are mitochondrial toxins.
Vitamin K2 Deficiency
Statins also inhibit the conversion of vitamin K1 to K2. K2 is critical because it prevents calcification of soft tissues, especially the arteries. Plants contain a high amount of vitamin K1, but virtually no vitamin K2 with the exception of fermented cabbage and soy in products such as sauerkraut, kimchi, and natto.
While a healthy person can convert some K1 to K2, we really aren't very efficient at doing so. On the other hand animal foods, including meat, organs, eggs, and dairy, tend to contain higher amounts of bioavailable vitamin K2.
Ironically, the current health recommendations for the prevention of heart disease are to limit or avoid the foods that have the best source of vitamin K2, and prescribe treatments that further depletes K2 which is critical to preventing calcification of arteries.
One study the authors mentioned involved performing highly sensitive coronary computer tomography angiograms (CCTA) on 2400 statin users and 4200 non-statin users. None of the participants had any known coronary artery disease. Statin use was “associated with a significant increase in the prevalence and extent of coronary plaques containing calcium.”
One might argue that someone can take supplements to counter the CoQ10 and K2 deficiencies. But let’s look at this another way.
What does a statin have to do with you having heart disease or the potential of having heart disease?
Are we statin deficient? Of course not.
We take this bizarre approach of prescribing some treatment that we would never put in our bodies naturally that depletes critical nutrients required for normal functioning biochemical processes, and avoid foods that contain those same critical nutrients. We then end up creating deficiencies for which we must supplement with less optimal forms of these critical nutrients in order to prevent the very thing we’re trying to prevent with the recommended approach.
I don’t get it. I mean, I get it from a business perspective because it’s incredibly profitable, but I don’t get how this is a good approach for actually improving health.
Cholesterol, Statins, and Mortality
A Japanese interventional study they reviewed showed an increasing risk of all-cause mortality, cancer, and cardiovascular disease once you lowered total cholesterol below 220mg/dL.
Another study done on U.S. veterans showed a higher, and increasing risk of coronary heart disease and diabetes mellitus the longer they took statins. Interestingly, all-cause mortality is lower among the statin user group which is contradictory to meta-analyses of statins. Regardless, this study would suggest that statins increase the risk of the very thing they are supposed to prevent.
Does LDL Block Arteries?
This is the trillion dollar question that until somewhat recently, nobody has really explored even though this is the hypothesis upon which cholesterol lowering medications such as statins are based.
There is an independent study, called The KETO Study, in the works now that has provided some interesting baseline data that calls into question the blanket recommendations of lowering LDL cholesterol.
This study enrolled 100 men who are classified as lean mass hyper responders who have been on a ketogenic (very high fat/very low carbohydrate) diet for an average of 4.7 years. Most people who go on a ketogenic diet do not necessarily experience an elevation in LDL levels, but this particular phenotype experiences a significant increase in LDL.
These participants who were otherwise considered metabolically healthy had an average LDL level of 272, and were recommended statin treatment but had declined. The researchers performed CCTA scans at the start of the trial to determine levels of plaque in their arteries and then will perform another scan after one year.
To get a comparison, they were able to match 80 participants from this study to participants of the Miami Heart Study who are also receiving CCTA scans. The participants of the Miami study had average LDL cholesterol of 127, less than half the average of the participants in the KETO Trial cohort.
The initial scans show no difference between calcium scores, plaques, or stenosis. How can there be no difference between these two groups if elevated LDL causes blockages in the arteries?
In the presentation of the data, the lead author points out a study in Denmark showed that out of 11,000 patients with a lifetime of elevated LDL cholesterol above 190, 50% of the subjects did not have coronary calcium. You can watch the presentation of the baseline data here.
So what gives?
None of this is to say that LDL isn’t somehow involved in blockages, but is cholesterol really the culprit, or is it just an unwitting participant simply doing its job and perhaps exacerbating an underlying condition that is the root cause of the problem?
People with familial hypercholesterolemia, a genetic disorder that results in incredibly high LDL levels, might benefit from cholesterol lowering drugs.
But will lowering LDL in the general population really do much in the long run anyway? The evidence doesn’t point to a major benefit for most people.
This is the problem with reductionism in medicine. The body is far too complex to just throw out blanket treatment recommendations to lower some arbitrary numbers of critical biomolecules that may have little or nothing to do with the actual problem.
How many people have been needlessly damaged by taking medications that weren’t necessary yet carry massive adverse risks?
Unfortunately, the current sick-care business model dictates a one size fits all approach because that is how profits are maximized. In the coming decades, we will begin to realize the vast amount of damage that has been wrought by the conventional medical complex.