3statins

Statins

Update in November 2024

I have a GRG colleague who disagrees and believes the evidence supports the use of statins.

Updates from June 2023.

Cholesterol fraud and statin harm

I just spoke to a cardiologist alum of Carleton College Dr. Dubroff, who sent me topic medical journal articles he has written the past few years showing that cholesterol levels are unrelated to risk of heart disease, that statins do not reduce the risk of heart attacks, and that statins have many harmful side effects that increase the risk of heart disease, cancer, depression, and more. I encourage you to read these and bring them to your physicians.

You may be old enough to recall when ulcers were caused by stress, and we should just learn to relax.  It took 20 years before medicine accepted the discovery that ulcers are caused by a bacterial infection that can be cured by antibiotics, or peptobismol!

Today we are learning that heart disease risk can be reduced by lifestyle change – diet and exercise – NOT by statins, whose use just benefits pharmaceutical companies.  Here is the new evidence. Links are to published medical journal articles:

If this convinces you to consider to stop taking statins, here is a doctor’s suggestion how to check.

1. Over the past 10 years cholesterol levels have been falling while the number of Americans dying of heart disease has been steadily climbing. This apparent paradox compels us to question whether lowering cholesterol is the best way to prevent coronary heart disease.
2. Cholesterol Paradox: a correlate does not a surrogate make: The global campaign to lower cholesterol by diet and drugs has failed to thwart the developing pandemic of coronary heart disease around the world. Some experts believe this failure is due to the explosive rise in obesity and diabetes, but it is equally plausible that the cholesterol hypothesis, which posits that lowering cholesterol prevents cardiovascular disease, is incorrect. The recently presented ACCELERATE trial dumbfounded many experts by failing to demonstrate any cardiovascular benefit of evacetrapib despite dramatically lowering low-density lipoprotein cholesterol and raising high- density lipoprotein cholesterol in high-risk patients with coronary disease. This clinical trial adds to a growing volume of knowledge that challenges the validity of the cholesterol hypothesis and the utility of cholesterol as a surrogate end point. Inadvertently, the cholesterol hypothesis may have even contributed to this pandemic.
3. Fat or fiction: the diet- heart hypothesis -The preponderance of evidence indicates that low-fat diets that reduce serum cholesterol do not reduce cardiovascular events or mortality. Specifically, diets that replace saturated fat with polyunsaturated fat do not convincingly reduce cardiovascular events or mortality. These conclusions stand in contrast to current testimony to the contrary, a behaviour called confirmation bias. Others have noted the limitations of targeting a single risk factor potentially lead to heart disease. There are several possible explanations. Foremost, we must consider that the diet-heart hypothesis is invalid or requires modification. Moreover, some experts may selectively cite evidence that validates their own viewpoint while disregarding evidence-based medicine opinion and debate.

Over the past 10 years cholesterol levels have been falling while the number of Americans dying of heart disease has been steadily climbing. This apparent paradox compels us to question whether lowering cholesterol is the best way to prevent coronary heart disease. A number of recent studies suggest that cholesterol, specifically LDL- C, may not be a primary risk factor for coronary heart disease and other markers, such as insulin resistance or remnant cholesterol, may be much more important. Furthermore, therapies designed to prevent coronary heart disease by lowering cholesterol with drugs or diet have yielded inconsistent results. Despite the widespread utilization of cholesterol-lowering statins in Europe, observational studies indicate that there has been no accompanying decline in coronary heart disease deaths. This new evidence should give us pause as we try to understand why the campaign to prevent heart disease by lowering cholesterol has not achieved its goals.

4. The Fallacy of OTC Statin Therapy – The report by Nissen et al (1) confirms that consumers eligible for nonprescription rosuvastatin therapy can be reliably identified through technology-assisted self-selection. Whether over- the-counter statin therapy for primary prevention would positively affect public health is debatable. We already have an over-the-counter preventive therapy for cardiovascular disease that is highly effective, widely available, and has no risk. It is called a healthy lifestyle and was completely ignored in this paper. The simplicity of taking a statin pill is likely to fuel patients’ complacency about being “protected” from heart disease, at the expense of engaging in more protective lifestyle interventions.
5. The health risk to you from taking a statin– Muscle Pain and Weakness, neuropathy, heart failure, dizziness, cognitive impairment, cancer, pancreatitis, and depression.

PRIOR TO JUNE 2023: I was recently asked to investigate information for a doctor to consider when deciding whether someone should take a statin to reduce cholesterol.  Here are the results from the scientific literature:

1. Background on cholesterol

Cholesterol is actually a class of molecules that exist in many forms to transport fat through our bloodstreams.  Most well known are HDL and LDL. High Density Lipoproteins – Lipo means fat, particularly cholesterol.  So lipoproteins are proteins that bind cholesterol.  Proteins are denser than cholesterol, like water vs. oil. Proteins binding more cholesterol are less dense.  LDL binds lots of cholesterol, HDL has much less cholesterol.  LDL transports cholesterol from your liver to your body, HDL takes it out of your body to the liver for elimination from your body.  So basically HDL is good, LDL is bad.

But what is worst is oxidized LDL.  Lipoproteins contain vitamin E, an antioxidant vitamin that is fat soluble, so it can prevent the cholesterol in LDL from being oxidized.  But if you have free radicals, loose electrons from a poor diet or lack of vitamins C and E, then the LDL gets oxidized.  Oxidized LDL is sticky, like when you whip cream.  The ox-LDL sticks to your artery walls – in the body and brain – leading to plaque, causing strokes and heart disease. Plaque begins forming at about age 4.  If you get enough antioxidants through diet and supplements, and reduce free radicals by avoiding saturated fat, you will be much healthier.

But it is currently too expensive for doctors to test ox-LDL in your body.  They used to just measure total cholesterol, but now are able to measure HDL and LDL separately.  The ratio of LDL to HDL is vital.  You want more HDL, and less LDL.  Exercise and fish oil in particular raise HDL.  Saturated fat – red meat and fried foods – raise LDL.  According to StatPearls, you should try to keep your cholesterol ratio LDL/HDL below 5, with the ideal cholesterol ratio being 3.5. Note this may have a large effect on whether you need statins to lower cholesterol.  If your ratio is 3.5, you may not need statins.

2. What is a safe cholesterol level?

People are considered to have high cholesterol (“hypercholesterolemia”) when certain levels are exceeded. From NIH, high cholesterol levels are not a medical condition on their own. Also, there are different opinions on what is considered to be too high. It is important to remember that high cholesterol is just one of many risk factors for cardiovascular disease. This means that cholesterol levels alone tell us little about a person’s risk. The risk of cardiovascular disease can only be properly assessed if all the factors are considered together: Age, gender, family history, smoking, blood pressure, HDL and LDL levels.  There is some disagreement about when cholesterol levels are “too high.”

The evidence derived from large observational studies, including the Framingham Study,²² the LRCP²³ and the PROCAM,^24,25 suggests that the total/HDL cholesterol ratio is a more powerful coronary risk predictor than independently-used total cholesterol, LDL cholesterol and HDL cholesterol. The greatest risk was observed in subjects with an LDL/HDL ratio >5 and triglycerides >200 mg/dL (2.24 mmol/L). In the placebo group of the AFCAPS/TexCAPS study,²⁷ baseline LDL cholesterol had no predictive value for the incidence of coronary events, whereas predictive value was found in HDL cholesterol and the total/HDL cholesterol and LDL/HDL cholesterol ratios, both with greater significance than HDL cholesterol by adjusted logistic regression. The total/HDL cholesterol index is therefore a good predictor of cardiovascular risk irrespective of other factors.

In general: The higher the ratio, the higher the risk. Most healthcare providers want the ratio to be below 5:1. A ratio below 3.5:1 is considered very good.  So if your HDL level is 100, you are fine if your total cholesterol is 350!

3. Are statins safe? By Mayo Clinic Staff

Doctors often prescribe statins for people with high cholesterol to lower their total cholesterol and reduce their risk of a heart attack or stroke. While statins are highly effective and safe for most people, they have been linked to muscle pain, digestive problems and mental fuzziness in some people who take them and may rarely cause liver damage.

One of the most common complaints of people taking statins is muscle pain. You may feel this pain as a soreness, tiredness or weakness in your muscles. The pain can be a mild discomfort, or it can be severe enough to make your daily activities difficult.

4. Are statins effective?

The results of this systematic review and meta-analysis indicate that use of statins, in moderate doses, lowered LDL-C levels 20% to 40% and reduced CHD mortality or nonfatal MI 25%, all-cause mortality 16%, and CHD mortality 23%.
The University of Zurich researchers used a computer model to assess the 10-year risk for cardiovascular disease “at which statins provide at least a 60 percent Trusted Source probability of net benefit.”

But in a Swiss study, they adjusted the results to take out any effects from “competing risk” of death that was not due to cardiovascular disease, as well as “baseline risk, frequencies of and preferences for statin benefits and harms.” The harms that they included in their calculations were “adverse events,” such as myopathy (muscle weakness), liver dysfunction, and onset of diabetes. The results showed that the 10-year cardiovascular risk thresholds at which benefits of statin use exceed the harms are consistently higher than those recommended in the guidelines.

For instance, in the case of men aged 70–75 years with no history of symptoms, the harms of taking statins were greater than the benefits until the risk of developing cardiovascular disease over 10 years was over 21 percent. For women aged 70–75 years, the 10-year risk required for benefit to outweigh harms was 22 percent.

A 2016 reviewTrusted Source published in The Lancet claims that the side effects of taking statins are widely exaggerated, and that the drugs are safe and effective. The review concluded that the benefits of statins outweigh the risks of an adverse reaction.

Most people with high cholesterol who start taking statins will need to do so for the rest of their lives. However, some may be able to stop if they successfully lower their cholesterol levels through diet, weight loss, exercise, or some other means.

Cholesterol structure

mar ‘22 – Our results are in agreement with the existing evidence about positive association between statins, vascular calcification, and increase on oxidized phospholipids that are harmful to life.

feb ‘22-Here is an article that reviews several studies involving statins. The summary is that statins do not reduce mortality. They do reliably reduce cholesterol levels, but there is a major debate as to whether this is helpful for overall health, cardiovascular or otherwise. https://sebastianrushworth.com/2020/07/28/do-statins-save-lives/

They do, indeed, reduce negative outcomes (19% to ≤ ~33%, at the cost of “bruised” or damaged mitochondria. The inhibition of cellular synthesis triggers & the limited upregulation of the Apo-B (LDL-P)-Receptors (mainly hepatic) with a small, but limited reduction in Apo-B (LDL-P) a.k.a. the atherogenic particles, which is what is the core driver of the disease process.

This can predispose Brain/CNS tissue to damage, resulting in memory loss & a potential acceleration of dementia-Alzheimer’s. The brain/CNS has no Apo-B (LDL-P)-Receptors, so inhibiting synthesis leaves these tissues particularly vulnerable.

2 common lipid disorders [in my opinion] should never receive statin therapy:

– Elevated Lp(a)

– Elevated serum xenosterols (plant sterols/cholesterol)

Not only does statin monotherapy provide ANY benefit, the data shows a clear pattern of INCREASED CV risk. Both parameters, when measured, INCREASE substantially with statin use.

‘20 – It has long been controversial whether or not a longevist, even one who fully guards against the negative cardiovascular effects of high cholesterol levels, should still take statins or not. The main reason for the negativity of most longevists toward statins (including me) is because statins inhibit the mevalonate pathway which is the same pathway that produces CoQ10, a very necessary mitochondrial compound. Because of this I have always recommended to anyone taking statins that they should generously supplement CoQ10.

However, the following review is a very complete review of the anti-aging benefits of statins which has started to cause me to change my mind about them, as long as I continue to take ample CoQ10 at the same time.

Effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on ageing: Molecular mechanismshttps://doi.org/10.1016/j.arr.2020.101024 Accumulating evidence has documented several pleiotropic
effects of statins in addition to their lipid-lowering properties. Recently, several studies have highlighted that statins may have the potential to delay the ageing process and inhibit the onset of senescence.

BUT A 2021 ARTICLE STATES THAT STATINS CAUSE HEART ATTACKS BY CALCIFYING ARTERIES! Our results are in agreement with the existing evidence about positive association between statins and vascular calcification. They enlighten to a certain extent the possible mechanisms through which statins may enhance calcium accumulation in arterial wall, namely, by inhibition of vitamin K dependent proteins and functions involved in vascular protection.

(see my essay on cholesterol with link to the statin paper)  https://nutritioninvestigator.org/cholesterol